Heat shock protein 27 plays a protective role in thoracic aortic dissection by promoting cell proliferation and inhibiting apoptosis

Sili Zou,Mingfang Liao,Lefeng Qu,Junlin Yang,Mark Green,Tong Huang,Jianjin Wu

doi:10.1186/s11658-017-0056-y

Sili Zou, Mingfang Liao + Show 5 more

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https://doi.org/10.1186/s11658-017-0056-y

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Abstract

BackgroundThoracic 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).MethodsHSP27 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 H2O2.ResultsHSP27 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 H2O2-induced inhibition of cell proliferation. Furthermore, HSP27 was found to decrease H2O2-induced cell apoptosis and oxidative stress.ConclusionsThese results suggest that HSP27 expression promotes VSMC viability, suppresses cell apoptosis, and confers protection against oxidative stress in TAD.

Highlights

Thoracic aortic dissection (TAD) is one of the most severe aortic diseases
The aim of this study is to explore the potential roles of heat shock protein 27 (HSP27) in the pathogenesis of TAD using vascular smooth muscle cells (VSMCs), and to compare the oxidative stress levels and HSP27 expression in the aortic tissue of patients with TAD and control subjects
HSP27 levels were higher in the aortic wall of patients with TAD and was mainly produced by VSMCs To confirm that HSP27 expression is altered in TAD, western blots were performed using the protein lysate from aortic tissues

Summary

Introduction

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). Thoracic aortic dissection (TAD) is one of the most severe aortic diseases. If the tear extends into the aortic wall media, pulsatile blood can tear it apart along the length of the aorta [2]. The aortic wall is constantly subjected to biological insults and hemodynamic stress, leading to aortic wall degeneration with the possibility of dissection or aneurysm [3]. The structural changes of the aortic wall over time include fragmentation of elastic fibers, focal or zonal necrosis of the media, and the transition of smooth muscle cells (SMCs) from a contractile to asynthetic phenotype [4].

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