PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23586526-12 2013 Thus, IGF-1 mitigation of microglial ROS and TNF-alpha responses maybe targets for novel therapeutics development to prevent SD, and perhaps migraine. Reactive Oxygen Species 37-40 insulin-like growth factor 1 Rattus norvegicus 6-11 24412273-9 2014 Exogenous IGF-I also inhibited the increase of H2O2-induced ROS generation, and the decrease of PTH 1-34-induced ROS generation in the presence of IGF-I and Nrf-2 siRNA. Reactive Oxygen Species 60-63 insulin-like growth factor 1 Rattus norvegicus 10-15 24412273-9 2014 Exogenous IGF-I also inhibited the increase of H2O2-induced ROS generation, and the decrease of PTH 1-34-induced ROS generation in the presence of IGF-I and Nrf-2 siRNA. Reactive Oxygen Species 113-116 insulin-like growth factor 1 Rattus norvegicus 10-15 24412273-9 2014 Exogenous IGF-I also inhibited the increase of H2O2-induced ROS generation, and the decrease of PTH 1-34-induced ROS generation in the presence of IGF-I and Nrf-2 siRNA. Reactive Oxygen Species 113-116 insulin-like growth factor 1 Rattus norvegicus 147-152 30659610-0 2019 ROS- and HIF1alpha-dependent IGFBP3 upregulation blocks IGF1 survival signaling and thereby mediates high-glucose-induced cardiomyocyte apoptosis. Reactive Oxygen Species 0-3 insulin-like growth factor 1 Rattus norvegicus 56-60 30659610-7 2019 As a result, briefly, our main findings are that hyperglycemia can induce cardiac IGFBP3 overexpression and secretion, that high levels of IGFBP3 can sequester IGF1 from IGF1 survival pathway, leading to apoptosis, and that IGFBP3 gene upregulation is hypoxia-inducible factor (HIF)1alpha-dependent and reactive oxygen species dependent. Reactive Oxygen Species 303-326 insulin-like growth factor 1 Rattus norvegicus 160-164 22370764-6 2012 We examined the effects of GH and IGF-I on reactive oxygen species (ROS) production in C2C12 myocytes. Reactive Oxygen Species 43-66 insulin-like growth factor 1 Rattus norvegicus 34-39 22362362-0 2012 ROS constitute a convergence nexus in the development of IGF1 resistance and impaired wound healing in a rat model of type 2 diabetes. Reactive Oxygen Species 0-3 insulin-like growth factor 1 Rattus norvegicus 57-61 22362362-4 2012 Cultured dermal fibroblasts from rats and full-thickness excisional wounds were used as models to test the premise that reactive oxygen species (ROS) play a causal role in the development of IGF1 resistance and impaired wound healing under different but pathophysiologically relevant clinical settings, including diabetes, dexamethasone-induced hypercortisolemia and TNFalpha-induced inflammation. Reactive Oxygen Species 120-143 insulin-like growth factor 1 Rattus norvegicus 191-195 22362362-4 2012 Cultured dermal fibroblasts from rats and full-thickness excisional wounds were used as models to test the premise that reactive oxygen species (ROS) play a causal role in the development of IGF1 resistance and impaired wound healing under different but pathophysiologically relevant clinical settings, including diabetes, dexamethasone-induced hypercortisolemia and TNFalpha-induced inflammation. Reactive Oxygen Species 145-148 insulin-like growth factor 1 Rattus norvegicus 191-195 22362362-10 2012 The ROS suppressors EUK-134 and alpha-lipoic acid, or small interfering RNA (siRNA)-mediated silencing of JNK expression, restored IGF1 sensitivity both in vitro and in vivo, and also ameliorated the impairment in IGF1-mediated wound responses during diabetes, inflammation and hypercortisolemia. Reactive Oxygen Species 4-7 insulin-like growth factor 1 Rattus norvegicus 131-135 22362362-10 2012 The ROS suppressors EUK-134 and alpha-lipoic acid, or small interfering RNA (siRNA)-mediated silencing of JNK expression, restored