The Experts below are selected from a list of 198 Experts worldwide ranked by ideXlab platform
Tian Ming - One of the best experts on this subject based on the ideXlab platform.
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Activation of the G Protein-Coupled Estrogen Receptor Prevented the Development of Acute Colitis by Protecting the Crypt Cell.
The Journal of pharmacology and experimental therapeutics, 2020Co-Authors: Qian Wang, Shiquan Chai, Kaixuan Liu, Guanyu Chen, Tian Ming, Jianbo Liu, Shuyu Wen, Jiayi WangAbstract:G protein-coupled estrogen receptor (GPER) might be involved in ulcerative colitis (UC), but the direct effect of GPER on UC is still unclear. We used male C57BL/6 mice to establish the acute colitis model with administration of dextran sulfate sodium and explored the effect of GPER on acute colitis and its possible mechanism. The selective GPER agonist G-1 inhibited weight loss and colon shortening and decreased the disease activity index for colitis and histologic damage in mice with colitis. All of these effects were prevented by a selective GPER blocker. G-1 administration prevented the dysfunction of tight junction protein expression and goblet Cells in colitis model and thus inhibited the increase of mucosal permeability in colitis-suffering mice significantly. GPER activation reduced expression of glucose-regulating peptide-78 and anti-CCAAT/enhancer-binding protein homologous protein and attenuated the three arms of the unfolded protein response in colitis. G-1 therapy inhibited the increase of cleavage caspase-3- and TUNEL-positive Cells in colonic Crypts in the colitis model, increased the number of Ki67- and bromodeoxyuridine-positive Cells in Crypts, and reversed the decrease of cyclin D1 and cyclin B1 expression in colitis, indicating its protective effect on Crypt Cells. In cultured CCD841 Cells, G-1 treatment fought against Cell injury induced by endoplasmic reticulum stress. These findings demonstrate that GPER activation prevents colitis by protecting the colonic Crypt Cells, which are associated with inhibition of endoplasmic reticulum stress. SIGNIFICANCE STATEMENT: We demonstrate that G protein-coupled estrogen receptor (GPER) activation prevents dextran sulfate sodium-induced acute colitis by protecting the Crypt Cells, showing that it inhibited the Crypt Cell apoptosis and protected proliferation of Crypt Cells, which resulted in protection of the intestinal mucosal barrier. This protective effect was achieved (at least in part) by inhibiting endoplasmic reticulum stress. Mucosal healing is regarded as a key therapeutic target for colitis, and GPER is expected to become a new therapeutic target for colitis.
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activation of g protein coupled estrogen receptor protects intestine from ischemia reperfusion injury in mice by protecting the Crypt Cell proliferation
Clinical Science, 2019Co-Authors: Shiquan Chai, Kaixuan Liu, Wanbing Feng, Tiantian Liu, Qian Wang, Rong Zhou, Shiming Chen, Liyan Wang, Guanyu Chen, Tian MingAbstract:The intestinal ischemia/reperfusion (I/R) injury is a common clinical event related with high mortality in patients undergoing surgery or trauma. Estrogen exerts salutary effect on intestinal I/R injury, but the receptor type is not totally understood. We aimed to identify whether the G protein-coupled estrogen receptor (GPER) could protect the intestine against I/R injury and explored the mechanism. Adult male C57BL/6 mice were subjected to intestinal I/R injury by clamping (45 min) of the superior mesenteric artery followed by 4 h of intestinal reperfusion. Our results revealed that the selective GPER blocker abolished the protective effect of estrogen on intestinal I/R injury. Selective GPER agonist G-1 significantly alleviated I/R-induced intestinal mucosal damage, neutrophil infiltration, up-regulation of TNF-α and cyclooxygenase-2 (Cox-2) expression, and restored impaired intestinal barrier function. G-1 could ameliorate the impaired Crypt Cell proliferation ability induced by I/R and restore the decrease in villus height and Crypt depth. The up-regulation of inducible nitric oxide synthase (iNOS) expression after I/R treatment was attenuated by G-1 administration. Moreover, selective iNOS inhibitor had a similar effect with G-1 on promoting the proliferation of Crypt Cells in the intestinal I/R model. Both GPER and iNOS were expressed in leucine-rich repeat containing G-protein coupled receptor 5 (Lgr5) positive stem Cells in Crypt. Together, these findings demonstrate that GPER activation can prompt epithelial Cell repair following intestinal injury, which occurred at least in part by inhibiting the iNOS expression in intestinal stem Cells (ISCs). GPER may be a novel therapeutic target for intestinal I/R injury.
