Thrombospondin‑2 is upregulated in patients with aortic dissection and enhances angiotensin II‑induced smooth muscle cell apoptosis

• Published in: Experimental and therapeutic medicine Vol. 20; no. 6; p. 150
• Main Authors: Qi, Liping, Wu, Kui, Shi, Shutian, Ji, Qingwei, Miao, Huangtai, Bin, Que
• Format: Journal Article
• Language: English
• Published: Athens Spandidos Publications UK Ltd 01.12.2020; D.A. Spandidos
• Subjects: Age; Antibodies; Aortic dissection; Apoptosis; Bone marrow; Cardiovascular disease; Heart failure; Hospitals; Investigations; Males; Mortality; Pain; Proteins; Smooth muscle; Beijing China
• ISSN: 1792-0981; 1792-1015
• DOI: 10.3892/etm.2020.9279

Thrombospondin-2 (TSP-2) is an important extracellular matrix protein that is involved in a variety of cardiovascular diseases, including viral myocarditis and abdominal aortic aneurysm. The present study aimed to investigate TSP-2 expression in patients with aortic dissection (AD). Aortas were obtained from patients with AD and healthy donors, and TSP-2 expression level in all samples was measured by western blotting and immunofluorescence assays. Blood samples were also collected from patients with AD and non-AD (NAD) subjects. Circulating TSP-2, tumor necrosis factor (TNF)-α and interleukin (IL)-6 levels in each sample were detected using ELISAs. In addition, the effect of TSP-2 on angiotensin II (Ang II)-induced smooth muscle cell (SMC) apoptosis was assessed in vitro. Compared with healthy donors, aortic TSP-2 expression level was significantly increased in patients with AD. Furthermore, TSP-2 was secreted primarily by SMCs, but also by endothelial cells. TSP-2 plasma expression level was also elevated in patients with AD compared with non-AD subjects. Furthermore, TSP-2 serum expression level was positively correlated with TNF-α and IL-6 expression levels in patients with AD. In addition, recombinant mouse TSP-2 treatment increased Bax mRNA expression and decreased Bcl2 mRNA expression in Ang II-treated SMCs; however, the effects were reversed following treatment with the NF-κB p65 signaling pathway inhibitor JSH-23 or with the anti-TNF-α and anti-IL-6 neutralizing antibodies. The present study demonstrated that TSP-2 expression was increased in the aortic tissues and plasma of patients with AD. These findings suggested that TSP-2 may participate in the progression of AD by activating the NF-κB p65 signaling pathway and amplifying the inflammatory response.