PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 20032081-9 2010 As both protein kinase C (PKC)alpha and beta are involved in VEGF-induced COX-2 expression and CREB activation, we investigated which isoform(s) of PKC was affected by RSG. Rosiglitazone 168-171 vascular endothelial growth factor A Homo sapiens 61-65 22752619-6 2012 The diminished bone regeneration in the DO model in rosiglitazone-treated animals was associated with a significant decrease in cell proliferation measured by the number of cells expressing proliferating cell nuclear antigen and neovascularization measured by both the number of vascular sinusoids and the number of cells producing proangiogenic vascular endothelial growth factor at the DO site. Rosiglitazone 52-65 vascular endothelial growth factor A Homo sapiens 346-380 21986923-0 2012 Rosiglitazone, a PPAR-gamma agonist, inhibits VEGF secretion by peripheral blood mononuclear cells and ROS production by human leukocytes. Rosiglitazone 0-13 vascular endothelial growth factor A Homo sapiens 46-50 21986923-1 2012 OBJECTIVE: To investigate the effects of rosiglitazone, a peroxisome proliferator-activated receptor-gamma agonist, on the secretion of vascular endothelial growth factor (VEGF) by peripheral blood mononuclear cells (PBMCs) and on the generation of reactive oxygen species (ROS) by leukocytes. Rosiglitazone 41-54 vascular endothelial growth factor A Homo sapiens 136-170 21986923-1 2012 OBJECTIVE: To investigate the effects of rosiglitazone, a peroxisome proliferator-activated receptor-gamma agonist, on the secretion of vascular endothelial growth factor (VEGF) by peripheral blood mononuclear cells (PBMCs) and on the generation of reactive oxygen species (ROS) by leukocytes. Rosiglitazone 41-54 vascular endothelial growth factor A Homo sapiens 172-176 21986923-4 2012 RESULTS: Rosiglitazone and calphostin C (a protein kinase C inhibitor) inhibited VEGF secretion by PBMCs by 63.7 and 62.3%, respectively. Rosiglitazone 9-22 vascular endothelial growth factor A Homo sapiens 81-85 21986923-6 2012 CONCLUSION: The results support the involvement of PKC as a direct, and/or NADPH-oxidase as an indirect, target for the action of rosiglitazone on VEGF secretion by PBMCs and ROS production in human leukocytes. Rosiglitazone 130-143 vascular endothelial growth factor A Homo sapiens 147-151 26081281-8 2015 In both human trophoblast cell and placental explants, we demonstrated that rosiglitazone, a PPARgamma agonist, 1) increased EG-VEGF secretion, 2) increased EG-VEGF and its receptors mRNA and protein expression, 3) increased placental vascularization via PROKR1 and PROKR2, and 4) inhibited trophoblast migration and invasion via PROKR2. Rosiglitazone 76-89 vascular endothelial growth factor A Homo sapiens 128-132 24787994-4 2014 The inhibitory effect of RSG on VM formation could be at least partially explained by an RSG-driven downregulation of vascular endothelial growth factor (VEGF) levels and phosphorylation of AKT, which is known to be important in VM. Rosiglitazone 25-28 vascular endothelial growth factor A Homo sapiens 118-152 24787994-4 2014 The inhibitory effect of RSG on VM formation could be at least partially explained by an RSG-driven downregulation of vascular endothelial growth factor (VEGF) levels and phosphorylation of AKT, which is known to be important in VM. Rosiglitazone 25-28 vascular endothelial growth factor A Homo sapiens 154-158 24787994-4 2014 The inhibitory effect of RSG on VM formation could be at least partially explained by an RSG-driven downregulation of vascular endothelial growth factor (VEGF) levels and phosphorylation of AKT, which is known to be important in VM. Rosiglitazone 89-92 vascular endothelial growth factor