IGF1 sensitivity both in vitro and in vivo, and also ameliorated the impairment in IGF1-mediated wound responses during diabetes, inflammation and hypercortisolemia. Reactive Oxygen Species 4-7 insulin-like growth factor 1 Rattus norvegicus 214-218 22362362-11 2012 Our data advance the notion that ROS constitute a convergence nexus for the development of IGF1 resistance and impaired wound healing under different but pathophysiologically relevant clinical settings, with a proof of concept for the beneficial effect of ROS suppressors. Reactive Oxygen Species 33-36 insulin-like growth factor 1 Rattus norvegicus 91-95 22362362-11 2012 Our data advance the notion that ROS constitute a convergence nexus for the development of IGF1 resistance and impaired wound healing under different but pathophysiologically relevant clinical settings, with a proof of concept for the beneficial effect of ROS suppressors. Reactive Oxygen Species 256-259 insulin-like growth factor 1 Rattus norvegicus 91-95 16999977-4 2006 The purpose of this study was to determine whether IGF-1 protects intestinal cells from ROS-induced apoptosis. Reactive Oxygen Species 88-91 insulin-like growth factor 1 Rattus norvegicus 51-56 18567639-15 2008 CONCLUSION: Our results suggest that Nox4 and Rac1 mediate IGF-I-induced ROS production and cell migration in VSMCs and that Nox4 is not regulated by Rac1. Reactive Oxygen Species 73-76 insulin-like growth factor 1 Rattus norvegicus 59-64 17522998-0 2007 Modulation of intracellular reactive oxygen species level in chondrocytes by IGF-1, FGF, and TGF-beta1. Reactive Oxygen Species 28-51 insulin-like growth factor 1 Rattus norvegicus 77-82 17522998-2 2007 The principal aim of this study was to test the capacity of three growth factors with established roles in cartilage, namely insulin-like growth factor (IGF)-1, fibroblast growth factor (FGF) and transforming growth factor (TGF)-beta 1, to alter intracellular reactive oxygen species (ROS) levels. Reactive Oxygen Species 260-283 insulin-like growth factor 1 Rattus norvegicus 125-159 17522998-2 2007 The principal aim of this study was to test the capacity of three growth factors with established roles in cartilage, namely insulin-like growth factor (IGF)-1, fibroblast growth factor (FGF) and transforming growth factor (TGF)-beta 1, to alter intracellular reactive oxygen species (ROS) levels. Reactive Oxygen Species 285-288 insulin-like growth factor 1 Rattus norvegicus 125-159 17522998-7 2007 TGF-beta1 significantly increased cellular ROS levels in mature and old cartilage whereas in marked contrast, IGF-1 significantly and age-dependently reduced ROS levels. Reactive Oxygen Species 158-161 insulin-like growth factor 1 Rattus norvegicus 110-115 17522998-9 2007 Pretreatment of rat cartilage with IGF-1 significantly enhanced the activity of GPX, without altering the activity of SOD or CAT, and protected chondrocytes against ROS-induced cell death. Reactive Oxygen Species 165-168 insulin-like growth factor 1 Rattus norvegicus 35-40 17522998-13 2007 In marked contrast, IGF-1 is a potent antioxidant in mature and aged rat and human chondrocytes, protecting cells against ROS-induced cell death probably through the enhancement of the activity of the antioxidant enzyme GPX. Reactive Oxygen Species 122-125 insulin-like growth factor 1 Rattus norvegicus 20-25 21350246-1 2011 The discovery that in invertebrates, disruption of the insulin/insulin-like growth factor (IGF)-1 pathway extends life span and increases resistance to oxidative injury led to the hypothesis that IGF-1 signaling may play a role in regulating cellular reactive oxygen species production, oxidative stress resistance, and consequentially, organismal life span in mammals. Reactive Oxygen