scholarly journals Role of Cyclic Strain Frequency in Regulating the Alignment of Vascular Smooth Muscle Cells In Vitro

2008 ◽  
Vol 94 (4) ◽  
pp. 1497-1507 ◽  
Author(s):  
Bo Liu ◽  
Ming-Juan Qu ◽  
Kai-Rong Qin ◽  
He Li ◽  
Zhen-Kun Li ◽  
...  
2021 ◽  
Author(s):  
Li Chen ◽  
Rongrong Zhang ◽  
Jinyin Li ◽  
Yiping Gao ◽  
Shilong Mao

Abstract Background: Calcium deposition in vascular smooth muscle cells (VSMCs) can lead to the rigidity of the vasculature and an increase of risk in cardiac events. This study aimed to explore the role of exosomal microRNA-151-3p (miR-151-3p) in the regulation of VSMC calcification. Methods: A cellular calcification model was established using the mouse primary aortic VSMCs by β-glycerophosphate treatment. The calcium deposition was evaluated by Alizarin Red staining. The expression of miR-151-3p in exosomes was evaluated by qRT-PCR. The relationship between miR-151-3p and Atg5 was determined by bioinformatics analysis and dual-luciferase gene reporter assay. The exosome derived from mouse VSMCs transfected with miR-151-3p mimics/inhibitor were isolated and used to stimulate VSMCs. The expression of Atg5, α-SMA, OPN, Runx2 and BMP2 was evaluated by western blot. An animal model was established to investigate the role of miR-151-3p in exosomes.Results: MiR-151-3p was significantly upregulated in the exosomes of VSMCs treated with β-glycerophosphate. Exosomes derived from calcific VSMCs increased the calcium deposition of general VSMCs without any treatment. Exosomes derived from miR-151-3p mimics transfected VSMCs increased the expression of Runx2 and BMP2, while reduced the expression of α-SMA and OPN in general VSMCs. and exosomes derived from miR-151-3p inhibitor transfected VSMCs reversed these effects in vitro. Meanwhile, miR-151-3p served as a ceRNA of Atg5 by directly binding to the 3'UTR of Atg5. Moreover, the expression of α-SMA, OPN, Runx2 and BMP2 in vivo was consistent with the results in VSMCs in vitro.Conclusion: Our study revealed that miR-151-3p in VSMCs-derived exosomes might induce calcium deposition through regulating Atg5 expression, suggesting that miR-151-3p might be a potential biomarker for vascular calcification.


2010 ◽  
Vol 17 (5) ◽  
pp. 503-509 ◽  
Author(s):  
Chie Aoki ◽  
Yoshiyuki Hattori ◽  
Atsuko Tomizawa ◽  
Teruo Jojima ◽  
Kikuo Kasai

2005 ◽  
Vol 96 (5) ◽  
pp. 567-575 ◽  
Author(s):  
David Morrow ◽  
Catherine Sweeney ◽  
Yvonne A. Birney ◽  
Philip M. Cummins ◽  
Dermot Walls ◽  
...  

2021 ◽  
Author(s):  
Jorge A. Aguilar-Pineda ◽  
Karin J. Vera-Lopez ◽  
Pallavi Shrivastava ◽  
Rita Nieto-Montesinos ◽  
Miguel A. Chávez-Fumagalli ◽  
...  

SUMMARYDespite the emerging evidence implying early vascular contributions to neurogenerative syndromes, the role of vascular smooth muscle cells (VSMCs) in the pathogenesis of Alzheimer’s disease is still not well understood. Herein, we show that VSMCs in brains of AD patients and the animal model of the disease, are deficient in multiple VSMC-contractile markers which correlated with Tau accumulation in brain arterioles. Ex vivo and in vitro experiments demonstrated that VSMCs undergo dramatic phenotypic transitions under AD-like conditions, adopting pro-inflammatory and synthetic phenotypes. Notably, these changes coincided with Tau hyperphosphorylation at residues Y18, T205 and S262. We also observed that loss of VSMC markers occurred in an age-dependent manner, and that expression of Sm22α and α-Sma proteins were inversely correlated with CD68 and Tau accumulation in brain arterioles of 3xTg-AD mice. Together, these findings further support the contribution of VSMCs in AD pathogenesis, and nominate VSMCs as potential novel therapeutic target in AD.Graphical Abstract


2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Fabiola Boccuto ◽  
Laura Tammè ◽  
Claudio Iaconetti ◽  
Jolanda Sabatino ◽  
Alberto Polimeni ◽  
...  

Abstract Aims Vascular smooth muscle cells (VSMCs) play a key role in the vessel wall, being active partaker in vascular remodelling and influencing multiple pathophysiological phenomena, such as progression of atherosclerosis, in-stent restenosis and vascular reactivity. Recently antisense oligonucleotides have shown promising results as a therapeutic option. The aim of this study was to analyse the expression profile and function of T-UCRs in vascular smooth muscle cells (VSMCs)—both in vitro and in vivo—and to evaluate the effects of their inhibition by the use of specific antisense oligonucleotides. Methods After obtaining cell cultures of vascular smooth muscle cells, we modified their phenotype varying growth conditions. A microarray and qRT-PCR expression profile analysis and a cell cycle analysis with cell proliferation/apoptosis/migration assay were performed. In vivo studies were performed on rat carotids after cell damage and administration of specific antisense oligonucleotides. Results There were significant differences in the expression of T-UCRs in VSMCs with a proliferating and quiescent phenotype. In particular, 5 T-UCRs were found to be upregulated in VSMCs. These types of cells were subsequently transfected with specific antisense oligonucleotides obtaining a reduction in their proliferative activity in particular with the inhibition of the T-UCRs uc.194 and uc.443 + A. MiR-10A and miR-34b-5p were identified with complementary sequences respectively to uc.194 and uc.443 + A. The increase of these miRs following the inhibition of the T-UCRs were closely related to the inhibition of the proliferative signals of VSMCs. Similarly, the same results were obtained in vivo. Conclusions The expression levels of non-coding RNAs uc.194 and uc. 443 + A increase in proliferating smooth muscle cells in vitro and in the vascular wall following damage, suggesting an important role of these molecules in the phenomenon of intra-stent restenosis. Through the inhibition of uc.194 and uc.443 + A using an antisense strategy, we demonstrated a reduction in cell proliferation and migration processes and, consequently, in the formation of neointima. A possible relationship was also highlighted between the aforementioned non-coding RNAs and some micro-RNAs (miR-10A and miR-34b-5p), negative regulators of the proliferative phenotype of VSMCs. The inhibition of the analysed T-UCRs would allow the maintenance of the contractile phenotype thanks to the activity of the miRs analysed in this study. Our results might pave the way for the identification of new therapeutic targets in order to prevent and reduce the incidence of intra-stent restenosis.


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