PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 11909638-7 2002 Retinoic acid, a vitamin A (retinol) metabolite, which alone had little effect on the HSP27 level, markedly enhanced the HSP27 accumulation stimulated by TGF-beta. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 154-162 15389595-0 2005 Regulation of proliferation and migration in retinoic acid treated C3H10T1/2 cells by TGF-beta isoforms. Tretinoin 45-58 transforming growth factor, beta 1 Mus musculus 86-94 15389595-8 2005 C3H10T1/2 cells treated with all-trans-retinoic acid (ATRA) and expressing relatively higher levels of osteoblastic gene markers such as alkaline phosphatase and collagen type I, lower levels of chondrocytic gene markers collagen type II and aggrecan, and unchanged levels of the adipose marker adipsin did not demonstrate significant chemokinesis or chemotaxis in response to TGF-beta1 or -beta3 at concentrations ranging from 10(-12) to 10(-9) g/ml. Tretinoin 54-58 transforming growth factor, beta 1 Mus musculus 377-396 12801520-9 2003 Retinoic acid, which alone failed to affect VEGF synthesis, markedly enhanced the VEGF synthesis stimulated by TGF-beta. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 111-119 12801520-10 2003 Retinoic acid enhanced the TGF-beta-increased levels of VEGF mRNA. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 27-35 12801520-11 2003 The amplifications by retinoic acid of TGF-beta-increased VEGF synthesis and levels of VEGF mRNA were reduced by PD98059 or SB203580. Tretinoin 22-35 transforming growth factor, beta 1 Mus musculus 39-47 12801520-12 2003 The combination of PD98059 and SB203580 almost completely suppressed the enhancement by retinoic acid of VEGF synthesis induced by TGF-beta. Tretinoin 88-101 transforming growth factor, beta 1 Mus musculus 131-139 12801520-13 2003 Taken together, our results strongly suggest that both p44/p42 MAP kinase and p38 MAP kinase take part in TGF-beta-stimulated VEGF synthesis in osteoblasts, and that retinoic acid upregulates the VEGF synthesis. Tretinoin 166-179 transforming growth factor, beta 1 Mus musculus 106-114 11909638-8 2002 Retinoic acid enhanced the TGF-beta-induced increase of mRNA for HSP27. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 27-35 11909638-9 2002 The amplification of TGF-beta-stimulated HSP27 accumulation by retinoic acid was reduced by PD98059 or SB203580. Tretinoin 63-76 transforming growth factor, beta 1 Mus musculus 21-29 10432387-13 1999 TGF-beta1 levels in mesangial cells stimulated with LPS/IFN-gamma in presence of ATRA or 13-cis-RA were also reduced indicating that TGF-beta1 did not mediate the suppressive effect of retinoids on iNOS. Tretinoin 81-85 transforming growth factor, beta 1 Mus musculus 0-9 10716749-0 2000 Treatment with all-trans-retinoic acid decreases levels of endogenous TGF-beta(1) in the mesenchyme of the developing mouse inner ear. Tretinoin 15-38 transforming growth factor, beta 1 Mus musculus 70-81 10716749-2 2000 METHODS: In this study, we examine the effects of atRA exposure on the endogenous expression of transforming growth factor-beta(1) (TGF-beta(1)), a signaling molecule that mediates the epithelial-mesenchymal interactions that guide the development of the capsule of the inner ear. Tretinoin 50-54 transforming growth factor, beta 1 Mus musculus 96-130 10716749-2 2000 METHODS: In this study, we examine the effects of atRA exposure on the endogenous expression of transforming growth factor-beta(1) (TGF-beta(1)), a signaling molecule that mediates the epithelial-mesenchymal interactions that guide the development of the capsule of the inner ear. Tretinoin 50-54 transforming growth factor, beta 1 Mus musculus 132-143 10716749-4 2000 Consistent with these in vivo findings, high-density cultures of E10.5 periotic mesenchyme plus otic epithelium, treated with doses of atRA that suppress chondrogenesis, showed significantly decreased levels of TGF-beta(1), as compared with TGF-beta(1) levels in untreated control cultures. Tretinoin 135-139 transforming growth factor, beta 1 Mus musculus 211-222 10716749-4 2000 Consistent with these in vivo findings, high-density cultures of E10.5 periotic mesenchyme plus otic epithelium, treated with doses of atRA that suppress chondrogenesis, showed significantly decreased levels of TGF-beta(1), as compared with TGF-beta(1) levels in untreated control cultures. Tretinoin 135-139 transforming growth factor, beta 1 Mus musculus 241-252 11669453-5 2001 Thus, a putative TGF-beta Inhibitory Element (TIE) adjacent to the retinoic acid response element (RARE) in the RAR-beta promoter is either non-functional, or requires promoter/enhancer elements not present in the promoter construct used in these experiments. Tretinoin 67-80 transforming growth factor, beta 1 Mus musculus 17-25 9839358-7 1998 The interactions between RA and TGF-beta s were very