MicroRNAs in ascending thoracic aortic aneurysms

Moushi, Areti; Pillar, Nir; Keravnou, Anna; Soteriou, Marinos; Shomron, Noam; Cariolou, Marios A.; Bashiardes, Evy

doi:10.1042/bsr20200218

Cited by 12 publications

(14 citation statements)

References 77 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CircRNAs can competitively bind to the miRNAs to alleviate the degeneration of the gene expression 21,22 . Differential expression of miRNAs has been previously reported in an aneurysmal sample and found to be associated with SMC apoptosis, inflammatory response, and ECM degradation in the aneurysm site 23–25 . In our study, we were able to confirm that circ_0008285 directly binds to miR‐150‐5p.…”

Section: Discussionsupporting

confidence: 78%

Circ_0008285 silencing suppresses angiotensin II‐induced vascular smooth muscle cell apoptosis in thoracic aortic aneurysm via miR‐150‐5p/BASP1 axis

et al. 2023

View full text Add to dashboard Cite

Background Vascular smooth muscle cells (VSMCs) are the predominant cell type of the aortic middle layer, the abnormal number or function of which has been demonstrated to have a role in thoracic aortic aneurysm (TAA). Here, this study aimed to identify the function of circ_0008285 in VSMC apoptosis. Methods Human VSMCs were treated with angiotensin II (Ang II) for functional experiments. Cell counting kit‐8, 5‐ethynyl‐2′‐deoxyuridine (EdU), and flow cytometry were applied for function analysis. The interaction between miR‐150‐5p and circ_0008285 or brain acid‐soluble protein 1 (BASP1) was also evaluated by dual‐luciferase reporter assay and RNA immunoprecipitation assay. Exosomes were isolated by the commercial kit. Results A highly expressed circ_0008285 was observed in the aortic tissues of TAA patients and Ang‐II‐induced VSMCs. Circ_0008285 deficiency dramatically reversed Ang‐II‐induced proliferation arrest and apoptosis promotion in VSMCs. Circ_0008285 functionally targeted miR‐150‐5p. MiR‐150‐5p inhibition attenuated the inhibitory effects of circ_0008285 silencing on Ang‐II‐evoked apoptosis in VSMCs. BASP1 was verified to be a target of miR‐150‐5p, and was proved to attenuate miR‐150‐5p‐triggered apoptosis arrest in Ang‐II‐stimulated VSMCs. Additionally, extracellular circ_0008285 was packaged into exosomes, which could be transferred into the recipient cells. Conclusion Circ_0008285 silencing could suppress Ang‐II‐induced VSMCs apoptosis via miR‐150‐5p/BASP1 axis, adding further understanding of the pathogenesis of TAA.

show abstract

Section: Discussionsupporting

confidence: 78%

Circ_0008285 silencing suppresses angiotensin II‐induced vascular smooth muscle cell apoptosis in thoracic aortic aneurysm via miR‐150‐5p/BASP1 axis

et al. 2023

View full text Add to dashboard Cite

show abstract

“…17 Boon et al, 18 based on animal models, showed that miRNA 29 inhibition with an-timiR (anti-miRNA) 29 agents, led to decreased MMP 2 and 9 expression in the aorta, increased expression of collagen and elastin genes and limitation of aneurysm progression. These results were confirmed by the Maegdefessel et al study, 19 where antimiR29 agents in murine models increased collagen production, inducing a fibrotic response in the aortic wall and, hence, slowed down aneurysm evolution. 20 miRNA 195 is also involved in extracellular matrix regulation.…”

Section: Discussionsupporting

confidence: 59%

Expression of Tissue microRNAs in Ascending Aortic Aneurysms and Dissections

et al. 2022

View full text Add to dashboard Cite

Little is known about the role of serum and tissue mediators in the progression of ascending aortic aneurysms and dissections. We examined how the tissue expression of microRNAs and matrix metalloproteinases (MMPs), as well as the serum levels of osteoprotegerin, adiponectin, and high sensitivity C-reactive protein (hsCRP) are associated with these entities. We enrolled 21 patients with ascending aortic aneurysm, 11 with acute Stanford type A aortic dissection and 18 controls. The serum levels of osteoprotegerin, adiponectin, and hsCRP, as well as the tissue expression of MMPs 2 and 9 and tissue microRNAs 29 and 195 were compared among groups. There was no difference regarding serum osteoprotegerin, adiponectin, and tissue MMP2 and MMP9 levels. hsCRP was higher in the dissection group ( P = .03). Tissue expression of microRNA 29 was 2.11-fold higher in the dissection ( P = .001) and 2.99-fold higher in the aneurysm group ( P < .001), compared with the control group. Tissue expression of microRNA 195 was 2.72-fold higher in the dissection ( P < .001) and 2.00-fold lower in the aneurysm group ( P = .08), compared with to the control group. These findings support the contribution of microRNAs in the progression of aneurysm formation and dissection, suggesting a role as potential biomarkers and future therapeutic targets.

show abstract

“…Meanwhile, elevated fibrillin-1 was proposed to be a possible biomarker for TAA due to its role as a scaffold protein for elastin in the aortic wall [ 23 ]. Several other potential biomarkers for TAA such as matrix metalloproteinases (MMPs) and miRNAs (hsa-miR-140-5p, hsa-miR-191-5p and hsa-miR-214-3p) have been reported [ 24 , 25 ]. Nonetheless, none of these proteins/molecules have been shown to have good diagnostic and/or predictive values for aortic aneurysms clinically in patients.…”

Section: Introductionmentioning

confidence: 99%