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MicroRNA-1298 is regulated by DNA methylation and affects vascular smooth muscle cell function by targeting connexin

Wei Hu1, Mian Wang1, Henghui Yin1

  • 1Division of Vascular Surgery, The Guangdong Engineering Laboratory for Diagnosis and Treatment of Vascular Diseases, The Vascular Surgical Disease Research Center of Guangdong Province, First Affiliated Hospital, Sun Yat-sen University, 58 Zhong Shan Er Road, Guangzhou, Guangdong 510080, China.

Cardiovascular Research
|May 31, 2015
PubMed
Abstract

Insights

MicroRNA-1298 (miR-1298) is down-regulated in arteriosclerosis obliterans (ASO) due to DNA hypermethylation. Restoring miR-1298 levels in vascular smooth muscle cells reduces cell proliferation and migration, offering a potential therapy for ASO.

Area of Science:

  • Vascular Biology
  • Epigenetics
  • Molecular Medicine

Background:

  • MicroRNAs (miRNAs) play critical roles in vascular diseases.
  • MicroRNA-1298 (miR-1298) is significantly downregulated in arteriosclerosis obliterans (ASO).
  • The precise function and regulation of miR-1298 in ASO remain largely unknown.

Purpose of the Study:

  • To investigate the expression, regulatory mechanisms, and functional role of miR-1298 in ASO.
  • To explore the relationship between miR-1298, DNA methylation, and vascular smooth muscle cell (VSMC) function.
  • To identify downstream targets of miR-1298 involved in ASO pathogenesis.

Main Methods:

  • Quantitative reverse-transcription PCR and in situ hybridization to assess miR-1298 expression.
  • Pyrosequencing and luciferase reporter assays to investigate DNA methylation and regulatory mechanisms.
  • In vitro studies using cultured VSMCs and an in vivo rat carotid balloon injury model to evaluate miR-1298 function.

Main Results:

  • miR-1298 is predominantly expressed in VSMCs and significantly downregulated in ASO arteries.
  • Hypermethylation of upstream CpG sites in ASO arteries correlates with miR-1298 downregulation.
  • miR-1298 re-expression inhibited VSMC proliferation and migration, targeting Connexin 43 (Cx43).
  • In vivo, miR-1298 re-delivery reduced neointimal formation by targeting Cx43.

Conclusions:

  • A novel pathway involving upstream DNA methylation, miR-1298, and Cx43 regulates VSMC function in ASO.
  • Modulating miR-1298 levels presents a potential therapeutic strategy for arteriosclerosis obliterans.
Keywords:
Arteriosclerosis obliteransConnexin 43MethylationSmooth muscle cellmicroRNA

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