complex. Tretinoin 25-27 transforming growth factor, beta 1 Mus musculus 32-40 9839358-10 1998 Differential regulation was evident, because RA treatment resulted in an increase in TGF-beta 1 mRNA steady levels followed by a decrease in the intracellular and extracellular forms of TGF-beta 1 protein. Tretinoin 45-47 transforming growth factor, beta 1 Mus musculus 85-95 9839358-10 1998 Differential regulation was evident, because RA treatment resulted in an increase in TGF-beta 1 mRNA steady levels followed by a decrease in the intracellular and extracellular forms of TGF-beta 1 protein. Tretinoin 45-47 transforming growth factor, beta 1 Mus musculus 186-196 9839358-12 1998 The increases in mRNA steady-state levels for TGF-beta 2 and TGF-beta 3, as for TGF-beta 1, were rapid and transient in nature, again arguing for direct mediation by RA. Tretinoin 166-168 transforming growth factor, beta 1 Mus musculus 80-90 9731743-0 1998 Differential expression and biological activity of retinoic acid-induced TGFbeta isoforms in embryonic palate mesenchymal cells. Tretinoin 51-64 transforming growth factor, beta 1 Mus musculus 73-80 9731743-1 1998 The effect of retinoic acid (RA) on TGF-beta mRNA expression and protein production in murine embryonic palate mesenchymal (MEPM) cells was examined by Northern blotting and TGF-beta bioassay in association with TGF-beta isoform-specific neutralizing antibodies. Tretinoin 14-27 transforming growth factor, beta 1 Mus musculus 36-44 9731743-11 1998 These data demonstrate a role for RA and RA-induced TGF-beta in the regulation of palate cell proliferation and GAG synthesis and suggest a role for TGF-beta in retinoid-induced cleft palate. Tretinoin 41-43 transforming growth factor, beta 1 Mus musculus 52-60 9731743-1 1998 The effect of retinoic acid (RA) on TGF-beta mRNA expression and protein production in murine embryonic palate mesenchymal (MEPM) cells was examined by Northern blotting and TGF-beta bioassay in association with TGF-beta isoform-specific neutralizing antibodies. Tretinoin 29-31 transforming growth factor, beta 1 Mus musculus 36-44 9731743-9 1998 Coincubation of heat-activated CM from RA-treated MEPM cells with pan-specific or TGF-beta2 or beta3-specific neutralizing antibodies partially relieved the inhibitory effect on 3H-thymidine incorporation, suggesting that this proliferative response was due to RA-induced TGF-beta. Tretinoin 39-41 transforming growth factor, beta 1 Mus musculus 82-90 9070313-0 1997 Retinoic acid induces the expression of germ-line C alpha transcript mainly by a TGF-beta-independent mechanism. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 81-89 9537245-8 1998 Because up-regulated expression of TGF-beta1 suppresses papilloma formation, these studies suggest a mechanism whereby RA can prevent papilloma eruption via a TGF-beta intermediate, but papillomas resistant to RA may have altered TGF-beta signaling and progress to carcinomas at an increased frequency. Tretinoin 119-121 transforming growth factor, beta 1 Mus musculus 35-44 9537245-8 1998 Because up-regulated expression of TGF-beta1 suppresses papilloma formation, these studies suggest a mechanism whereby RA can prevent papilloma eruption via a TGF-beta intermediate, but papillomas resistant to RA may have altered TGF-beta signaling and progress to carcinomas at an increased frequency. Tretinoin 119-121 transforming growth factor, beta 1 Mus musculus 35-43 9537245-8 1998 Because up-regulated expression of TGF-beta1 suppresses papilloma formation, these studies suggest a mechanism whereby RA can prevent papilloma eruption via a TGF-beta intermediate, but papillomas resistant to RA may have altered TGF-beta signaling and progress to carcinomas at an increased frequency. Tretinoin 119-121 transforming growth factor, beta 1 Mus musculus 159-167 9070313-8 1997 These results suggest that the major induction pathway of I alpha C alpha was not mediated by active TGF-beta and that RA at physiological concentrations may be involved in IgA isotype switching in vivo in a TGF-beta-independent manner. Tretinoin 119-121 transforming growth factor, beta 1 Mus musculus 208-216 7497526-10 1995 These findings suggest that RA induces IgA production by (IL-5 + LPS)-stimulated B-cells in TGF-beta-independent and TGF-beta-dependent manners. Tretinoin 28-30 transforming growth factor, beta 1 Mus musculus 92-100 7497526-10 1995 These findings suggest that RA induces IgA production by (IL-5 + LPS)-stimulated B-cells in TGF-beta-independent and TGF-beta-dependent manners. Tretinoin 28-30 transforming growth factor, beta 1 Mus musculus 117-125 8370078-9 1993 TGF-beta activity in the culture medium was also determined, finding that RA rapidly stimulates secretion of biologically active TGF-beta, the elevation being evident after 1 day of culture. Tretinoin 74-76 transforming growth factor, beta 1 Mus musculus 