GPR 30 reduces myocardial infarct area and fibrosis in female ovariectomized mice by activating the PI3K/AKT pathway
GPR 30 reduces myocardial infarct area and fibrosis in female ovariectomized mice by activating the PI3K/AKT pathway
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GPR 30 通过激活 PI3K/AKT 通路减少雌性卵巢切除小鼠的心肌梗塞面积和纤维化
DOI：
10.1016/j.lfs.2019.03.049
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发表时间：
2019-06
期刊：
影响因子：
6.1
通讯作者：
Liu Jincheng
中科院分区：
文献类型：
--
作者：
Wang Xiaowu;Lu Linhe;Tan Yanzhen;Jiang Liqing;Zhao Minggao;Gao Erhe;Yu Shiqiang;Liu Jincheng
AimsEstrogen plays an important role in cardioprotection. Animal experiments showed that the G-protein coupled estrogen receptor 30 (GPR30) specific agonist G1 could reduce post-ischemic dysfunction and inhibit cardiac fibroblast proliferation. However, the underlying mechanism of action is not clear. The current study tests the hypothesis that GPR30 reduces myocardial infarct area and fibrosis in female ovariectomized (OVX) mice by activating the PI3K/AKT pathway.Main methodsIn this study, we established a myocardial infarction (MI) animal model derived from OVX C57BL/6 female mice, and investigated the effect of G1 on cardiac function by echocardiography and Hemodynamics, morphology and expression of fibrosis-related and apoptosis-related proteins by Masson's trichrome and H&E, Immunofluorescence, Western blotting and TUNEL.Key findingsCombination with OVX significantly increased myocardial fibrosis and MI area compared to MI treatment alone, as determined by echocardiography and hemodynamics. Further addition of G1 changed the expression of apoptosis-related proteins, decreased the levels of tumor necrosis factor-α and interleukin-10, and reduced the degree of myocardial fibrosis and myocardial infarct area. Primary cultured cardiac fibroblasts (CFs) were subjected to hypoxia/serum deprivation (H/SD) simulating the in vivo ischemia model. When the PI3K/AKT pathway was inhibited by wortmanin in H/SD CFs, G1 failed to induce significant changes in the expression of apoptosis-related proteins.SignificanceIt suggested that GPR30 may improve cardiac function in female OVX mice by activating the PI3K/AKT pathway and reducing myocardial infarct size and fibrosis.
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DOI：
10.1016/j.jacbts.2016.08.008
发表时间：
2016-12
期刊：
JACC. Basic to translational science
影响因子：
--
作者：
Knezevic T;Myers VD;Su F;Wang J;Song J;Zhang XQ;Gao E;Gao G;Muniswamy M;Gupta MK;Gordon J;Weiner KN;Rabinowitz J;Ramsey FV;Tilley DG;Khalili K;Cheung JY;Feldman AM
通讯作者：
Feldman AM
影响因子：
20.1
作者：
Tao L;Wang Y;Gao E;Zhang H;Yuan Y;Lau WB;Chan L;Koch WJ;Ma XL
通讯作者：
Ma XL
G蛋白偶联的雌激素受体GPER在健康和疾病中。
DOI：
10.1038/nrendo.2011.122
发表时间：
2011-08-16
期刊：
Nature reviews. Endocrinology
影响因子：
--
作者：
通讯作者：
--
G蛋白偶联的雌激素受体GPER/GPR30作为心血管功能的调节剂。
影响因子：
4
作者：
Meyer, Matthias R.;Prossnitz, Eric R.;Barton, Matthias
通讯作者：
Barton, Matthias
影响因子：
4.6
作者：
Sivasinprasasn S;Tanajak P;Pongkan W;Pratchayasakul W;Chattipakorn SC;Chattipakorn N
通讯作者：
Chattipakorn N