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MiR-126 Affects Brain-Heart Interaction after Cerebral Ischemic Stroke

Jieli Chen1,2, Chengcheng Cui3, Xiaoping Yang4

  • 1Henry Ford Hospital Neurology, Detroit, MI, 48202, USA. jieli@neuro.hfh.edu.

Translational Stroke Research
|January 20, 2017
PubMed

Insights

Ischemic stroke impairs cardiac function by decreasing microRNA-126 (miR-126) levels. This reduction contributes to heart inflammation, fibrosis, and hypertrophy, highlighting miR-126

Area of Science:

  • Cardiovascular Research
  • Neuroscience
  • Molecular Biology

Background:

  • Cardiovascular diseases are significantly more prevalent in individuals with neurological deficits.
  • MicroRNA-126 (miR-126) plays a crucial role in vascular health, influencing remodeling and fibrosis.
  • Emerging evidence suggests miR-126's involvement in the pathogenesis of cardiovascular diseases and stroke.

Purpose of the Study:

  • To investigate the hypothesis that reduced miR-126 expression following ischemic stroke contributes to cardiac dysfunction.
  • To elucidate the specific role of endothelial cell-derived miR-126 in post-stroke cardiac health.

Main Methods:

  • Utilized wild-type, endothelial cell-specific miR-126 knockout, and control mice subjected to distal middle cerebral artery occlusion (dMCAo) to model ischemic stroke.
  • Assessed cardiac hemodynamics and function using transthoracic Doppler echocardiography.
  • Quantified miR-126 expression, target gene and protein levels (VCAM-1, MCP-1), cardiac hypertrophy, fibrosis, inflammation, and oxidative stress at 28 days post-stroke.

Main Results:

  • Ischemic stroke in wild-type mice led to decreased cardiac ejection fraction, increased myocyte hypertrophy, fibrosis, inflammation, and oxidative stress.
  • Stroke significantly reduced serum and cardiac miR-126 levels while increasing expression of miR-126 target genes (VCAM-1, MCP-1).
  • Mice lacking endothelial miR-126 exhibited exacerbated cardiac dysfunction, hypertrophy, fibrosis, and inflammation post-stroke compared to controls.

Conclusions:

  • Ischemic stroke directly induces cardiac dysfunction.
  • Decreased miR-126 expression, particularly from endothelial cells, is a key mechanism contributing to cardiac dysfunction after stroke.
  • Restoring miR-126 levels may offer a therapeutic strategy for post-stroke cardiac complications.

Keywords:
Brain-heart interactionCardiac dysfunctionCardiomyocyteIschemiaMicroRNA-126Stroke

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