0-8 8585424-2 1995 We hypothesize that the expression of this more osteoblastic phenotype subsequent to RA exposure is the result of the treated cell"s extracellular matrix (ECM) becoming a repository and active source of putative osteoinductive growth factors including, specifically, select members of the TGF-beta superfamily. Tretinoin 85-87 transforming growth factor, beta 1 Mus musculus 289-297 7556459-1 1995 We have previously shown that both transforming growth factor-beta (TGF-beta) and retinoic acid (RA) regulate the expression of cellular retinoic acid binding proteins (CRABP) I and II and TGF-beta 3 mRNAs in primary cultures of murine embryonic palate mesenchymal (MEPM) cells. Tretinoin 137-150 transforming growth factor, beta 1 Mus musculus 68-76 7556459-4 1995 Induction by 3.3 microM RA was abrogated by simultaneous treatment with TGF-beta 1 (5 ng/ml). Tretinoin 24-26 transforming growth factor, beta 1 Mus musculus 72-82 7547504-9 1995 In contrast, the osteoinductive effect of matrix from retinoic acid-treated cells was blocked with both vgr-1 and TGF-beta 1 antibodies, suggesting that TGF-beta 1 may act prior to vgr-1 during osteoblastic differentiation. Tretinoin 54-67 transforming growth factor, beta 1 Mus musculus 114-124 7547504-9 1995 In contrast, the osteoinductive effect of matrix from retinoic acid-treated cells was blocked with both vgr-1 and TGF-beta 1 antibodies, suggesting that TGF-beta 1 may act prior to vgr-1 during osteoblastic differentiation. Tretinoin 54-67 transforming growth factor, beta 1 Mus musculus 153-163 8370078-9 1993 TGF-beta activity in the culture medium was also determined, finding that RA rapidly stimulates secretion of biologically active TGF-beta, the elevation being evident after 1 day of culture. Tretinoin 74-76 transforming growth factor, beta 1 Mus musculus 129-137 2087681-12 1990 RA exposure altered the expression of TFG-alpha, TGF-beta 1, and TGF-beta 2, but significant effects on EGF were not found. Tretinoin 0-2 transforming growth factor, beta 1 Mus musculus 49-59 8385738-3 1993 Because transforming growth factor-beta (TGF beta) superfamily members, including the different TGF beta isoforms and the bone morphogenetic proteins (BMPs), are thought to play a role in regulating bone and cartilage formation, and because exogenous TGF beta and BMP-2 have already been found to modulate osteoblastic differentiation of C26 and 10T1/2 cells, we evaluated the endogenous expression of these factors in both cell lines cultured in the presence or absence of retinoic acid. Tretinoin 474-487 transforming growth factor, beta 1 Mus musculus 41-49 8385738-3 1993 Because transforming growth factor-beta (TGF beta) superfamily members, including the different TGF beta isoforms and the bone morphogenetic proteins (BMPs), are thought to play a role in regulating bone and cartilage formation, and because exogenous TGF beta and BMP-2 have already been found to modulate osteoblastic differentiation of C26 and 10T1/2 cells, we evaluated the endogenous expression of these factors in both cell lines cultured in the presence or absence of retinoic acid. Tretinoin 474-487 transforming growth factor, beta 1 Mus musculus 96-104 8385738-3 1993 Because transforming growth factor-beta (TGF beta) superfamily members, including the different TGF beta isoforms and the bone morphogenetic proteins (BMPs), are thought to play a role in regulating bone and cartilage formation, and because exogenous TGF beta and BMP-2 have already been found to modulate osteoblastic differentiation of C26 and 10T1/2 cells, we evaluated the endogenous expression of these factors in both cell lines cultured in the presence or absence of retinoic acid. Tretinoin 474-487 transforming growth factor, beta 1 Mus musculus 96-104 1638993-5 1992 Exposure of early neural plate stage embryos to retinoic acid caused reduced expression of TGF beta 1 and TGF beta 2 proteins but had no effect on TGF beta 3. Tretinoin 48-61 transforming growth factor, beta 1 Mus musculus 91-101 1638993-8 1992 The down-regulation of intracellular TGF beta 1 was observed up to 48 hours after initial exposure to retinoic acid while some down-regulation of TGF beta 2 was still seen up to 60 hours after initial exposure. Tretinoin 102-115 transforming growth factor, beta 1 Mus musculus 37-47 1545145-3 1992 Immunochemical methods have shown an increase in TGF-beta 1 and, to a lesser extent, of TGF-beta 2 in the epidermis following retinoic acid treatment. Tretinoin 126-139 transforming growth factor, beta 1 Mus musculus 49-59 1545145-5 1992 This study suggests that TGF-beta may mediate the effect of retinoic acids on dermal repair through the stimulation of collagen gene expression. Tretinoin 60-74 transforming growth factor, beta 1 Mus musculus 25-33 30864551-1 2019 BACKGROUND: All-trans retinoic acid (ATRA) potentiates TGF-beta-dependent regulatory