A Homo sapiens 118-152 24787994-4 2014 The inhibitory effect of RSG on VM formation could be at least partially explained by an RSG-driven downregulation of vascular endothelial growth factor (VEGF) levels and phosphorylation of AKT, which is known to be important in VM. Rosiglitazone 89-92 vascular endothelial growth factor A Homo sapiens 154-158 20032081-10 2010 RSG only reduced VEGF- and PMA-stimulated PKCalpha membrane translocation. Rosiglitazone 0-3 vascular endothelial growth factor A Homo sapiens 17-21 19797172-7 2009 Organ culture revealed reduced vascular endothelial growth factor in SESs receiving RSG compared to RSG animals receiving bare metal stent or PESs. Rosiglitazone 84-87 vascular endothelial growth factor A Homo sapiens 31-65 19923143-9 2010 The peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonist, rosiglitazone, attenuated HG-induced PKC but not HG- or BK- induced MAPK p42/44 activation and reduced HG-stimulated VEGF, along with IL-6, CCL-2 and TGF-beta secretion. Rosiglitazone 75-88 vascular endothelial growth factor A Homo sapiens 192-196 19797172-8 2009 Quantitative polymerase chain reaction in human aortic endothelial cells (HAECs) revealed that sirolimus (but not paclitaxel) inhibited RSG-induced vascular endothelial growth factor transcription. Rosiglitazone 136-139 vascular endothelial growth factor A Homo sapiens 148-182 16840174-0 2006 Rosiglitazone antagonizes vascular endothelial growth factor signaling and nuclear factor of activated T cells activation in cardiac valve endothelium. Rosiglitazone 0-13 vascular endothelial growth factor A Homo sapiens 26-60 19760125-5 2009 Matrine displayed synergistic effects with existing anticancer agents celecoxib (the inhibitor of cyclooxygenase-2), trichostatin A (the histone deacetylase inhibitor) and rosiglitazone against the proliferation and VEGF excretions in MDA-MB-231 cells. Rosiglitazone 172-185 vascular endothelial growth factor A Homo sapiens 216-220 19693712-10 2009 Moreover, ovaries from NV animals had decreased levels of the pro-angiogenic growth factors vascular endothelial growth factor (VEGF) and endocrine gland-derived VEGF both of which were increased with rosiglitazone treatment. Rosiglitazone 201-214 vascular endothelial growth factor A Homo sapiens 128-132 19693712-10 2009 Moreover, ovaries from NV animals had decreased levels of the pro-angiogenic growth factors vascular endothelial growth factor (VEGF) and endocrine gland-derived VEGF both of which were increased with rosiglitazone treatment. Rosiglitazone 201-214 vascular endothelial growth factor A Homo sapiens 162-166 18810647-0 2008 PPAR gamma ligands, rosiglitazone and pioglitazone, inhibit bFGF- and VEGF-mediated angiogenesis. Rosiglitazone 20-33 vascular endothelial growth factor A Homo sapiens 70-74 18810647-1 2008 OBJECTIVE: To study the effect of peroxisome proliferator-activated receptor-gamma (PPAR gamma) agonists, pioglitazone and rosiglitazone, on vascular endothelial growth factor (VEGF)- and basic fibroblast growth factor (bFGF)-induced angiogenesis and on endothelial cell migration. Rosiglitazone 123-136 vascular endothelial growth factor A Homo sapiens 141-175 18810647-1 2008 OBJECTIVE: To study the effect of peroxisome proliferator-activated receptor-gamma (PPAR gamma) agonists, pioglitazone and rosiglitazone, on vascular endothelial growth factor (VEGF)- and basic fibroblast growth factor (bFGF)-induced angiogenesis and on endothelial cell migration. Rosiglitazone 123-136 vascular endothelial growth factor A Homo sapiens 177-181 18810647-4 2008 RESULTS: Pioglitazone and rosiglitazone inhibited the pro-angiogenic effects of bFGF and VEGF in the CAM model significantly (P < 0.001) to the same extent. Rosiglitazone 