热休克蛋白 27 通过促进细胞增殖和抑制细胞凋亡在胸主动脉夹层中发挥保护作用。
Heat shock protein 27 plays a protective role in thoracic aortic dissection by promoting cell proliferation and inhibiting apoptosis.
机构信息
Department of Vascular and Endovascular Surgery, Changzheng Hospital, the Second Military Medical University, 415 Fengyang Road, Shanghai, People's Republic of China.
DICAT Biomedical Computation Centre, Vancouver, BC Canada.
出版信息
Cell Mol Biol Lett. 2017 Nov 28;22:24. doi: 10.1186/s11658-017-0056-y. eCollection 2017.
BACKGROUND
Thoracic aortic dissection (TAD) is one of the most severe aortic diseases. The study aimed to explore the potential role of heat shock protein 27 (HSP27) in the pathogenesis of TAD using an in vitro model of oxidative stress in vascular smooth muscle cells (VSMCs).
METHODS
HSP27 was analyzed in aortic surgical specimens from 12 patients with TAD and 8 healthy controls. A lentiviral vector was used to overexpress HSP27 in rat aortic VSMCs. Cell proliferation and apoptosis were measured under oxidative stress induced by HO.
RESULTS
HSP27 expression was significantly higher in aortic tissue from patients with TAD and VSMCs in the aortic media were the main cell type producing HSP27. Elevated oxidative stress was also detected in the TAD samples. Overexpression of HSP27 significantly attenuated HO-induced inhibition of cell proliferation. Furthermore, HSP27 was found to decrease HO-induced cell apoptosis and oxidative stress.
CONCLUSIONS
These results suggest that HSP27 expression promotes VSMC viability, suppresses cell apoptosis, and confers protection against oxidative stress in TAD.
背景
胸主动脉夹层（TAD）是最严重的主动脉疾病之一。本研究旨在通过血管平滑肌细胞（VSMC）氧化应激的体外模型，探讨热休克蛋白 27（HSP27）在 TAD 发病机制中的潜在作用。
方法
分析了 12 例 TAD 患者和 8 例健康对照者的主动脉手术标本中的 HSP27。使用慢病毒载体过表达大鼠主动脉 VSMC 中的 HSP27。在 HO 诱导的氧化应激下测量细胞增殖和凋亡。
结果
TAD 患者的主动脉组织中 HSP27 表达明显升高，主动脉中层的 VSMC 是产生 HSP27 的主要细胞类型。TAD 样本中也检测到氧化应激升高。过表达 HSP27 可显著减轻 HO 诱导的细胞增殖抑制。此外，发现 HSP27 可降低 HO 诱导的细胞凋亡和氧化应激。
结论
这些结果表明，HSP27 表达促进 VSMC 活力，抑制细胞凋亡，并在 TAD 中提供抗氧化应激保护。
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