T cells (Treg) induction, while it inhibits pro-inflammatory interleukin-17-producing T helper cells (Th17) differentiation. Tretinoin 22-35 transforming growth factor, beta 1 Mus musculus 55-63 3496961-3 1987 Addition of the differentiation agents N,N-dimethylformamide (DMF) or retinoic acid simultaneously with TGF-beta blocked the ability of TGF-beta to induce mitogenesis. Tretinoin 70-83 transforming growth factor, beta 1 Mus musculus 136-144 31586630-5 2019 In Peyer"s patches (PP), ATRA/TGF-beta MPs up-regulated tolerogenic dendritic cells (tolDCs) (CD11c+CD11b-CD103+), while the proportion of mature dendritic cells was not altered. Tretinoin 25-29 transforming growth factor, beta 1 Mus musculus 30-38 1366990-2 1990 We determined that TGF-beta activity increases approximately 25-100% when the mouse EC cell line, F9, is induced to differentiate with retinoic acid (RA). Tretinoin 135-148 transforming growth factor, beta 1 Mus musculus 19-27 1366990-2 1990 We determined that TGF-beta activity increases approximately 25-100% when the mouse EC cell line, F9, is induced to differentiate with retinoic acid (RA). Tretinoin 150-152 transforming growth factor, beta 1 Mus musculus 19-27 30864551-1 2019 BACKGROUND: All-trans retinoic acid (ATRA) potentiates TGF-beta-dependent regulatory T cells (Treg) induction, while it inhibits pro-inflammatory interleukin-17-producing T helper cells (Th17) differentiation. Tretinoin 37-41 transforming growth factor, beta 1 Mus musculus 55-63 29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 41-54 transforming growth factor, beta 1 Mus musculus 439-446 29926545-0 2019 The Effects of Retinoic Acid and MAPK Inhibitors on Phosphorylation of Smad2/3 Induced by Transforming Growth Factor beta1. Tretinoin 15-28 transforming growth factor, beta 1 Mus musculus 90-122 29926545-2 2019 We investigated the effect of RA and the role of these signaling molecules on the phosphorylation of Smad2/3 (p-Smad2/3) induced by TGF-beta1. Tretinoin 30-32 transforming growth factor, beta 1 Mus musculus 132-141 29926545-7 2019 RESULTS: When A549 cells were pre-stimulated with TGF-beta1 prior to RA treatment, RA completely inhibited the p-Smad2/3. Tretinoin 69-71 transforming growth factor, beta 1 Mus musculus 50-59 29926545-11 2019 In a bleomycin-induced lung injury mouse model, RA decreased the expression of TGF-beta1 and Smad3 at 1 and 3 weeks. Tretinoin 48-50 transforming growth factor, beta 1 Mus musculus 79-88 29926545-12 2019 CONCLUSION: RA had inhibitory effects on the phosphorylation of Smad induced by TGF-beta1 in vitro, and RA also decreased the expression of TGF-beta1 at 1 and 3 weeks in vivo. Tretinoin 12-14 transforming growth factor, beta 1 Mus musculus 80-89 29926545-12 2019 CONCLUSION: RA had inhibitory effects on the phosphorylation of Smad induced by TGF-beta1 in vitro, and RA also decreased the expression of TGF-beta1 at 1 and 3 weeks in vivo. Tretinoin 12-14 transforming growth factor, beta 1 Mus musculus 140-160 29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 56-58 transforming growth factor, beta 1 Mus musculus 218-225 29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 56-58 transforming growth factor, beta 1 Mus musculus 439-446 25586558-4 2015 IL-21 and retinoic acid (RA) induce IgA(+) B-cell development and IgA production and drives autocrine TGFbeta1 production to initiate IgA CSR. Tretinoin 10-23 transforming growth factor, beta 1 Mus musculus 102-110 29876477-3 2018 This data report describes the effect of retinoic acid (RA) and/or anti-interferon-gamma (IFNgamma) antibody supplementation on up-regulation of CD8alpha and Foxp3 in Eed CD4+ T cells, the effect of dose or timing of TGFbeta treatment on CD4+ T cell identity of Eed, adding further information regarding the conditions that induces CD8alpha, and mRNA expression changes of genes encoding polycomb repressive complex 2 (PRC2) subunits by TGFbeta treatment. Tretinoin 41-54 transforming growth factor, beta 1 Mus musculus 218-225 26333706-14 2015 The levels of Foxp3, TGF-beta, and IL-10 mRNA, as well as the percentage of CD4+CD25+Foxp3+ T cells, were higher in the ATRA group than in theAR group. Tretinoin 120-124 transforming growth factor, beta 1 Mus musculus 21-29 25887926-5 2015 Moreover, with the presence of TGF-beta, ATRA upregulated CD4(+)CD25(+)Foxp3(+)Treg cells and suppressed Th17 cells in the blood, spleen and draining lymph nodes of recipient mice, as well as enhanced the Foxp3 expression and inhibited the RORgammat expression in grafts and peripheral blood mononuclear cells (PBMCs). Tretinoin 41-45 transforming growth factor, beta 1 Mus musculus 31-39 25477235-4 2014 We found that atRA inhibited MEPM-cell proliferation by downregulating TGF-beta/Smad signaling and that TGF-beta3 treatment was able to antagonize RA signaling. Tretinoin 14-18 transforming growth factor, beta 1 Mus musculus 71-79 25381698-2 2015 Retinoic acid (RA), a natural metabolite of vitamin A, has been reported to enhance the differentiation of Treg cells in the presence of TGF-beta. