| 李圣维,夏国际,熊墨煌,应 如,徐劲松.内质网应激促进肺动脉平滑肌细胞的表型转化[J].,2018,(3):458-462 |
| 内质网应激促进肺动脉平滑肌细胞的表型转化 |
| Endoplasmic Reticulum Stress induced Phenotypic Modulation in Pulmonary Arterial Smooth Muscle Cells |
| 投稿时间：2017-04-27 修订日期：2017-05-23 |
| DOI：10.13241/j.cnki.pmb.2018.03.012 |
| 中文关键词: 内质网应激 肺动脉高压 血管重塑 平滑肌细胞表型转化 |
| 英文关键词: Endoplasmic reticulum stress Pulmonary hypertension Vascular remodeling Phenotypic modulation in pulmonary ar- terial smooth muscle cells |
| 基金项目:江西省自然科学基金面上项目(20161BAB205280)；江西省卫计委科技计划面上项目(20151294)；军区医学科技创新课题面上项目(14MS066) ；江西省自然科学基金项目( 20171BAB215003) |
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| 中文摘要: |
| 摘要 目的：探讨内质网应激(ERS)对肺动脉平滑肌细胞表型转化的影响。方法：采用胶原酶I消化法培养原代大鼠肺动脉平滑肌细胞(PASMCs)，用衣霉素(TM)或4-苯基丁酸(4-PBA)诱导或抑制内ERS，MTS法评价细胞增殖情况，western blot和定量RT-PCR检测蛋白和mRNA表达情况。结果：TM呈浓度依赖性诱导内质网应激标志物GRP78和XBP1 mRNA表达；较低浓度的TM促进PASMCs增殖，高浓度(5 μg/mol)使细胞凋亡；TM使PASMCs表达SM22 alpha减少，分泌I型胶原增加；4-PBA预处理可逆转TM诱导PASMCs的SM22 alpha减少和I型胶原分泌增加。结论：内质网应激促进肺动脉平滑肌细胞表型转化，可能是内质网应激参与肺动脉高压的机制之一。 |
| 英文摘要: |
| ABSTRACT Objective: To explore the effect of Endoplasmic reticulum stress (ERS) on phenotypic modulation of pulmonary arterial smooth muscle cells. Methods: Collagenase I digestion methods were applied for culturing primary PASMCs of rats. TM or 4-PBA were used to induce or inhibit ERS. MTS were proliferation assay. Western blot and RT-PCR were used to investigate the protein and mRNA levels. Results: TM induced the expression of ERS marker GRP78 and XBP1 of PASMCs in a concentration-dependent way. Low con- centration of TM made the PASMCs proliferation while too high concentration would make the cells apoptosis. TM reduced the expres- sion of SM22 alpha whild up-regulated the expression of collagen I in PASMCs. Meanwhile, 4-PBA which were used to inhibited ERS would restored the expression of SM22 alpha and collagen I. Conclusion: Endoplasmic reticulum stress induced phenotypic modulation in pulmonary arterial smooth muscle cells, which might be one of the mechanisms of pulmonary hypertension. |
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