The Activation of Peroxisome Proliferator-activated Receptor γ Enhances Insulin Signaling Pathways Via Up-regulating Chemerin Expression in High Glucose Treated HTR-8/SVneo Cells

Abstract. Objective:. To investigate whether peroxisome proliferator-activated receptor γ (PPARγ) agonists, rosiglitazone and GW1929, activate the phosphatidylinositol 3-kinase (PI3K)-AKT/protein kinase B pathway and the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase1/...

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Main Authors: Xuan Zhou, Li-Jie Wei, Jia-Qi Li, Jing-Yi Zhang, Sheng-Lan Zhu, Hui-Ting Zhang, Jing Jia, Jun Yu, Shao-Shuai Wang, Ling Feng, Dan-Dan Shi
Format: Article
Language:English
Published: Wolters Kluwer Health 2020-07-01
Series:Maternal-Fetal Medicine
Online Access:http://journals.lww.com/10.1097/FM9.0000000000000044
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author Xuan Zhou
Li-Jie Wei
Jia-Qi Li
Jing-Yi Zhang
Sheng-Lan Zhu
Hui-Ting Zhang
Jing Jia
Jun Yu
Shao-Shuai Wang
Ling Feng
Dan-Dan Shi
author_facet Xuan Zhou
Li-Jie Wei
Jia-Qi Li
Jing-Yi Zhang
Sheng-Lan Zhu
Hui-Ting Zhang
Jing Jia
Jun Yu
Shao-Shuai Wang
Ling Feng
Dan-Dan Shi
author_sort Xuan Zhou
collection DOAJ
description Abstract. Objective:. To investigate whether peroxisome proliferator-activated receptor γ (PPARγ) agonists, rosiglitazone and GW1929, activate the phosphatidylinositol 3-kinase (PI3K)-AKT/protein kinase B pathway and the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase1/2 (ERK1/2) pathway by upgrading the expression of chemerin. Methods:. The HTR-8/SVneo trophoblastic cells were cultured in vitro in high glucose concentration (25 mmol/L) to mimic gestational diabetic phenotypes. We transfected small interfering RNA into HTR-8/SVneo cells to silence two receptors of chemerin, that are chemokine-like receptor 1 (CMKLR1) and G protein-coupled receptor1 (GPR1). And recombinant human chemerin, PPARγ agonists (rosiglitazone, 10 μmol/L and GW1929, 10 μmol/L) and PPARγ inhibitor (GW9662, 5 μmol/L) were additionally added to the medium, respectively. The existence of chemerin was verified by immunocytochemistry, and the expressions of PPARγ, chemerin, and its receptors as well as insulin signaling-related factors PI3K, AKT2, and MAPK (ERK1/2) were detected by real time quantitative-polymerase chain reaction and western blot. Results:. Chemerin existed in the HTR-8/SVneo cells. Effects of chemerin on PI3K-AKT pathway and MAPK (ERK1/2) pathway were dependent on the density of chemerin. When rosiglitazone and GW1929 were added to the medium, the mRNA levels of PI3K, AKT2, and MAPK1 were upregulated (P < 0.05). Conversely, GW9662 downregulated the mRNA levels of AKT2 and MAPK1 (P < 0.05). Rosiglitazone and GW1929 increased the protein levels of PPARγ, chemerin, CMKLR1 and GPR1 (P < 0.05). Rosiglitazone and GW1929 had no effect on the expression of PI3K p110β and phospho-AKT2 without CMKLR1 (P > 0.05). Meanwhile, the expression of phospho-ERK2 remained unaffected in the absence of GPR1 (P > 0.05). Conclusion:. Both rosiglitazone and GW1929 have the effect of improving insulin signaling pathways via upgrading the level of chemerin in high glucose treated HTR-8/SVneo cells.