Shiquan Chai - One of the best experts on this subject based on the ideXlab platform.
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Activation of the G Protein-Coupled Estrogen Receptor Prevented the Development of Acute Colitis by Protecting the Crypt Cell.
The Journal of pharmacology and experimental therapeutics, 2020Co-Authors: Qian Wang, Shiquan Chai, Kaixuan Liu, Guanyu Chen, Tian Ming, Jianbo Liu, Shuyu Wen, Jiayi WangAbstract:G protein-coupled estrogen receptor (GPER) might be involved in ulcerative colitis (UC), but the direct effect of GPER on UC is still unclear. We used male C57BL/6 mice to establish the acute colitis model with administration of dextran sulfate sodium and explored the effect of GPER on acute colitis and its possible mechanism. The selective GPER agonist G-1 inhibited weight loss and colon shortening and decreased the disease activity index for colitis and histologic damage in mice with colitis. All of these effects were prevented by a selective GPER blocker. G-1 administration prevented the dysfunction of tight junction protein expression and goblet Cells in colitis model and thus inhibited the increase of mucosal permeability in colitis-suffering mice significantly. GPER activation reduced expression of glucose-regulating peptide-78 and anti-CCAAT/enhancer-binding protein homologous protein and attenuated the three arms of the unfolded protein response in colitis. G-1 therapy inhibited the increase of cleavage caspase-3- and TUNEL-positive Cells in colonic Crypts in the colitis model, increased the number of Ki67- and bromodeoxyuridine-positive Cells in Crypts, and reversed the decrease of cyclin D1 and cyclin B1 expression in colitis, indicating its protective effect on Crypt Cells. In cultured CCD841 Cells, G-1 treatment fought against Cell injury induced by endoplasmic reticulum stress. These findings demonstrate that GPER activation prevents colitis by protecting the colonic Crypt Cells, which are associated with inhibition of endoplasmic reticulum stress. SIGNIFICANCE STATEMENT: We demonstrate that G protein-coupled estrogen receptor (GPER) activation prevents dextran sulfate sodium-induced acute colitis by protecting the Crypt Cells, showing that it inhibited the Crypt Cell apoptosis and protected proliferation of Crypt Cells, which resulted in protection of the intestinal mucosal barrier. This protective effect was achieved (at least in part) by inhibiting endoplasmic reticulum stress. Mucosal healing is regarded as a key therapeutic target for colitis, and GPER is expected to become a new therapeutic target for colitis.
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activation of g protein coupled estrogen receptor protects intestine from ischemia reperfusion injury in mice by protecting the Crypt Cell proliferation
Clinical Science, 2019Co-Authors: Shiquan Chai, Kaixuan Liu, Wanbing Feng, Tiantian Liu, Qian Wang, Rong Zhou, Shiming Chen, Liyan Wang, Guanyu Chen, Tian MingAbstract:The intestinal ischemia/reperfusion (I/R) injury is a common clinical event related with high mortality in patients undergoing surgery or trauma. Estrogen exerts salutary effect on intestinal I/R injury, but the receptor type is not totally understood. We aimed to identify whether the G protein-coupled estrogen receptor (GPER) could protect the intestine against I/R injury and explored the mechanism. Adult male C57BL/6 mice were subjected to intestinal I/R injury by clamping (45 min) of the superior mesenteric artery followed by 4 h of intestinal reperfusion. Our results revealed that the selective GPER blocker abolished the protective effect of estrogen on intestinal I/R injury. Selective GPER agonist G-1 significantly alleviated I/R-induced intestinal mucosal damage, neutrophil infiltration, up-regulation of TNF-α and cyclooxygenase-2 (Cox-2) expression, and restored impaired intestinal barrier function. G-1 could ameliorate the impaired Crypt Cell proliferation ability induced by I/R and restore the decrease in villus height and Crypt depth. The up-regulation of inducible nitric oxide synthase (iNOS) expression after I/R treatment was attenuated by G-1 administration. Moreover, selective iNOS inhibitor had a similar effect with G-1 on promoting the proliferation of Crypt Cells in the intestinal I/R model. Both GPER and iNOS were expressed in leucine-rich repeat containing G-protein coupled receptor 5 (Lgr5) positive stem Cells in Crypt. Together, these findings demonstrate that GPER activation can prompt epithelial Cell repair following intestinal injury, which occurred at least in part by inhibiting the iNOS expression in intestinal stem Cells (ISCs). GPER may be a novel therapeutic target for intestinal I/R injury.
