GPR 30 reduces myocardial infarct area and fibrosis in female ovariectomized mice by activating the PI3K/AKT pathway
Estrogen 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. T...
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| Veröffentlicht in: | Life sciences (1973) 2019-06, Vol.226, p.22-32 |
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| creator | Wang, Xiaowu Lu, Linhe Tan, Yanzhen Jiang, Liqing Zhao, Minggao Gao, Erhe Yu, Shiqiang Liu, Jincheng |
| description | Estrogen 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.
In 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.
Combination 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.
It suggested that GPR30 may improve cardiac function in female OVX mice by activating the PI3K/AKT pathway and reducing myocardial infarct size and fibrosis. |
| doi_str_mv | 10.1016/j.lfs.2019.03.049 |
| format | Article |
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In 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.
Combination 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.
It suggested that GPR30 may improve cardiac function in female OVX mice by activating the PI3K/AKT pathway and reducing myocardial infarct size and fibrosis.</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2019.03.049</identifier><identifier>PMID: 30905784</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Animal models ; Animals ; Apoptosis ; Benzodioxoles - pharmacokinetics ; Cardiac fibroblasts ; Cardioprotection ; Cell Proliferation ; Computer simulation ; Deprivation ; Disease Models, Animal ; Echocardiography ; Estrogens ; Female ; Fibroblasts ; Fibroblasts - metabolism ; Fibrosis ; Fibrosis - metabolism ; G-protein coupled estrogen receptor 30 (GPR30) ; Heart - physiology ; Hemodynamics ; Hypoxia ; Hypoxia/serum deprivation (H/SD) ; Immunofluorescence ; In vivo methods and tests ; Interleukin 10 ; Ischemia ; Mice ; Mice, Inbred C57BL ; Morphology ; Myocardial infarction ; Myocardial infarction (MI) ; Myocardial Infarction - metabolism ; Myocardium - metabolism ; Ovariectomy ; Phosphatidylinositol 3-Kinases ; Proteins ; Proto-Oncogene Proteins c-akt ; Quinolines ; Receptors, Estrogen - metabolism ; Receptors, Estrogen - physiology ; Receptors, G-Protein-Coupled - agonists ; Receptors, G-Protein-Coupled - metabolism ; Receptors, G-Protein-Coupled - physiology ; Signal Transduction ; Tumor necrosis factor-α ; Western blotting</subject><ispartof>Life sciences (1973), 2019-06, Vol.226, p.22-32</ispartof><rights>2019 Elsevier Inc.</rights><rights>Copyright © 2019 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier BV Jun 1, 2019</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c381t-2f6424422187643bcb3325fe61271f67bc9253d2827fea089f6e02d9c14511783</citedby><cites>FETCH-LOGICAL-c381t-2f6424422187643bcb3325fe61271f67bc9253d2827fea089f6e02d9c14511783</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.lfs.2019.03.049$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30905784$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Xiaowu</creatorcontrib><creatorcontrib>Lu, Linhe</creatorcontrib><creatorcontrib>Tan, Yanzhen</creatorcontrib><creatorcontrib>Jiang, Liqing</creatorcontrib><creatorcontrib>Zhao, Minggao</creatorcontrib><creatorcontrib>Gao, Erhe</creatorcontrib><creatorcontrib>Yu, Shiqiang</creatorcontrib><creatorcontrib>Liu, Jincheng</creatorcontrib><title>GPR 30 reduces myocardial infarct area and fibrosis in female ovariectomized mice by activating the PI3K/AKT pathway</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>Estrogen 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.
In 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.
Combination 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.