Species 251-274 insulin-like growth factor 1 Rattus norvegicus 196-201 18567639-0 2008 Insulin-like growth factor-I induces reactive oxygen species production and cell migration through Nox4 and Rac1 in vascular smooth muscle cells. Reactive Oxygen Species 37-60 insulin-like growth factor 1 Rattus norvegicus 0-28 18567639-1 2008 AIMS: We showed previously that insulin-like growth factor-I (IGF-I)-induced vascular smooth muscle cells (VSMCs) proliferation through the production of reactive oxygen species (ROS). Reactive Oxygen Species 154-177 insulin-like growth factor 1 Rattus norvegicus 32-60 18567639-1 2008 AIMS: We showed previously that insulin-like growth factor-I (IGF-I)-induced vascular smooth muscle cells (VSMCs) proliferation through the production of reactive oxygen species (ROS). Reactive Oxygen Species 154-177 insulin-like growth factor 1 Rattus norvegicus 62-67 18567639-1 2008 AIMS: We showed previously that insulin-like growth factor-I (IGF-I)-induced vascular smooth muscle cells (VSMCs) proliferation through the production of reactive oxygen species (ROS). Reactive Oxygen Species 179-182 insulin-like growth factor 1 Rattus norvegicus 32-60 18567639-1 2008 AIMS: We showed previously that insulin-like growth factor-I (IGF-I)-induced vascular smooth muscle cells (VSMCs) proliferation through the production of reactive oxygen species (ROS). Reactive Oxygen Species 179-182 insulin-like growth factor 1 Rattus norvegicus 62-67 18567639-2 2008 However, how IGF-I-induced ROS was unknown. Reactive Oxygen Species 27-30 insulin-like growth factor 1 Rattus norvegicus 13-18 18567639-3 2008 The aim of this study is to investigate the mechanisms by which IGF-I induces ROS production in VSMCs. Reactive Oxygen Species 78-81 insulin-like growth factor 1 Rattus norvegicus 64-69 18567639-7 2008 VSMCs from Sprague-Dawley rat thoracic aortas were used in this work.IGF-I enhanced ROS production in rat VSMCs. Reactive Oxygen Species 84-87 insulin-like growth factor 1 Rattus norvegicus 69-74 18567639-10 2008 Either knockdown of Nox4 or inactivation of Rac1 impaired IGF-I-induced ROS. Reactive Oxygen Species 72-75 insulin-like growth factor 1 Rattus norvegicus 58-63 17462533-0 2007 Insulin-like growth factor-I (IGF-I) induces epidermal growth factor receptor transactivation and cell proliferation through reactive oxygen species. Reactive Oxygen Species 125-148 insulin-like growth factor 1 Rattus norvegicus 0-28 17462533-0 2007 Insulin-like growth factor-I (IGF-I) induces epidermal growth factor receptor transactivation and cell proliferation through reactive oxygen species. Reactive Oxygen Species 125-148 insulin-like growth factor 1 Rattus norvegicus 30-35 17462533-6 2007 IGF-I stimulated ROS production and Src activation. Reactive Oxygen Species 17-20 insulin-like growth factor 1 Rattus norvegicus 0-5 17462533-7 2007 Antioxidants inhibited IGF-I-induced ROS generation and activation of EGFR, ERK, and Src. Reactive Oxygen Species 37-40 insulin-like growth factor 1 Rattus norvegicus 23-28 17462533-10 2007 These results suggest that (1) IGF-I induces EGFR activation through production of ROS and ROS-mediated Src activation in VSMCs, and (2) EGFR transactivation is required for IGF-I-induced VSMC proliferation. Reactive Oxygen Species 83-86 insulin-like growth factor 1 Rattus norvegicus 31-36 17462533-10 2007 These results suggest that (1) IGF-I induces EGFR activation through production of ROS and ROS-mediated Src activation in VSMCs, and (2) EGFR transactivation is required for IGF-I-induced VSMC proliferation. Reactive Oxygen Species 91-94 insulin-like growth factor 1 Rattus norvegicus 31-36 16999977-11 2006 CONCLUSIONS: PI3-K pathway is activated during ROS-induced intestinal epithelial cell injury; IGF-1 exerted an