Qian Wang - One of the best experts on this subject based on the ideXlab platform.
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Activation of the G Protein-Coupled Estrogen Receptor Prevented the Development of Acute Colitis by Protecting the Crypt Cell.
The Journal of pharmacology and experimental therapeutics, 2020Co-Authors: Qian Wang, Shiquan Chai, Kaixuan Liu, Guanyu Chen, Tian Ming, Jianbo Liu, Shuyu Wen, Jiayi WangAbstract:G protein-coupled estrogen receptor (GPER) might be involved in ulcerative colitis (UC), but the direct effect of GPER on UC is still unclear. We used male C57BL/6 mice to establish the acute colitis model with administration of dextran sulfate sodium and explored the effect of GPER on acute colitis and its possible mechanism. The selective GPER agonist G-1 inhibited weight loss and colon shortening and decreased the disease activity index for colitis and histologic damage in mice with colitis. All of these effects were prevented by a selective GPER blocker. G-1 administration prevented the dysfunction of tight junction protein expression and goblet Cells in colitis model and thus inhibited the increase of mucosal permeability in colitis-suffering mice significantly. GPER activation reduced expression of glucose-regulating peptide-78 and anti-CCAAT/enhancer-binding protein homologous protein and attenuated the three arms of the unfolded protein response in colitis. G-1 therapy inhibited the increase of cleavage caspase-3- and TUNEL-positive Cells in colonic Crypts in the colitis model, increased the number of Ki67- and bromodeoxyuridine-positive Cells in Crypts, and reversed the decrease of cyclin D1 and cyclin B1 expression in colitis, indicating its protective effect on Crypt Cells. In cultured CCD841 Cells, G-1 treatment fought against Cell injury induced by endoplasmic reticulum stress. These findings demonstrate that GPER activation prevents colitis by protecting the colonic Crypt Cells, which are associated with inhibition of endoplasmic reticulum stress. SIGNIFICANCE STATEMENT: We demonstrate that G protein-coupled estrogen receptor (GPER) activation prevents dextran sulfate sodium-induced acute colitis by protecting the Crypt Cells, showing that it inhibited the Crypt Cell apoptosis and protected proliferation of Crypt Cells, which resulted in protection of the intestinal mucosal barrier. This protective effect was achieved (at least in part) by inhibiting endoplasmic reticulum stress. Mucosal healing is regarded as a key therapeutic target for colitis, and GPER is expected to become a new therapeutic target for colitis.
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activation of g protein coupled estrogen receptor protects intestine from ischemia reperfusion injury in mice by protecting the Crypt Cell proliferation
Clinical Science, 2019Co-Authors: Shiquan Chai, Kaixuan Liu, Wanbing Feng, Tiantian Liu, Qian Wang, Rong Zhou, Shiming Chen, Liyan Wang, Guanyu Chen, Tian MingAbstract:The intestinal ischemia/reperfusion (I/R) injury is a common clinical event related with high mortality in patients undergoing surgery or trauma. Estrogen exerts salutary effect on intestinal I/R injury, but the receptor type is not totally understood. We aimed to identify whether the G protein-coupled estrogen receptor (GPER) could protect the intestine against I/R injury and explored the mechanism. Adult male C57BL/6 mice were subjected to intestinal I/R injury by clamping (45 min) of the superior mesenteric artery followed by 4 h of intestinal reperfusion. Our results revealed that the selective GPER blocker abolished the protective effect of estrogen on intestinal I/R injury. Selective GPER agonist G-1 significantly alleviated I/R-induced intestinal mucosal damage, neutrophil infiltration, up-regulation of TNF-α and cyclooxygenase-2 (Cox-2) expression, and restored impaired intestinal barrier function. G-1 could ameliorate the impaired Crypt Cell proliferation ability induced by I/R and restore the decrease in villus height and Crypt depth. The up-regulation of inducible nitric oxide synthase (iNOS) expression after I/R treatment was attenuated by G-1 administration. Moreover, selective iNOS inhibitor had a similar effect with G-1 on promoting the proliferation of Crypt Cells in the intestinal I/R model. Both GPER and iNOS were expressed in leucine-rich repeat containing G-protein coupled receptor 5 (Lgr5) positive stem Cells in Crypt. Together, these findings demonstrate that GPER activation can prompt epithelial Cell repair following intestinal injury, which occurred at least in part by inhibiting the iNOS expression in intestinal stem Cells (ISCs). GPER may be a novel therapeutic target for intestinal I/R injury.
