Key result
Talin-1 expression was significantly downregulated in the media of aortic dissection samples compared with normal controls, and its in vitro knockdown promoted vascular smooth muscle cell proliferation and migration.
Why the study?
Does Talin-1 downregulation increase proliferation and migration of vascular smooth muscle cells in aortic dissection?
Case-Control (n=20)
No
Does Talin-1 downregulation increase proliferation and migration of vascular smooth muscle cells in aortic dissection?
Talin-1 is downregulated in aortic dissection and its inhibition promotes vascular smooth muscle cell proliferation and migration, suggesting a potential role in the pathogenesis of aortic dissection.
Talin-1 loss may contribute to aortic dissection progression; hypothesis-generating and should not yet change practice.
BACKGROUND: This study aimed to assessed whether Talin-1 is involved in the pathogenesis of aortic dissection via regulating vascular smooth muscle cell (VSMC) biological function. METHODS: Human aortic samples were obtained from organ donors who died from nonvascular diseases as normal controls and from patients undergoing surgical repair of thoracic aortic dissection. The expression level and distribution of Talin-1 were detected using westernblot analysis and immunohistochemistry in each sample. We inhibited the expression of Talin-1 via RNA interference in VSMCs. VSMC proliferation was detected by Cell-counting Kit-8 analyses. Scratch test and flow cytometry were used to identify the migration and apoptosis ability. Antibody microarray analysis and qRT-PCR were used to detect some protein and mRNA changes which were induced by Talin-1 downregulation. RESULTS: Talin-1 was significantly downregulated in the media of aortic dissection samples compared with controls (P < 0.05). Talin-1 knockdown significantly induced VSMC proliferation and migration in vitro. Proteins which involved in cell cycle can be regulated by downregulating Talin-1. Down regulation of Talin-1 can significanly increased the expression of anaphase-promoting complex subunit 2 (APC2) and decreased p19 alternative reading frame (p19ARF), Cullin-3, and beta actin's expression. CONCLUSIONS: Talin-1 induces VSMCs proliferation and migration. It downregulated in aortic dissection, which might play a potential role in the development of aortic dissection.
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Wei et al. (2017) conducted a case-control in Aortic Dissection (n=20). Aortic dissection vs. Normal aorta (organ donors) was evaluated on Talin-1 protein expression in aortic media (p=<0.05). Talin-1 expression was significantly downregulated in the media of aortic dissection samples compared with normal controls, and its in vitro knockdown promoted vascular smooth muscle cell proliferation and migration.
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