It suggested that GPR30 may improve cardiac function in female OVX mice by activating the PI3K/AKT pathway and reducing myocardial infarct size and fibrosis.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Animal models</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Benzodioxoles - pharmacokinetics</subject><subject>Cardiac fibroblasts</subject><subject>Cardioprotection</subject><subject>Cell Proliferation</subject><subject>Computer simulation</subject><subject>Deprivation</subject><subject>Disease Models, Animal</subject><subject>Echocardiography</subject><subject>Estrogens</subject><subject>Female</subject><subject>Fibroblasts</subject><subject>Fibroblasts - metabolism</subject><subject>Fibrosis</subject><subject>Fibrosis - metabolism</subject><subject>G-protein coupled estrogen receptor 30 (GPR30)</subject><subject>Heart - physiology</subject><subject>Hemodynamics</subject><subject>Hypoxia</subject><subject>Hypoxia/serum deprivation (H/SD)</subject><subject>Immunofluorescence</subject><subject>In vivo methods and tests</subject><subject>Interleukin 10</subject><subject>Ischemia</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Morphology</subject><subject>Myocardial infarction</subject><subject>Myocardial infarction (MI)</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardium - metabolism</subject><subject>Ovariectomy</subject><subject>Phosphatidylinositol 3-Kinases</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt</subject><subject>Quinolines</subject><subject>Receptors, Estrogen - metabolism</subject><subject>Receptors, Estrogen - physiology</subject><subject>Receptors, G-Protein-Coupled - agonists</subject><subject>Receptors, G-Protein-Coupled - metabolism</subject><subject>Receptors, G-Protein-Coupled - physiology</subject><subject>Signal Transduction</subject><subject>Tumor necrosis factor-α</subject><subject>Western blotting</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1v1DAQhi0EotvCD-CCLHFOOv6KE3GqqtJWrUSFytly7DH1apMstnfR8utxtYUjpznMM-_ofQj5wKBlwLrzdbsJueXAhhZEC3J4RVas10MDnWCvyQqAy0ZwUCfkNOc1ACilxVtyImAApXu5IuX64RsVQBP6ncNMp8PibPLRbmicg02uUJvQUjt7GuKYlhxz3dCAk90gXfY2RXRlmeJv9HSKDul4oNaVuLclzj9oeUL6cCvuzi_uHunWlqdf9vCOvAl2k_H9yzwj379cPV7eNPdfr28vL-4bJ3pWGh46yaXkvHbqpBjdKARXATvGNQudHt3AlfC85zqghX4IHQL3g2NSMaZ7cUY-HXO3afm5w1zMetmlub40nEuutWJKVYodKVfb5YTBbFOcbDoYBubZs1mb6tk8ezYgTPVcbz6-JO_GCf2_i79iK_D5CGDtt4-YTHYRZ4c-purL-CX-J_4P3G2L_g</recordid><startdate>20190601</startdate><enddate>20190601</enddate><creator>Wang, Xiaowu</creator><creator>Lu, Linhe</creator><creator>Tan, Yanzhen</creator><creator>Jiang, Liqing</creator><creator>Zhao, Minggao</creator><creator>Gao, Erhe</creator><creator>Yu, Shiqiang</creator><creator>Liu, Jincheng</creator><general>Elsevier Inc</general><general>Elsevier BV</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20190601</creationdate><title>GPR 30 reduces myocardial infarct area and fibrosis in female ovariectomized mice by activating the PI3K/AKT pathway</title><author>Wang, Xiaowu ; Lu, Linhe ; Tan, Yanzhen ; Jiang, Liqing ; Zhao, Minggao ; Gao, Erhe ; Yu, Shiqiang ; Liu, Jincheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c381t-2f6424422187643bcb3325fe61271f67bc9253d2827fea089f6e02d9c14511783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Animal models</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Benzodioxoles - pharmacokinetics</topic><topic>Cardiac fibroblasts</topic><topic>Cardioprotection</topic><topic>Cell Proliferation</topic><topic>Computer simulation</topic><topic>Deprivation</topic><topic>Disease Models, Animal</topic><topic>Echocardiography</topic><topic>Estrogens</topic><topic>Female</topic><topic>Fibroblasts</topic><topic>Fibroblasts - metabolism</topic><topic>Fibrosis</topic><topic>Fibrosis - metabolism</topic><topic>G-protein