Guanyu Chen - One of the best experts on this subject based on the ideXlab platform.
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Activation of the G Protein-Coupled Estrogen Receptor Prevented the Development of Acute Colitis by Protecting the Crypt Cell.
The Journal of pharmacology and experimental therapeutics, 2020Co-Authors: Qian Wang, Shiquan Chai, Kaixuan Liu, Guanyu Chen, Tian Ming, Jianbo Liu, Shuyu Wen, Jiayi WangAbstract:G protein-coupled estrogen receptor (GPER) might be involved in ulcerative colitis (UC), but the direct effect of GPER on UC is still unclear. We used male C57BL/6 mice to establish the acute colitis model with administration of dextran sulfate sodium and explored the effect of GPER on acute colitis and its possible mechanism. The selective GPER agonist G-1 inhibited weight loss and colon shortening and decreased the disease activity index for colitis and histologic damage in mice with colitis. All of these effects were prevented by a selective GPER blocker. G-1 administration prevented the dysfunction of tight junction protein expression and goblet Cells in colitis model and thus inhibited the increase of mucosal permeability in colitis-suffering mice significantly. GPER activation reduced expression of glucose-regulating peptide-78 and anti-CCAAT/enhancer-binding protein homologous protein and attenuated the three arms of the unfolded protein response in colitis. G-1 therapy inhibited the increase of cleavage caspase-3- and TUNEL-positive Cells in colonic Crypts in the colitis model, increased the number of Ki67- and bromodeoxyuridine-positive Cells in Crypts, and reversed the decrease of cyclin D1 and cyclin B1 expression in colitis, indicating its protective effect on Crypt Cells. In cultured CCD841 Cells, G-1 treatment fought against Cell injury induced by endoplasmic reticulum stress. These findings demonstrate that GPER activation prevents colitis by protecting the colonic Crypt Cells, which are associated with inhibition of endoplasmic reticulum stress. SIGNIFICANCE STATEMENT: We demonstrate that G protein-coupled estrogen receptor (GPER) activation prevents dextran sulfate sodium-induced acute colitis by protecting the Crypt Cells, showing that it inhibited the Crypt Cell apoptosis and protected proliferation of Crypt Cells, which resulted in protection of the intestinal mucosal barrier. This protective effect was achieved (at least in part) by inhibiting endoplasmic reticulum stress. Mucosal healing is regarded as a key therapeutic target for colitis, and GPER is expected to become a new therapeutic target for colitis.
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activation of g protein coupled estrogen receptor protects intestine from ischemia reperfusion injury in mice by protecting the Crypt Cell proliferation
Clinical Science, 2019Co-Authors: Shiquan Chai, Kaixuan Liu, Wanbing Feng, Tiantian Liu, Qian Wang, Rong Zhou, Shiming Chen, Liyan Wang, Guanyu Chen, Tian MingAbstract:The intestinal ischemia/reperfusion (I/R) injury is a common clinical event related with high mortality in patients undergoing surgery or trauma. Estrogen exerts salutary effect on intestinal I/R injury, but the receptor type is not totally understood. We aimed to identify whether the G protein-coupled estrogen receptor (GPER) could protect the intestine against I/R injury and explored the mechanism. Adult male C57BL/6 mice were subjected to intestinal I/R injury by clamping (45 min) of the superior mesenteric artery followed by 4 h of intestinal reperfusion. Our results revealed that the selective GPER blocker abolished the protective effect of estrogen on intestinal I/R injury. Selective GPER agonist G-1 significantly alleviated I/R-induced intestinal mucosal damage, neutrophil infiltration, up-regulation of TNF-α and cyclooxygenase-2 (Cox-2) expression, and restored impaired intestinal barrier function. G-1 could ameliorate the impaired Crypt Cell proliferation ability induced by I/R and restore the decrease in villus height and Crypt depth. The up-regulation of inducible nitric oxide synthase (iNOS) expression after I/R treatment was attenuated by G-1 administration. Moreover, selective iNOS inhibitor had a similar effect with G-1 on promoting the proliferation of Crypt Cells in the intestinal I/R model. Both GPER and iNOS were expressed in leucine-rich repeat containing G-protein coupled receptor 5 (Lgr5) positive stem Cells in Crypt. Together, these findings demonstrate that GPER activation can prompt epithelial Cell repair following intestinal injury, which occurred at least in part by inhibiting the iNOS expression in intestinal stem Cells (ISCs). GPER may be a novel therapeutic target for intestinal I/R injury.
