{"title":"Galectin-3 介导了 PDGF 对肺动脉高压的影响。","authors":"Shaomei Guo, Ziming Feng","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Aims: </strong>The present study aimed to perform in vitro experiments to investigate whether Galectin-3 (Gal-3) mediates the effect of platelet-derived growth factor (PDGF) on pulmonary arterial smooth muscle cells (PASMC) proliferation, apoptosis and migration, and to reveal the mechanism of how Gal-3 functions in the pathogenesis of pulmonary arterial hypertension (PAH).</p><p><strong>Methods: </strong>Pulmonary arterial smooth muscle cells (PASMC) were treated with various concentration of PDGF for indicated times, and the expression of Gal-3 was analyzed by western blotting. Gal-3 siRNA was transfected into the PASMC to knock down endogenous Gal-3. MTT assay was performed to examine cell proliferation. Transwell-migration assay was used to determine cell migration ability. Cell apoptosis rate was determined by flow cytometric analysis.</p><p><strong>Results: </strong>The result showed that the expression of Gal-3 protein was induced by PDGF in a dose- and a time-dependent manner. PDGF contributes to the progression of PAH by inducing cell proliferation and migration, as well as inhibiting cell apoptosis of PASMC. However, these effects of PDGF on PASMC were attenuated by Gal-3 knockdown.</p><p><strong>Conclusion: </strong>The present study provided potential evidence about the role of Gal-3 in the pathophysiological mechanisms of PAH. This study firstly demonstrated that Gal-3 could be induced by PDGF in PASMC, and mediates the effect of PDGF on PASMC proliferation, apoptosis and migration, thus contributing to the pathogenesis of PAH.</p>","PeriodicalId":13892,"journal":{"name":"International journal of clinical and experimental medicine","volume":"8 9","pages":"15302-7"},"PeriodicalIF":0.2000,"publicationDate":"2015-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4658907/pdf/","citationCount":"0","resultStr":"{\"title\":\"Galectin-3 mediates the effect of PDGF on pulmonary arterial hypertension.\",\"authors\":\"Shaomei Guo, Ziming Feng\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Aims: </strong>The present study aimed to perform in vitro experiments to investigate whether Galectin-3 (Gal-3) mediates the effect of platelet-derived growth factor (PDGF) on pulmonary arterial smooth muscle cells (PASMC) proliferation, apoptosis and migration, and to reveal the mechanism of how Gal-3 functions in the pathogenesis of pulmonary arterial hypertension (PAH).</p><p><strong>Methods: </strong>Pulmonary arterial smooth muscle cells (PASMC) were treated with various concentration of PDGF for indicated times, and the expression of Gal-3 was analyzed by western blotting. Gal-3 siRNA was transfected into the PASMC to knock down endogenous Gal-3. MTT assay was performed to examine cell proliferation. Transwell-migration assay was used to determine cell migration ability. Cell apoptosis rate was determined by flow cytometric analysis.</p><p><strong>Results: </strong>The result showed that the expression of Gal-3 protein was induced by PDGF in a dose- and a time-dependent manner. PDGF contributes to the progression of PAH by inducing cell proliferation and migration, as well as inhibiting cell apoptosis of PASMC. However, these effects of PDGF on PASMC were attenuated by Gal-3 knockdown.</p><p><strong>Conclusion: </strong>The present study provided potential evidence about the role of Gal-3 in the pathophysiological mechanisms of PAH. This study firstly demonstrated that Gal-3 could be induced by PDGF in PASMC, and mediates the effect of PDGF on PASMC proliferation, apoptosis and migration, thus contributing to the pathogenesis of PAH.</p>\",\"PeriodicalId\":13892,\"journal\":{\"name\":\"International journal of clinical and experimental medicine\",\"volume\":\"8 9\",\"pages\":\"15302-7\"},\"PeriodicalIF\":0.2000,\"publicationDate\":\"2015-09-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4658907/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International journal of clinical and experimental medicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2015/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q4\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International journal of clinical and experimental medicine","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2015/1/1 0:00:00","PubModel":"eCollection","JCR":"Q4","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
Galectin-3 mediates the effect of PDGF on pulmonary arterial hypertension.
Aims: The present study aimed to perform in vitro experiments to investigate whether Galectin-3 (Gal-3) mediates the effect of platelet-derived growth factor (PDGF) on pulmonary arterial smooth muscle cells (PASMC) proliferation, apoptosis and migration, and to reveal the mechanism of how Gal-3 functions in the pathogenesis of pulmonary arterial hypertension (PAH).
Methods: Pulmonary arterial smooth muscle cells (PASMC) were treated with various concentration of PDGF for indicated times, and the expression of Gal-3 was analyzed by western blotting. Gal-3 siRNA was transfected into the PASMC to knock down endogenous Gal-3. MTT assay was performed to examine cell proliferation. Transwell-migration assay was used to determine cell migration ability. Cell apoptosis rate was determined by flow cytometric analysis.
Results: The result showed that the expression of Gal-3 protein was induced by PDGF in a dose- and a time-dependent manner. PDGF contributes to the progression of PAH by inducing cell proliferation and migration, as well as inhibiting cell apoptosis of PASMC. However, these effects of PDGF on PASMC were attenuated by Gal-3 knockdown.
Conclusion: The present study provided potential evidence about the role of Gal-3 in the pathophysiological mechanisms of PAH. This study firstly demonstrated that Gal-3 could be induced by PDGF in PASMC, and mediates the effect of PDGF on PASMC proliferation, apoptosis and migration, thus contributing to the pathogenesis of PAH.
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