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 137-145 25381698-2 2015 Retinoic acid (RA), a natural metabolite of vitamin A, has been reported to enhance the differentiation of Treg cells in the presence of TGF-beta. Tretinoin 15-17 transforming growth factor, beta 1 Mus musculus 137-145 25477235-8 2014 Moreover, after deletion of TGIF, both the effects of atRA on TGF-beta-dependent protein expression and the effects of TGF-beta on RA-dependent protein expression were lost. Tretinoin 54-58 transforming growth factor, beta 1 Mus musculus 62-70 24576683-0 2014 Retinoic acid induced repair in the lung of adult hyperoxic mice, reducing transforming growth factor-beta1 (TGF-beta1) mediated abnormal alterations. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 75-107 24576683-0 2014 Retinoic acid induced repair in the lung of adult hyperoxic mice, reducing transforming growth factor-beta1 (TGF-beta1) mediated abnormal alterations. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 109-118 24576683-10 2014 This positive effect of retinoic acid resulted from the inhibition of Smad3/TGF-beta1 signaling via reduced Smad4 mRNA and increased Smad7 protein expression. Tretinoin 24-37 transforming growth factor, beta 1 Mus musculus 76-85 24576683-11 2014 Retinoic acid also induced alveolarization and restricted Smad3/TGF-beta1 signaling by decreasing Smad4 mRNA in healthy mice. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 64-73 24576683-12 2014 Thus, retinoic acid helped repair Smad3/TGF-beta1-induced lung damage in hyperoxic mice. Tretinoin 6-19 transforming growth factor, beta 1 Mus musculus 40-49 24410928-0 2014 All-trans-retinoic acid ameliorates the inflammation by inducing transforming growth factor beta 1 and interleukin 10 in mouse epididymitis. Tretinoin 0-23 transforming growth factor, beta 1 Mus musculus 65-98 24410928-7 2014 RESULTS: Our results demonstrate that atRA ameliorates the inflammation in mouse epididymitis by decreasing the expression of the pro-inflammatory cytokines and increasing the expression of anti-inflammatory factors including TGF-beta1 and IL-10. Tretinoin 38-42 transforming growth factor, beta 1 Mus musculus 226-235 24410928-8 2014 Our results show that the upregulating effect of atRA on TGF-beta1 was mediated by RARalpha, and the enhancing effect of atRA on IL-10 expression was mediated via RARbeta. Tretinoin 49-53 transforming growth factor, beta 1 Mus musculus 57-66 23744644-0 2013 Retinoic acid, acting as a highly specific IgA isotype switch factor, cooperates with TGF-beta1 to enhance the overall IgA response. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 86-95 24404978-8 2014 RK in the presence of ATRA also increased the levels of mRNAs of osteocalcin, alpha1(I) collagen, and TGF-betas (TGF-beta1, TGF-beta2, and TGF-beta3) compared with ATRA only. Tretinoin 22-26 transforming growth factor, beta 1 Mus musculus 113-122 23657628-6 2013 We found that RA significantly enhanced TGF-beta-induced expression of Foxp3 on naive and committed T cells in vitro and that this was blocked by an antagonist of RARalpha (RARi). Tretinoin 14-16 transforming growth factor, beta 1 Mus musculus 40-48 21481001-0 2011 Folic acid rescue of ATRA-induced cleft palate by restoring the TGF-beta signal and inhibiting apoptosis. Tretinoin 21-25 transforming growth factor, beta 1 Mus musculus 64-72 22116001-2 2012 Retinoic acid (RA) enhances induction of CD4(+) Tregs in the presence of TGFbeta. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 73-80 22116001-2 2012 Retinoic acid (RA) enhances induction of CD4(+) Tregs in the presence of TGFbeta. Tretinoin 15-17 transforming growth factor, beta 1 Mus musculus 73-80 22116001-4 2012 We found that in vitro, RA-treated T cells expressed high levels of Foxp3 in the presence of recombinant TGFbeta. Tretinoin 24-26 transforming growth factor, beta 1 Mus musculus 105-112 22116001-10 2012 Our data support the hypothesis that RPE cells produce RA, thereby enabling bystander T cells to be converted into Tregs through TGFbeta promotion, which can then participate in the establishment of immune tolerance in the eye. Tretinoin 55-57 transforming growth factor, beta 1 Mus musculus 129-136 23733880-4 2013 CD103(+) DCs, but not pDCs or lung macrophages, upregulated the expression of retinaldehyde dehydrogenase 2 (aldh1a2), which is key for the production of retinoic acid, a cofactor for TGF-beta for Foxp3 induction. Tretinoin 154-167 transforming growth factor, beta 1 Mus musculus 184-192 22707713-8 2012 LFA-1/ICAM-1-stimulated human and mouse T-cells were refractory to TGF-beta-mediated induction of FOXP3(+) (forkhead box P3) and RORgammat(+) (retinoic acid-related orphan nuclear