Kaixuan Liu - One of the best experts on this subject based on the ideXlab platform.
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Activation of the G Protein-Coupled Estrogen Receptor Prevented the Development of Acute Colitis by Protecting the Crypt Cell.
The Journal of pharmacology and experimental therapeutics, 2020Co-Authors: Qian Wang, Shiquan Chai, Kaixuan Liu, Guanyu Chen, Tian Ming, Jianbo Liu, Shuyu Wen, Jiayi WangAbstract:G protein-coupled estrogen receptor (GPER) might be involved in ulcerative colitis (UC), but the direct effect of GPER on UC is still unclear. We used male C57BL/6 mice to establish the acute colitis model with administration of dextran sulfate sodium and explored the effect of GPER on acute colitis and its possible mechanism. The selective GPER agonist G-1 inhibited weight loss and colon shortening and decreased the disease activity index for colitis and histologic damage in mice with colitis. All of these effects were prevented by a selective GPER blocker. G-1 administration prevented the dysfunction of tight junction protein expression and goblet Cells in colitis model and thus inhibited the increase of mucosal permeability in colitis-suffering mice significantly. GPER activation reduced expression of glucose-regulating peptide-78 and anti-CCAAT/enhancer-binding protein homologous protein and attenuated the three arms of the unfolded protein response in colitis. G-1 therapy inhibited the increase of cleavage caspase-3- and TUNEL-positive Cells in colonic Crypts in the colitis model, increased the number of Ki67- and bromodeoxyuridine-positive Cells in Crypts, and reversed the decrease of cyclin D1 and cyclin B1 expression in colitis, indicating its protective effect on Crypt Cells. In cultured CCD841 Cells, G-1 treatment fought against Cell injury induced by endoplasmic reticulum stress. These findings demonstrate that GPER activation prevents colitis by protecting the colonic Crypt Cells, which are associated with inhibition of endoplasmic reticulum stress. SIGNIFICANCE STATEMENT: We demonstrate that G protein-coupled estrogen receptor (GPER) activation prevents dextran sulfate sodium-induced acute colitis by protecting the Crypt Cells, showing that it inhibited the Crypt Cell apoptosis and protected proliferation of Crypt Cells, which resulted in protection of the intestinal mucosal barrier. This protective effect was achieved (at least in part) by inhibiting endoplasmic reticulum stress. Mucosal healing is regarded as a key therapeutic target for colitis, and GPER is expected to become a new therapeutic target for colitis.
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activation of g protein coupled estrogen receptor protects intestine from ischemia reperfusion injury in mice by protecting the Crypt Cell proliferation
Clinical Science, 2019Co-Authors: Shiquan Chai, Kaixuan Liu, Wanbing Feng, Tiantian Liu, Qian Wang, Rong Zhou, Shiming Chen, Liyan Wang, Guanyu Chen, Tian MingAbstract:The intestinal ischemia/reperfusion (I/R) injury is a common clinical event related with high mortality in patients undergoing surgery or trauma. Estrogen exerts salutary effect on intestinal I/R injury, but the receptor type is not totally understood. We aimed to identify whether the G protein-coupled estrogen receptor (GPER) could protect the intestine against I/R injury and explored the mechanism. Adult male C57BL/6 mice were subjected to intestinal I/R injury by clamping (45 min) of the superior mesenteric artery followed by 4 h of intestinal reperfusion. Our results revealed that the selective GPER blocker abolished the protective effect of estrogen on intestinal I/R injury. Selective GPER agonist G-1 significantly alleviated I/R-induced intestinal mucosal damage, neutrophil infiltration, up-regulation of TNF-α and cyclooxygenase-2 (Cox-2) expression, and restored impaired intestinal barrier function. G-1 could ameliorate the impaired Crypt Cell proliferation ability induced by I/R and restore the decrease in villus height and Crypt depth. The up-regulation of inducible nitric oxide synthase (iNOS) expression after I/R treatment was attenuated by G-1 administration. Moreover, selective iNOS inhibitor had a similar effect with G-1 on promoting the proliferation of Crypt Cells in the intestinal I/R model. Both GPER and iNOS were expressed in leucine-rich repeat containing G-protein coupled receptor 5 (Lgr5) positive stem Cells in Crypt. Together, these findings demonstrate that GPER activation can prompt epithelial Cell repair following intestinal injury, which occurred at least in part by inhibiting the iNOS expression in intestinal stem Cells (ISCs). GPER may be a novel therapeutic target for intestinal I/R injury.