coupled estrogen receptor 30 (GPR30)</topic><topic>Heart - physiology</topic><topic>Hemodynamics</topic><topic>Hypoxia</topic><topic>Hypoxia/serum deprivation (H/SD)</topic><topic>Immunofluorescence</topic><topic>In vivo methods and tests</topic><topic>Interleukin 10</topic><topic>Ischemia</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Morphology</topic><topic>Myocardial infarction</topic><topic>Myocardial infarction (MI)</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardium - metabolism</topic><topic>Ovariectomy</topic><topic>Phosphatidylinositol 3-Kinases</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt</topic><topic>Quinolines</topic><topic>Receptors, Estrogen - metabolism</topic><topic>Receptors, Estrogen - physiology</topic><topic>Receptors, G-Protein-Coupled - agonists</topic><topic>Receptors, G-Protein-Coupled - metabolism</topic><topic>Receptors, G-Protein-Coupled - physiology</topic><topic>Signal Transduction</topic><topic>Tumor necrosis factor-α</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Xiaowu</creatorcontrib><creatorcontrib>Lu, Linhe</creatorcontrib><creatorcontrib>Tan, Yanzhen</creatorcontrib><creatorcontrib>Jiang, Liqing</creatorcontrib><creatorcontrib>Zhao, Minggao</creatorcontrib><creatorcontrib>Gao, Erhe</creatorcontrib><creatorcontrib>Yu, Shiqiang</creatorcontrib><creatorcontrib>Liu, Jincheng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Xiaowu</au><au>Lu, Linhe</au><au>Tan, Yanzhen</au><au>Jiang, Liqing</au><au>Zhao, Minggao</au><au>Gao, Erhe</au><au>Yu, Shiqiang</au><au>Liu, Jincheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>GPR 30 reduces myocardial infarct area and fibrosis in female ovariectomized mice by activating the PI3K/AKT pathway</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>2019-06-01</date><risdate>2019</risdate><volume>226</volume><spage>22</spage><epage>32</epage><pages>22-32</pages><issn>0024-3205</issn><eissn>1879-0631</eissn><abstract>Estrogen 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.
In 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.
Combination 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.
It suggested that GPR30 may improve cardiac function in female OVX mice by activating the PI3K/AKT pathway and reducing myocardial infarct size and fibrosis.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>30905784</pmid><doi>10.1016/j.lfs.2019.03.049</doi><tpages>11</tpages></addata></record> |
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| ispartof | Life sciences (1973), 2019-06, Vol.226, p.22-32 |
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| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Animal models Animals Apoptosis Benzodioxoles - pharmacokinetics Cardiac fibroblasts Cardioprotection Cell Proliferation Computer simulation Deprivation Disease Models, Animal Echocardiography Estrogens Female Fibroblasts Fibroblasts - metabolism Fibrosis Fibrosis - metabolism G-protein coupled estrogen receptor 30 (GPR30) Heart - physiology Hemodynamics Hypoxia Hypoxia/serum deprivation (H/SD) Immunofluorescence In vivo methods and tests Interleukin 10 Ischemia Mice Mice, Inbred C57BL Morphology Myocardial infarction Myocardial infarction (MI) Myocardial Infarction - metabolism Myocardium - metabolism Ovariectomy Phosphatidylinositol 3-Kinases Proteins Proto-Oncogene Proteins c-akt Quinolines Receptors, Estrogen - metabolism Receptors, Estrogen - physiology Receptors, G-Protein-Coupled - agonists Receptors, G-Protein-Coupled - metabolism Receptors, G-Protein-Coupled - physiology Signal Transduction Tumor necrosis factor-α Western blotting |
| title | GPR 30 reduces myocardial infarct area and fibrosis in female ovariectomized mice by activating the PI3K/AKT pathway |
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