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Essential Role of Smooth Muscle STIM1 in Hypertension and Cardiovascular Dysfunction

Modar Kassan1, Karima Ait-Aissa1, Eman Radwan1

  • 1From the Department of Physiology, Hypertension and Renal Center of Excellence, Tulane University, New Orleans, LA (M.K., K.M.); Department of Physiological Sciences, EVMS, Norfolk, VA (M.K., K.A.-A., E.R., V.M., S.H., S.B., K.M.); Department of Cellular and Molecular Physiology, Penn State University College of Medicine, Hershey, PA (W.Z., M.T); and Department of Internal Medicine, University of Iowa, Iowa City (K.M., M.G., K.I.).

Arteriosclerosis, Thrombosis, and Vascular Biology
|July 30, 2016
PubMed

Insights

Stromal interaction molecule 1 (STIM1) in smooth muscle drives hypertension and cardiovascular damage by increasing endoplasmic reticulum stress. Blocking STIM1 or CHOP protects against these conditions, highlighting STIM1 as a therapeutic target.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Hypertension Research

Background:

  • Chronic hypertension is a major risk factor for cardiovascular diseases, heart failure, and stroke.
  • Stromal interaction molecule 1 (STIM1) expression is implicated in cardiovascular pathologies.

Purpose of the Study:

  • To investigate the role of smooth muscle STIM1 in angiotensin II-induced hypertension and associated cardiovascular pathologies.
  • To elucidate the mechanisms linking STIM1, endoplasmic reticulum stress, and vascular dysfunction.

Main Methods:

  • Utilized angiotensin II infusion in wild-type mice and mice with smooth muscle-specific STIM1 deficiency (Stim1(SMC-/-)).
  • Assessed cardiac hypertrophy, fibrosis, endothelial dysfunction, and vascular nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity.
  • Examined the role of CCAAT-enhancer-binding protein homologous protein (CHOP) by using CHOP knockout mice (CHOP(-/-)).

Main Results:

  • Angiotensin II infusion induced hypertension, cardiac hypertrophy, fibrosis, and endothelial dysfunction, with increased STIM1 expression.
  • Mice lacking smooth muscle STIM1 (Stim1(SMC-/-)) or CHOP (CHOP(-/-)) were resistant to these pathologies.
  • Smooth muscle STIM1 mediated endoplasmic reticulum stress-induced vascular dysfunction via TGF-β and NADPH oxidase pathways.
  • Hypertensive wild-type mice exhibited increased vascular NADPH oxidase activity and reduced eNOS/cGMP/nitrite signaling, which was prevented in Stim1(SMC-/-) and CHOP(-/-) mice.

Conclusions:

  • Smooth muscle STIM1 is crucial for developing hypertension and associated cardiovascular pathologies.
  • STIM1-dependent endoplasmic reticulum stress contributes to vascular dysfunction in hypertension.
  • Targeting smooth muscle STIM1 offers a potential therapeutic strategy for cardiovascular diseases.
Abstract

Keywords:
ER stresscardiac hypertrophyendothelial nitric oxide synthasehypertensionnicotinamide adenine dinucleotide phosphatestromal interaction molecule 1vascular reactivity

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