Brahma-related gene 1 inhibits proliferation and migration of human aortic smooth muscle cells by directly up-regulating Ras-related associated with diabetes in the pathophysiologic processes of aortic dissection

Liao, Wei-Lin; Tan, Mengwei; Yuan, Yuan; Wang, Guokun; Wang, Chong; Tang, Hao; Zhao, Xu

doi:10.1016/j.jtcvs.2015.08.010

Cited by 24 publications

(19 citation statements)

References 34 publications

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“…Müller BT, et al and Wang L, et al have reported that VSMCs from AD tissues seem to proliferate faster than normal aorta tissues and the genes that participate in proliferation showed an elevated level of expression [35, 36]. Furthermore, VSMC migration is also acknowledged as a crucial issue in AD pathogenesis [37, 38]. Our vitro functional experiments verified that downregulation of Talin-1 drastically enhanced the proliferation and migration capability of VSMCs which implied the occurrence of a positive pathological remodeling that was harmful to AD development.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of Talin-1 expression associates with increased proliferation and migration of vascular smooth muscle cells in aortic dissection

Wei

Sun

et al. 2017

BMC Cardiovasc Disord

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BackgroundThis study aimed to assessed whether Talin-1 is involved in the pathogenesis of aortic dissection via regulating vascular smooth muscle cell (VSMC) biological function.MethodsHuman 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.ResultsTalin-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.ConclusionsTalin-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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Section: Discussionmentioning

confidence: 99%

Downregulation of Talin-1 expression associates with increased proliferation and migration of vascular smooth muscle cells in aortic dissection

Wei

Sun

et al. 2017

BMC Cardiovasc Disord

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“…Further study confirms that Talin-1 regulates VSMC apoptosis and finally causes pathologic vascular remodeling to change vascular media structure and function and lead to TAD [22]. Many genes such as Sirtuin-1, PCSK9, and brahmarelated gene 1 had been reported to be associated with the pathophysiologic processes of TAD through influence proliferation and migration of VSMCs [23][24][25].…”

Section: Discussionmentioning

confidence: 54%

Integration of Gene Expression Profile Data to Verify Hub Genes of Patients with Stanford A Aortic Dissection

Wang

et al. 2019

BioMed Research International

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Thoracic aortic dissection (TAD) is a catastrophic disease worldwide, but the pathogenic genes and pathways are largely unclear. This study aims at integrating two gene expression profile datasets and verifying hub genes and pathways involved in TAD as well as exploring potential molecular mechanisms. We will combine our mRNAs expression profile (6 TAD tissues versus 6 non-TAD tissues) and GSE52093 downloaded from the Gene Expression Omnibus (GEO) database. The two mRNAs expression profiles contained 13 TAD aortic tissues and 11 non-TAD tissues. The two expression profile datasets were integrated and we found out coexpression of differentially expressed genes (DEGs) using bioinformatics methods. The gene ontology and pathway enrichment of DEGs were performed by DAVID and Kyoto Encyclopedia of Genes and Genomes online analyses, respectively. The protein-protein interaction networks of the DEGs were constructed according to the data from the STRING database. Cytohubber calculating result shows the top 10 hub genes with CDC20, AURKA, RFC4, MCM4, TYMS, MCM2, DLGAP5, FANCI, BIRC5, and POLE2. Module analysis revealed that TAD was associated with significant pathways including cell cycle, vascular smooth muscle contraction, and adrenergic signaling in cardiomyocytes. The qRT-PCR result showed that the expression levels of all the hub genes were significantly increased in OA samples (p < 0.05), and these candidate genes could be used as potential diagnostic biomarkers and therapeutic targets of TAD.

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“…A 96-well plate was used for the assay, and the detailed procedures were performed as per our previous description, with modifications. 24 A total of 10 mL of CCK8 solution was added at 0, 24, 48, 72, and 96 hours after adenovirus transfection. Then, the cultures were incubated at 37 C with 5.0% carbon dioxide for 1.5 hours.…”

Section: Cell Proliferationmentioning

confidence: 99%

“…Then we evaluated the proliferation, migration, and apoptosis capabilities of VSMCs transfected with Ad-NANOG, which were considered as important functions of VSMCs in the pathogenesis of TAD. 8,24,29 We used CCK8 assay to evaluate the proliferation function of VSMCs. We found that VSMCs transfected with Ad-NANOG showed an enhanced proliferation function at 24, 48, 72, and 96 hours after transfection (Figure 4, A).…”

Section: Nanog Overexpression Promoted the Expression Of Opn And Vsmcmentioning

confidence: 99%

“…However, the relationship between NANOG and other genes that may result in TAD remains to be studied. 3,11,24 Fourth, we focused on the aortic media and VSMCs, aortic endothelial and adventitial cells were not included in the present study. We believe aortic endothelial and adventitial cells also play a role in TAD and need to be further investigated.…”

Section: Limitationsmentioning

confidence: 99%

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Mechanisms of aortic dissection smooth muscle cell phenotype switch

Yang

Song

et al. 2017

The Journal of Thoracic and Cardiovascular Surgery

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Brahma-related gene 1 inhibits proliferation and migration of human aortic smooth muscle cells by directly up-regulating Ras-related associated with diabetes in the pathophysiologic processes of aortic dissection

Abstract: Our study illustrated that Brg1 inhibited the proliferation and migration capacity of HASMCs, via the mechanism of direct up-regulation of RRAD, thus playing an important role in the pathophysiologic processes of aortic dissection.

Cited by 24 publications

References 34 publications

Downregulation of Talin-1 expression associates with increased proliferation and migration of vascular smooth muscle cells in aortic dissection

Downregulation of Talin-1 expression associates with increased proliferation and migration of vascular smooth muscle cells in aortic dissection

Integration of Gene Expression Profile Data to Verify Hub Genes of Patients with Stanford A Aortic Dissection

Mechanisms of aortic dissection smooth muscle cell phenotype switch

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