receptor gammat) Th17 differentiation. Tretinoin 143-156 transforming growth factor, beta 1 Mus musculus 67-75 22250783-15 2012 ATRA may ease the bleomycin-induced pulmonary fibrosis by inhibiting the expression of IL-6 and TGF-beta, shifting the Treg/Th17 ratio and reducing the secretion of IL-17A. Tretinoin 0-4 transforming growth factor, beta 1 Mus musculus 96-104 21481001-11 2011 Apoptosis and TGFbeta signaling in MEPM cells were involved in folic acid rescued ATRA-induced cleft palate. Tretinoin 82-86 transforming growth factor, beta 1 Mus musculus 14-21 21481001-2 2011 To gain more insight into the molecular pathways affected by FA, TGF-beta signaling and apoptosis in mouse embryonic palatal mesenchymal (MEPM) cells of all-trans retinoic acid (ATRA)-induced cleft palate in organ culture were tested. Tretinoin 163-176 transforming growth factor, beta 1 Mus musculus 65-73 21481001-2 2011 To gain more insight into the molecular pathways affected by FA, TGF-beta signaling and apoptosis in mouse embryonic palatal mesenchymal (MEPM) cells of all-trans retinoic acid (ATRA)-induced cleft palate in organ culture were tested. Tretinoin 178-182 transforming growth factor, beta 1 Mus musculus 65-73 20869773-2 2010 Likewise, it is shown that all-trans retinoic acid (ATRA) can greatly enhance TGF-beta-induced Treg conversion, a phenomenon which has mainly been studied in C57BL/6 mice. Tretinoin 37-50 transforming growth factor, beta 1 Mus musculus 78-86 21152098-0 2010 Identification of retinoic acid in a high content screen for agents that overcome the anti-myogenic effect of TGF-beta-1. Tretinoin 18-31 transforming growth factor, beta 1 Mus musculus 110-120 21152098-7 2010 Only all-trans retinoic acid and 9-cis retinoic acid allowed a maximal level of C2C12 cell differentiation in the presence of TGF-beta1; the angiotensin-converting enzyme inhibitor captopril and 10 nM estrogen provided partial rescue. Tretinoin 15-28 transforming growth factor, beta 1 Mus musculus 126-135 21152098-8 2010 Vitamin D was a potent inhibitor of retinoic acid-induced myogenesis in the presence of TGF-beta1. Tretinoin 36-49 transforming growth factor, beta 1 Mus musculus 88-97 21152098-10 2010 CONCLUSIONS/SIGNIFICANCE: Retinoic acid alleviated the anti-myogenic effect of TGF-beta1 by a Smad3-independent mechanism. Tretinoin 26-39 transforming growth factor, beta 1 Mus musculus 79-88 21931768-0 2011 All-trans retinoic acid promotes TGF-beta-induced Tregs via histone modification but not DNA demethylation on Foxp3 gene locus. Tretinoin 10-23 transforming growth factor, beta 1 Mus musculus 33-41 21931768-1 2011 BACKGROUND: It has been documented all-trans retinoic acid (atRA) promotes the development of TGF-beta-induced CD4(+)Foxp3(+) regulatory T cells (iTreg) that play a vital role in the prevention of autoimmune responses, however, molecular mechanisms involved remain elusive. Tretinoin 45-58 transforming growth factor, beta 1 Mus musculus 94-102 21931768-1 2011 BACKGROUND: It has been documented all-trans retinoic acid (atRA) promotes the development of TGF-beta-induced CD4(+)Foxp3(+) regulatory T cells (iTreg) that play a vital role in the prevention of autoimmune responses, however, molecular mechanisms involved remain elusive. Tretinoin 60-64 transforming growth factor, beta 1 Mus musculus 94-102 21931768-3 2011 METHODOLOGY/PRINCIPAL FINDINGS: Addition of atRA to naive CD4(+)CD25(-) cells stimulated with anti-CD3/CD28 antibodies in the presence of TGF-beta not only increased Foxp3(+) iTreg differentiation, but maintained Foxp3 expression through apoptosis inhibition. Tretinoin 44-48 transforming growth factor, beta 1 Mus musculus 138-146 20846163-4 2010 We reported recently that two substances (ATRA and thalidomide) have preventive effects on pulmonary fibrosis by inhibiting IL-6-dependent proliferation and TGF-beta1-dependent transdifferentiation of lung fibroblasts. Tretinoin 42-46 transforming growth factor, beta 1 Mus musculus 157-166 20944006-5 2010 RA promoted bone marrow-derived DC production of bioactive TGF-beta by inhibiting suppressor of cytokine signaling 3 expression and thereby enhancing STAT3 activation. Tretinoin 0-2 transforming growth factor, beta 1 Mus musculus 59-67 20869773-2 2010 Likewise, it is shown that all-trans retinoic acid (ATRA) can greatly enhance TGF-beta-induced Treg conversion, a phenomenon which has mainly been studied in C57BL/6 mice. Tretinoin 52-56 transforming growth factor, beta 1 Mus musculus 78-86 20869773-3 2010 Here we show that, although purified naive cells are highly susceptible to Treg generation, total CD4(+) T-cell populations from different mouse strains display significantly different sensitivities to TGF-beta/ATRA-induced Treg conversion. Tretinoin 211-215 transforming growth factor, beta 1 Mus musculus 202-210 20412539-0 2010 Retinoic acid attenuates acute heart rejection by increasing regulatory T cell and repressing differentiation of Th17 cell in the presence of TGF-beta. