Protective effect of HSP27 in atherosclerosis and coronary heart disease by inhibiting reactive oxygen species

Abstract Objective To clarify the mechanism of heat shock protein 27 (HSP27) as a diagnostic biomarker in coronary heart disease (CHD) and atherosclerosis (AS). Method Expressions of HSP27 in patients with CHD and healthy controls were determined by enzyme‐linked immunosorbent assay and the expressions of HSP27 in aortas of patients with CHD and healthy controls were measured by immunohistochemistry. Receiver operating characteristic curve was applied to assess the diagnostic performance of HSP27 in CHD. ApoE −/− mice were included and accordingly grouped. The expressions of HSP27 in AS plaque were measured by quantitative real‐time polymerase chain reaction, immunohistochemistry, and Western blot analysis. AS plaque was observed using hematoxylin and eosin staining. DHE was used to detect reactive oxygen species (ROS) levels in aortas. The expressions of mitochondrial apoptosis‐related proteins were measured by Western blot analysis. Cell apoptosis was determined by TUNEL staining. Results HSP27 was highly expressed in patients with CHD than in healthy controls ( P < 0.01). In comparison to the normal group, the model group had increased the relative positive area of HSP27 and higher expressions of HSP27, Bax, caspase‐3, and apoptosis index (AI) but decreased Bcl‐2 expression in AS plaque, as well as larger plaque areas and elevated ROS levels in the aorta (all P < 0.05). The HSP27‐small interfering RNA group had increased expressions of Bax, caspase‐3, and AI but decreased Bcl‐2 and HSP27 expressions in AS plaque, as well as larger plaque areas, the relative positive area of HSP27 and higher ROS levels in aorta when compared with those in the model group (all P < 0.05). Conclusion HSP27 exerts its protective role by suppressing ROS and AS progression by inhibiting mitochondria apoptosis pathway in CHD.