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Cited by 280

The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.

MicroRNA‐26a is a novel regulator of vascular smooth muscle cell function

Open access
Leeper, Nicholas J., Raiesdana, Azad, Kojima, Yoko, Chun, Hyung J., Azuma, Junya, Maegdefessel, Lars, Kundu, Ramendra K., Quertermous, Thomas, Tsao, Philip S., Spin, Joshua M.·2011·Journal of Cellular Physiology

Abstract

Aberrant smooth muscle cell (SMC) plasticity has been implicated in a variety of vascular disorders including atherosclerosis, restenosis, and abdominal aortic aneurysm (AAA) formation. While the pathways governing this process remain unclear, epigenetic regulation by specific microRNAs (miRNAs) has been demonstrated in SMCs. We hypothesized that additional miRNAs might play an important role in determining vascular SMC phenotype. Microarray analysis of miRNAs was performed on human aortic SMCs undergoing phenotypic switching in response to serum withdrawal, and identified 31 significantly regulated entities. We chose the highly conserved candidate miRNA‐26a for additional studies. Inhibition of miRNA‐26a accelerated SMC differentiation, and also promoted apoptosis, while inhibiting proliferation and migration. Overexpression of miRNA‐26a blunted differentiation. As a potential mechanism, we investigated whether miRNA‐26a influences TGF‐β‐pathway signaling. Dual‐luciferase reporter assays demonstrated enhanced SMAD signaling with miRNA‐26a inhibition, and the opposite effect with miRNA‐26a overexpression in transfected human cells. Furthermore, inhibition of miRNA‐26a increased gene expression of SMAD‐1 and SMAD‐4, while overexpression inhibited SMAD‐1. MicroRNA‐26a was also found to be downregulated in two mouse models of AAA formation (2.5‐ to 3.8‐fold decrease, P < 0.02) in which enhanced switching from contractile to synthetic phenotype occurs. In summary, miRNA‐26a promotes vascular SMC proliferation while inhibiting cellular differentiation and apoptosis, and alters TGF‐β pathway signaling. MicroRNA‐26a represents an important new regulator of SMC biology and a potential therapeutic target in AAA disease. J. Cell. Physiol. 226: 1035–1043, 2011. © 2010 Wiley‐Liss, Inc.

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Metadata

Authors
Leeper, N. J., Raiesdana, A., Kojima, Y., Chun, H. J., Azuma, J., Maegdefessel, L., Kundu, R. K., Quertermous, T., Tsao, P. S., & Spin, J. M.
Venue
Journal of Cellular Physiology
Publisher
Wiley
Published
2011-01-25
Volume
226
Issue
4
Pages
1035-1043
ISSN
  • 0021-9541 (ISSN-L)
  • 1097-4652
OpenAlex
W2047493201
Cited by
280
References
41
FWCI
6.50
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: MicroRNA‐26a is a novel regulator of vascular smooth muscle cell function. https://app.cochat.ai/papers/10.1002/jcp.22422
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Leeper, N. J., Raiesdana, A., Kojima, Y., Chun, H. J., Azuma, J., Maegdefessel, L., Kundu, R. K., Quertermous, T., Tsao, P. S., & Spin, J. M. (2011). MicroRNA‐26a is a novel regulator of vascular smooth muscle cell function. Journal of Cellular Physiology. https://doi.org/10.1002/jcp.22422

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