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spelling doaj.art-0754ff29907e429abc6ae3cd69e13fc32022-12-22T01:40:52ZengWolters Kluwer HealthMaternal-Fetal Medicine2641-58952020-07-012313114010.1097/FM9.0000000000000044202007000-00002The Activation of Peroxisome Proliferator-activated Receptor γ Enhances Insulin Signaling Pathways Via Up-regulating Chemerin Expression in High Glucose Treated HTR-8/SVneo CellsXuan Zhou0Li-Jie Wei1Jia-Qi Li2Jing-Yi Zhang3Sheng-Lan Zhu4Hui-Ting Zhang5Jing Jia6Jun Yu7Shao-Shuai Wang8Ling Feng9Dan-Dan Shi10Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.Department of Obstetrics and Gynecology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.Abstract. Objective:. To investigate whether peroxisome proliferator-activated receptor γ (PPARγ) agonists, rosiglitazone and GW1929, activate the phosphatidylinositol 3-kinase (PI3K)-AKT/protein kinase B pathway and the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase1/2 (ERK1/2) pathway by upgrading the expression of chemerin. Methods:. The HTR-8/SVneo trophoblastic cells were cultured in vitro in high glucose concentration (25 mmol/L) to mimic gestational diabetic phenotypes. We transfected small interfering RNA into HTR-8/SVneo cells to silence two receptors of chemerin, that are chemokine-like receptor 1 (CMKLR1) and G protein-coupled receptor1 (GPR1). And recombinant human chemerin, PPARγ agonists (rosiglitazone, 10 μmol/L and GW1929, 10 μmol/L) and PPARγ inhibitor (GW9662, 5 μmol/L) were additionally added to the medium, respectively. The existence of chemerin was verified by immunocytochemistry, and the expressions of PPARγ, chemerin, and its receptors as well as insulin signaling-related factors PI3K, AKT2, and MAPK (ERK1/2) were detected by real time quantitative-polymerase chain reaction and western blot. Results:. Chemerin existed in the HTR-8/SVneo cells. Effects of chemerin on PI3K-AKT pathway and MAPK (ERK1/2) pathway were dependent on the density of chemerin. When rosiglitazone and GW1929 were added to the medium, the mRNA levels of PI3K, AKT2, and MAPK1 were upregulated (P < 0.05). Conversely, GW9662 downregulated the mRNA levels of AKT2 and MAPK1 (P < 0.05). Rosiglitazone and GW1929 increased the protein levels of PPARγ, chemerin, CMKLR1 and GPR1 (P < 0.05). Rosiglitazone and GW1929 had no effect on the expression of PI3K p110β and phospho-AKT2 without CMKLR1 (P > 0.05). Meanwhile, the expression of phospho-ERK2 remained unaffected in the absence of GPR1 (P > 0.05). Conclusion:. Both rosiglitazone and GW1929 have the effect of improving insulin signaling pathways via upgrading the level of chemerin in high glucose treated HTR-8/SVneo cells.http://journals.lww.com/10.1097/FM9.0000000000000044
spellingShingle Xuan Zhou
Li-Jie Wei
Jia-Qi Li
Jing-Yi Zhang
Sheng-Lan Zhu
Hui-Ting Zhang
Jing Jia
Jun Yu
Shao-Shuai Wang
Ling Feng
Dan-Dan Shi
The Activation of Peroxisome Proliferator-activated Receptor γ Enhances Insulin Signaling Pathways Via Up-regulating Chemerin Expression in High Glucose Treated HTR-8/SVneo Cells
Maternal-Fetal Medicine
title The Activation of Peroxisome Proliferator-activated Receptor γ Enhances Insulin Signaling Pathways Via Up-regulating Chemerin Expression in High Glucose Treated HTR-8/SVneo Cells
title_full The Activation of Peroxisome Proliferator-activated Receptor γ Enhances Insulin Signaling Pathways Via Up-regulating Chemerin Expression in High Glucose Treated HTR-8/SVneo Cells
title_fullStr The Activation of Peroxisome Proliferator-activated Receptor γ Enhances Insulin Signaling Pathways Via Up-regulating Chemerin Expression in High Glucose Treated HTR-8/SVneo Cells
title_full_unstemmed The Activation of Peroxisome Proliferator-activated Receptor γ Enhances Insulin Signaling Pathways Via Up-regulating Chemerin Expression in High Glucose Treated HTR-8/SVneo Cells
title_short The Activation of Peroxisome Proliferator-activated Receptor γ Enhances Insulin Signaling Pathways Via Up-regulating Chemerin Expression in High Glucose Treated HTR-8/SVneo Cells
title_sort activation of peroxisome proliferator activated receptor γ enhances insulin signaling pathways via up regulating chemerin expression in high glucose treated htr 8 svneo cells
url http://journals.lww.com/10.1097/FM9.0000000000000044
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