26-39 vascular endothelial growth factor A Homo sapiens 89-93 18810275-6 2008 Rosiglitazone reduced the VEGF induced angiogenesis of HUVEC in dose-dependent manner through PPARgamma-dependent pathway. Rosiglitazone 0-13 vascular endothelial growth factor A Homo sapiens 26-30 16840174-7 2006 VEGF-induced proliferation and migration of human pulmonary valve endothelial cells (HPVECs) were inhibited by rosiglitazone (ROSI), a specific ligand of PPARgamma activation, suggesting that PPARgamma disrupts VEGF signaling in the valve endothelium. Rosiglitazone 111-124 vascular endothelial growth factor A Homo sapiens 0-4 16840174-7 2006 VEGF-induced proliferation and migration of human pulmonary valve endothelial cells (HPVECs) were inhibited by rosiglitazone (ROSI), a specific ligand of PPARgamma activation, suggesting that PPARgamma disrupts VEGF signaling in the valve endothelium. Rosiglitazone 111-124 vascular endothelial growth factor A Homo sapiens 211-215 16840174-7 2006 VEGF-induced proliferation and migration of human pulmonary valve endothelial cells (HPVECs) were inhibited by rosiglitazone (ROSI), a specific ligand of PPARgamma activation, suggesting that PPARgamma disrupts VEGF signaling in the valve endothelium. Rosiglitazone 126-130 vascular endothelial growth factor A Homo sapiens 0-4 16840174-7 2006 VEGF-induced proliferation and migration of human pulmonary valve endothelial cells (HPVECs) were inhibited by rosiglitazone (ROSI), a specific ligand of PPARgamma activation, suggesting that PPARgamma disrupts VEGF signaling in the valve endothelium. Rosiglitazone 126-130 vascular endothelial growth factor A Homo sapiens 211-215 16840174-8 2006 ROSI also antagonized VEGF-mediated NFATc1 nuclear translocation in HPVECs, suggesting that PPARgamma inhibits VEGF signaling of NFATc1 activation in the valve. Rosiglitazone 0-4 vascular endothelial growth factor A Homo sapiens 22-26 16840174-8 2006 ROSI also antagonized VEGF-mediated NFATc1 nuclear translocation in HPVECs, suggesting that PPARgamma inhibits VEGF signaling of NFATc1 activation in the valve. Rosiglitazone 0-4 vascular endothelial growth factor A Homo sapiens 111-115 16297938-5 2006 Effects of rosiglitazone on angiogenesis were assessed by vascular endothelial growth factor (VEGF)-induced tube formation and wound-healing migration. Rosiglitazone 11-24 vascular endothelial growth factor A Homo sapiens 58-92 16297938-5 2006 Effects of rosiglitazone on angiogenesis were assessed by vascular endothelial growth factor (VEGF)-induced tube formation and wound-healing migration. Rosiglitazone 11-24 vascular endothelial growth factor A Homo sapiens 94-98 16297938-9 2006 Rosiglitazone markedly decreased VEGF-induced tube formation and endothelial cell migration, which might be explained by a disorganization of the actin cytoskeleton. Rosiglitazone 0-13 vascular endothelial growth factor A Homo sapiens 33-37 16400517-6 2005 Treatment of transformed and primary endometrial cells with rosiglitazone, a synthetic PPARgamma agonist, or prostaglandin 15-deoxy-Delta12-14 J(2), a naturally occurring eicosanoid ligand, decreased VEGF protein secretion. Rosiglitazone 60-73 vascular endothelial growth factor A Homo sapiens 200-204 16400517-7 2005 In transiently transfected Ishikawa cells, rosiglitazone repressed VEGF gene promoter-luciferase activation with an IC(50) approximately approximately 50 nM. Rosiglitazone 43-56 vascular endothelial growth factor A Homo sapiens 67-71 11334422-5 2001 We further demonstrated that troglitazone, as well as rosiglitazone, at the plasma concentrations observed in patients, increased VEGF mRNA levels in 3T3-L1 adipocytes. Rosiglitazone 54-67 vascular endothelial growth factor A Homo sapiens 130-134