MicroRNA-133a regulates insulin-like growth factor-1 receptor expression and vascular smooth muscle cell

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Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
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Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

6.8K

Song Gao1, Michael Wassler2, Lulu Zhang2

  • 1The Texas Heart Institute at St. Luke's Hospital, Houston, TX, USA; The University of Texas Medical School at Houston, Houston, TX, USA.

Atherosclerosis
|January 10, 2014
PubMed
Abstract

Insights

MicroRNA-133a (miR-133a) promotes vascular smooth muscle cell (VSMC) growth by increasing IGF-1 receptor (IGF-1R) expression and mRNA stability. Reduced miR-133a in atherosclerosis impairs VSMC proliferation.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Atherosclerosis Research

Background:

  • MicroRNA-133a (miR-133a) and insulin-like growth factor-1 (IGF-1) are key regulators of cardiovascular cell proliferation.
  • Understanding their interplay is crucial for developing atherosclerosis treatments.

Purpose of the Study:

  • To investigate the effect of miR-133a on IGF-1 receptor (IGF-1R) expression and vascular smooth muscle cell (VSMC) proliferation in a murine model of atherosclerosis.
  • To elucidate the role of miR-133a in regulating IGF-1R mRNA stability.

Main Methods:

  • Analysis of IGF-1R and miR-133a expression in wild-type (WT) and apolipoprotein-E deficient (ApoE(-/-)) mouse aortas using immuno-fluorescence, immuno-blotting, and qRT-PCR.
  • Assessment of VSMC proliferation in response to IGF-1 stimulation and manipulation of miR-133a levels using inhibitors and precursors.
  • Luciferase reporter assays to evaluate the direct interaction between miR-133a and IGF-1R 3'UTR.
  • Measurement of IGF-1R mRNA half-life in VSMC from WT and ApoE(-/-) mice.

Main Results:

  • ApoE(-/-) aortas exhibited lower levels of both IGF-1R and miR-133a compared to WT.
  • ApoE(-/-) VSMC showed reduced proliferation in IGF-1-containing medium.
  • miR-133a inhibition decreased IGF-1R expression and VSMC growth, while miR-133a precursor increased IGF-1R levels and promoted proliferation.
  • miR-133a overexpression did not inhibit luciferase activity in the IGF-1R 3'UTR reporter system.
  • IGF-1R mRNA half-life was shorter in ApoE(-/-) VSMC and was modulated by miR-133a levels.

Conclusions:

  • MiR-133a enhances IGF-1R expression by prolonging IGF-1R mRNA half-life.
  • Reduced miR-133a in atherosclerosis is linked to decreased IGF-1R levels and impaired VSMC growth.
  • Administering miR-133a precursors may improve IGF-1-stimulated VSMC survival and proliferation in atherosclerosis.
Keywords:
ArteryAtherosclerosisInsulin-like growth factorMicroRNASmooth muscle cell

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