anti-apoptotic effect during this response by PI3-K activation. Reactive Oxygen Species 47-50 insulin-like growth factor 1 Rattus norvegicus 94-99 16870182-3 2006 We study here: (a) if hyperosmotic stress triggers reactive oxygen species (ROS) generation and in turn whether they regulate NFkappaB and (b) if insulin-like growth factor-1 (IGF-1) modulates ROS production and NFkappaB activation in hyperosmotically-stressed cardiomyocytes. Reactive Oxygen Species 193-196 insulin-like growth factor 1 Rattus norvegicus 146-174 16870182-3 2006 We study here: (a) if hyperosmotic stress triggers reactive oxygen species (ROS) generation and in turn whether they regulate NFkappaB and (b) if insulin-like growth factor-1 (IGF-1) modulates ROS production and NFkappaB activation in hyperosmotically-stressed cardiomyocytes. Reactive Oxygen Species 193-196 insulin-like growth factor 1 Rattus norvegicus 176-181 16870182-9 2006 IGF-1 prevents NFkappaB activation by a ROS-independent mechanism. Reactive Oxygen Species 40-43 insulin-like growth factor 1 Rattus norvegicus 0-5 9059547-7 1997 CONCLUSION: Reactive oxygen species increased vascular smooth muscle cell synthesis of IGF I and reduced levels of the inhibitory IGF binding protein-4. Reactive Oxygen Species 12-35 insulin-like growth factor 1 Rattus norvegicus 87-92 9605472-2 1998 The respiratory control ratio, which is an index of oxidative phosphorylation and therefore reflects the ability of mitochondria to produce ATP, is reduced by 50% within the first 2 h after the beginning of apoptosis, insulin-like growth factor I (IGF-I), actinomicin D or cycloheximide, previously reported to inhibit apoptosis, fully prevent the impairment of cellular respiration while scavengers of reactive oxygen species partially inhibit apoptosis and restore cellular respiration. Reactive Oxygen Species 403-426 insulin-like growth factor 1 Rattus norvegicus 218-246 9605472-2 1998 The respiratory control ratio, which is an index of oxidative phosphorylation and therefore reflects the ability of mitochondria to produce ATP, is reduced by 50% within the first 2 h after the beginning of apoptosis, insulin-like growth factor I (IGF-I), actinomicin D or cycloheximide, previously reported to inhibit apoptosis, fully prevent the impairment of cellular respiration while scavengers of reactive oxygen species partially inhibit apoptosis and restore cellular respiration. Reactive Oxygen Species 403-426 insulin-like growth factor 1 Rattus norvegicus 248-253 9059547-8 1997 Furthermore, reactive oxygen species-induced DNA synthesis was inhibited by an anti-IGF I antiserum. Reactive Oxygen Species 13-36 insulin-like growth factor 1 Rattus norvegicus 84-89 9059547-0 1997 Reactive oxygen species stimulate insulin-like growth factor I synthesis in vascular smooth muscle cells. Reactive Oxygen Species 0-23 insulin-like growth factor 1 Rattus norvegicus 34-62 9059547-1 1997 OBJECTIVES: The objective was to study potential regulation of insulin-like growth factor I (IGF I), its binding proteins, and the IGF I receptor by reactive oxygen species in vascular smooth muscle cells. Reactive Oxygen Species 149-172 insulin-like growth factor 1 Rattus norvegicus 63-91 9059547-1 1997 OBJECTIVES: The objective was to study potential regulation of insulin-like growth factor I (IGF I), its binding proteins, and the IGF I receptor by reactive oxygen species in vascular smooth muscle cells. Reactive Oxygen Species 149-172 insulin-like growth factor 1 Rattus norvegicus 93-98 9059547-9 1997 These findings suggest that the autocrine IGF I system plays an important role in vascular smooth muscle cell growth responses to reactive oxygen species. Reactive Oxygen Species 130-153 insulin-like growth factor 1 Rattus norvegicus 42-47