- Upregulation of lincRNA-p21 in thoracic aortic aneurysms is involved in the regulation of proliferation and apoptosis of vascular smooth muscle cells by activating TGF-β1 signaling pathway.
Upregulation of lincRNA-p21 in thoracic aortic aneurysms is involved in the regulation of proliferation and apoptosis of vascular smooth muscle cells by activating TGF-β1 signaling pathway.
Long intergenic noncoding RNA-p21 (lincRNA-p21) has been proved in the pathogenesis of aortic aneurysms, while its functionality in thoracic aortic aneurysms (TAA) and the mechanism of function remains unclear. Therefore our study aimed to investigate the role of lincRNA-p21 in TAA. Aortic media specimens and blood samples were collected from both patients with TAA and healthy controls. Expression of lincRNA-p21 in those tissues was detected by reverse-transcription quantitative polymerase chain reaction (qRT-PCR). Diagnostic values of lincRNA-p21 in aortic media and blood for TAA were evaluated by receiver operating characteristic curve analysis. LincRNA-p21 overexpression human vascular smooth muscle cells (VSMCs) were prepared and the effects of lincRNA-p21 overexpression on cell proliferation and apoptosis were explored by cell counting kit-8 assay and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay, respectively. Expression of lincRNA-p21 and transforming growth factor β1 (TGF-β1) in VSMCs with different treatment was detected by qRT-PCR and Western blot analysis, respectively. Expression of lincRNA-p21 in aortic media tissues and blood was significantly upregulated in TAA patients than in healthy controls. Expression of lincRNA-p21 in aortic media and blood can be used to effectively distinguish TAA patients form healthy controls. LincRNA-p21 overexpression inhibited proliferation and promoted apoptosis of VSMCs, while TGF-β1 inhibitor reduced those effects. LincRNA-p21 overexpression upregulated TGF-β1 expression, while TGF-β1 activator showed no significant effects on lincRNA-p21 expression in VSMC. LincRNA-p21 participates in TAA by regulating the proliferation and apoptosis of VSMCs through the activation of TGF-β1 signaling pathway.