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 142-150 20412539-1 2010 Retinoic acid (RA), in a transforming growth factor beta (TGF-beta)-dependent manner, promotes differentiation of regulatory T cells (Tregs) but inhibits the differentiation of Th17 cells in vitro from naive CD4(+) T cells. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 58-66 20412539-1 2010 Retinoic acid (RA), in a transforming growth factor beta (TGF-beta)-dependent manner, promotes differentiation of regulatory T cells (Tregs) but inhibits the differentiation of Th17 cells in vitro from naive CD4(+) T cells. Tretinoin 15-17 transforming growth factor, beta 1 Mus musculus 58-66 20484817-4 2010 Here, we present evidence that endogenous RA acts as a major regulatory signal integrating Wnt and Tgfbeta pathways in the control of Fgf10 expression during induction of the mouse primordial lung. Tretinoin 42-44 transforming growth factor, beta 1 Mus musculus 99-106 20039314-7 2010 Treatment of iPSCs-derived embryoid bodies (EBs) with transforming growth factor beta 1 (TGF-beta1) in the presence of retinoic acid enhanced generation of MSC-like cells. Tretinoin 119-132 transforming growth factor, beta 1 Mus musculus 54-87 20230754-0 2010 Retinoic acid regulates differentiation of the secondary heart field and TGFbeta-mediated outflow tract septation. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 73-80 20039314-7 2010 Treatment of iPSCs-derived embryoid bodies (EBs) with transforming growth factor beta 1 (TGF-beta1) in the presence of retinoic acid enhanced generation of MSC-like cells. Tretinoin 119-132 transforming growth factor, beta 1 Mus musculus 89-98 20110732-0 2010 Kidneys of Alb/TGF-beta1 transgenic mice are deficient in retinoic acid and exogenous retinoic acid shows dose-dependent toxicity. Tretinoin 58-71 transforming growth factor, beta 1 Mus musculus 15-24 20172352-3 2010 It is well known that in the gut, a subset of dendritic cells produces retinoic acid (RA), which together with transforming growth factor (TGF-beta) is able to differentiate naive T cells into Treg. Tretinoin 71-84 transforming growth factor, beta 1 Mus musculus 139-147 19443527-4 2009 Previously, it was reported that all-trans-retinoic acid (ATRA) inhibited the production and function of IL-6 and transforming growth factor (TGF)-beta1 in experiments using lung fibroblasts. Tretinoin 33-56 transforming growth factor, beta 1 Mus musculus 114-152 19443527-4 2009 Previously, it was reported that all-trans-retinoic acid (ATRA) inhibited the production and function of IL-6 and transforming growth factor (TGF)-beta1 in experiments using lung fibroblasts. Tretinoin 58-62 transforming growth factor, beta 1 Mus musculus 114-152 19204112-0 2009 Contrasting roles for all-trans retinoic acid in TGF-beta-mediated induction of Foxp3 and Il10 genes in developing regulatory T cells. Tretinoin 32-45 transforming growth factor, beta 1 Mus musculus 49-57 20110732-0 2010 Kidneys of Alb/TGF-beta1 transgenic mice are deficient in retinoic acid and exogenous retinoic acid shows dose-dependent toxicity. Tretinoin 86-99 transforming growth factor, beta 1 Mus musculus 15-24 18400747-7 2008 Retinoic acid has also been shown to suppress loss of Foxp3 induced by TGF-beta1. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 71-80 19255510-1 2009 We previously showed that atRA (all-trans Retinoic Acid, atRA) inhibites chondrogenesis by downregulation of TGF-beta/Smad signaling. Tretinoin 26-30 transforming growth factor, beta 1 Mus musculus 109-117 19255510-1 2009 We previously showed that atRA (all-trans Retinoic Acid, atRA) inhibites chondrogenesis by downregulation of TGF-beta/Smad signaling. Tretinoin 32-55 transforming growth factor, beta 1 Mus musculus 109-117 19255510-1 2009 We previously showed that atRA (all-trans Retinoic Acid, atRA) inhibites chondrogenesis by downregulation of TGF-beta/Smad signaling. Tretinoin 57-61 transforming growth factor, beta 1 Mus musculus 109-117 19255510-8 2009 Further examinations revealed that TGIF exerted a pivotal role in regulating crosstalk of RA and TGF-beta signaling, since siRNA knockdown of TGIF partially abolished the ability of atRA to suppress TGF-beta3-induced chondrogenesis, whereas forced expression of TGIF blocked the ability of TGF-beta3 to relieve atRA-mediated the suppression of chondrogenesis. Tretinoin 182-186 transforming growth factor, beta 1 Mus musculus 97-105 19255510-8 2009 Further examinations revealed that TGIF exerted a pivotal role in regulating crosstalk of RA and TGF-beta signaling, since siRNA knockdown of TGIF partially abolished the ability of atRA to suppress TGF-beta3-induced chondrogenesis, whereas forced expression of TGIF blocked the ability of TGF-beta3 to relieve atRA-mediated the suppression