PPARδ的激活通过抑制糖酵解减轻PDGF-BB诱导的肺动脉平滑肌细胞表型转化
R34%R363.2%R543.2; 目的:探讨过氧化物酶体增殖物激活受体δ(PPARδ)激动剂GW501516对血小板源性生长因子BB(PDGF-BB)诱导的大鼠肺动脉平滑肌细胞(PASMCs)表型转化和糖酵解的影响及其机制.方法:以20 μg/L PDGF-BB作为诱导剂,建立PASMCs表型转化及糖酵解的细胞模型,通过GW501516或糖酵解抑制剂2-脱氧葡萄糖(2-DG)干预24 h,检测PASMCs表型和糖酵解的变化.设置缺氧诱导因子1α(HIF-1α)抑制剂LW6为阳性对照组,通过GW501516和(或)HIF-1α稳定剂二甲基草酰甘氨酸(DMOG)干预24 h,测定细胞外乳酸含量...
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| Published in | 中国病理生理杂志 Vol. 39; no. 6; pp. 988 - 995 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | Chinese |
| Published |
武汉市第一医院心血管内科,湖北 武汉 430022
01.06.2023
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1000-4718 |
| DOI | 10.3969/j.issn.1000-4718.2023.06.004 |
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| Abstract | R34%R363.2%R543.2; 目的:探讨过氧化物酶体增殖物激活受体δ(PPARδ)激动剂GW501516对血小板源性生长因子BB(PDGF-BB)诱导的大鼠肺动脉平滑肌细胞(PASMCs)表型转化和糖酵解的影响及其机制.方法:以20 μg/L PDGF-BB作为诱导剂,建立PASMCs表型转化及糖酵解的细胞模型,通过GW501516或糖酵解抑制剂2-脱氧葡萄糖(2-DG)干预24 h,检测PASMCs表型和糖酵解的变化.设置缺氧诱导因子1α(HIF-1α)抑制剂LW6为阳性对照组,通过GW501516和(或)HIF-1α稳定剂二甲基草酰甘氨酸(DMOG)干预24 h,测定细胞外乳酸含量及葡萄糖摄取量的变化;检测PPARδ、血管平滑肌细胞表型标志蛋白、HIF-1α及糖酵解相关蛋白表达,探讨GW501516抑制PASMCs表型转化及糖酵解的机制.结果:PDGF-BB刺激可抑制PASMCs内PPARδ表达,而GW501516处理可促进PPARδ表达(P＜0.05).GW501516上调PASMCs收缩表型标志蛋白平滑肌22α蛋白(SM22α)和α-平滑肌肌动蛋白(α-SMA)表达,下调合成表型标志蛋白波形蛋白(vimentin)和骨桥蛋白(OPN)表达,减少细胞外乳酸生成,抑制细胞对葡萄糖的摄取(P＜0.05),而2-DG在抑制PASMCs表型转化及糖酵解方面的作用与GW501516相似.LW6和GW501516可抑制糖酵解与细胞表型转化,抑制HIF-1α、葡萄糖转运体1(GlUT1)、丙酮酸脱氢酶激酶1(PDK1)、乳酸脱氢酶A(LDHA)和单羧酸转运体蛋白4(MCT4)表达,同时促进丙酮酸脱氢酶(PDH)表达(P＜0.05),而DMOG可逆转GW501516的上述作用(P＜0.05).结论:PPARδ激动剂GW501516可通过抑制糖酵解而抑制PDGF-BB诱导的PASMCs表型转化,其机制可能与抑制HIF-1α的表达有关. |
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| AbstractList | R34%R363.2%R543.2; 目的:探讨过氧化物酶体增殖物激活受体δ(PPARδ)激动剂GW501516对血小板源性生长因子BB(PDGF-BB)诱导的大鼠肺动脉平滑肌细胞(PASMCs)表型转化和糖酵解的影响及其机制.方法:以20 μg/L PDGF-BB作为诱导剂,建立PASMCs表型转化及糖酵解的细胞模型,通过GW501516或糖酵解抑制剂2-脱氧葡萄糖(2-DG)干预24 h,检测PASMCs表型和糖酵解的变化.设置缺氧诱导因子1α(HIF-1α)抑制剂LW6为阳性对照组,通过GW501516和(或)HIF-1α稳定剂二甲基草酰甘氨酸(DMOG)干预24 h,测定细胞外乳酸含量及葡萄糖摄取量的变化;检测PPARδ、血管平滑肌细胞表型标志蛋白、HIF-1α及糖酵解相关蛋白表达,探讨GW501516抑制PASMCs表型转化及糖酵解的机制.结果:PDGF-BB刺激可抑制PASMCs内PPARδ表达,而GW501516处理可促进PPARδ表达(P＜0.05).GW501516上调PASMCs收缩表型标志蛋白平滑肌22α蛋白(SM22α)和α-平滑肌肌动蛋白(α-SMA)表达,下调合成表型标志蛋白波形蛋白(vimentin)和骨桥蛋白(OPN)表达,减少细胞外乳酸生成,抑制细胞对葡萄糖的摄取(P＜0.05),而2-DG在抑制PASMCs表型转化及糖酵解方面的作用与GW501516相似.LW6和GW501516可抑制糖酵解与细胞表型转化,抑制HIF-1α、葡萄糖转运体1(GlUT1)、丙酮酸脱氢酶激酶1(PDK1)、乳酸脱氢酶A(LDHA)和单羧酸转运体蛋白4(MCT4)表达,同时促进丙酮酸脱氢酶(PDH)表达(P＜0.05),而DMOG可逆转GW501516的上述作用(P＜0.05).结论:PPARδ激动剂GW501516可通过抑制糖酵解而抑制PDGF-BB诱导的PASMCs表型转化,其机制可能与抑制HIF-1α的表达有关. |
| Author | 陈昌贵 贺立群 易春峰 王栋 |
| AuthorAffiliation | 武汉市第一医院心血管内科,湖北 武汉 430022 |
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| Author_FL | YI Chunfeng HE Liqun WANG Dong CHEN Changgui |
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| Copyright | Copyright © Wanfang Data Co. Ltd. All Rights Reserved. |
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| DocumentTitle_FL | Activation of PPARδ suppresses phenotypic switching of PDGF-BB-in-duced pulmonary artery smooth muscle cells via inhibition of glycolysis |
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| Keywords | 糖酵解 过氧化物酶体增殖物激活受体δ 肺动脉平滑肌细胞 缺氧诱导因子1α 血小板源性生长因子BB |
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| Title | PPARδ的激活通过抑制糖酵解减轻PDGF-BB诱导的肺动脉平滑肌细胞表型转化 |
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