of chondrogenesis. Tretinoin 311-315 transforming growth factor, beta 1 Mus musculus 97-105 19255510-9 2009 Furthermore, we demonstrated that the effects of atRA on TGF-beta-dependent gene activation and of TGF-beta on RA-dependent gene activation are mediated by TGIF with siRNA to downregulate TGIF. Tretinoin 49-53 transforming growth factor, beta 1 Mus musculus 57-65 18397230-6 2008 In vitro studies disclosed that the administration of ATRA reduced (i) the production of TGF-beta1, IL-6 and collagen from HSCs, (ii) TGF-beta-dependent transdifferentiation of the cells and IL-6-dependent cell proliferation and (iii) the activities of nuclear factor-kappaB p65 and p38mitogen-activated protein kinase, which stimulate the production of TGF-beta1 and IL-6, which could be the mechanism underlying the preventive effect of ATRA on liver fibrosis. Tretinoin 54-58 transforming growth factor, beta 1 Mus musculus 89-98 18397230-6 2008 In vitro studies disclosed that the administration of ATRA reduced (i) the production of TGF-beta1, IL-6 and collagen from HSCs, (ii) TGF-beta-dependent transdifferentiation of the cells and IL-6-dependent cell proliferation and (iii) the activities of nuclear factor-kappaB p65 and p38mitogen-activated protein kinase, which stimulate the production of TGF-beta1 and IL-6, which could be the mechanism underlying the preventive effect of ATRA on liver fibrosis. Tretinoin 54-58 transforming growth factor, beta 1 Mus musculus 89-97 18397230-6 2008 In vitro studies disclosed that the administration of ATRA reduced (i) the production of TGF-beta1, IL-6 and collagen from HSCs, (ii) TGF-beta-dependent transdifferentiation of the cells and IL-6-dependent cell proliferation and (iii) the activities of nuclear factor-kappaB p65 and p38mitogen-activated protein kinase, which stimulate the production of TGF-beta1 and IL-6, which could be the mechanism underlying the preventive effect of ATRA on liver fibrosis. Tretinoin 54-58 transforming growth factor, beta 1 Mus musculus 354-363 18400747-8 2008 Retinoic acid in the presence of TGF-beta1 reduced STAT6 binding to the Foxp3 promoter and enhanced histone acetylation, thereby reverting the effect of IL-4. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 33-42 17637747-0 2008 Retinoic acid induces TGFbeta-dependent autocrine fibroblast growth. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 22-29 17634193-0 2007 Inhibition of Tgf beta signaling by endogenous retinoic acid is essential for primary lung bud induction. Tretinoin 47-60 transforming growth factor, beta 1 Mus musculus 14-22 17785809-4 2007 Retinoic acid can promote TGF-beta1-dependent generation of FoxP3+ regulatory T cells but decrease the TGF-beta1- and IL-6-dependent generation of inflammatory Th17 cells in mouse T cells. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 26-35 17785809-4 2007 Retinoic acid can promote TGF-beta1-dependent generation of FoxP3+ regulatory T cells but decrease the TGF-beta1- and IL-6-dependent generation of inflammatory Th17 cells in mouse T cells. Tretinoin 0-13 transforming growth factor, beta 1 Mus musculus 103-112 17634193-6 2007 RA rescue of the lung phenotype was associated with low levels of Smad2 phosphorylation and downregulation of Tgfbeta targets in Raldh2-null foreguts. Tretinoin 0-2 transforming growth factor, beta 1 Mus musculus 110-117 17634193-9 2007 Our data support a novel mechanism of RA-Tgfbeta-Fgf10 interactions in the developing foregut, in which endogenous RA controls Tgfbeta activity in the prospective lung field to allow local expression of Fgf10 and induction of lung buds. Tretinoin 38-40 transforming growth factor, beta 1 Mus musculus 41-48 17634193-9 2007 Our data support a novel mechanism of RA-Tgfbeta-Fgf10 interactions in the developing foregut, in which endogenous RA controls Tgfbeta activity in the prospective lung field to allow local expression of Fgf10 and induction of lung buds. Tretinoin 38-40 transforming growth factor, beta 1 Mus musculus 127-134 16096774-4 2005 Recent studies in vitro show that retinoic acid (RA) downregulates the release of MCP-1 and TGF-beta1 by tumor cells. Tretinoin 34-47 transforming growth factor, beta 1 Mus musculus 92-101 16096774-4 2005 Recent studies in vitro show that retinoic acid (RA) downregulates the release of MCP-1 and TGF-beta1 by tumor cells. Tretinoin 49-51 transforming growth factor, beta 1 Mus musculus 92-101 15799023-0 2005 Transforming growth factor-beta1 signaling participates in the physiological and pathological regulation of mouse inner ear development by all-trans retinoic acid. Tretinoin 149-162 transforming growth factor, beta 1 Mus musculus 0-32 15799023-9 2005 CONCLUSIONS: Our findings support a role for TGFbeta in the physiological and pathological effects of RA on inner ear development. Tretinoin 102-104 transforming growth factor, beta 1 Mus musculus 45-52