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Lactate Promotes Synthetic Phenotype in Vascular Smooth Muscle Cells.

Libang Yang1, Ling Gao1, Thomas Nickel1

  • 1From the Division of Cardiology, Department of Medicine (L.Y., T.N., C.J., B.Y.), Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Department of Medicine (A.G., C.H., Z.G.) and Department of Paediatrics (G.R.G.), University of Minnesota Medical School, Minneapolis; Department of Biomedical Engineering, University of Alabama at Birmingham (L.G., J.Z.); and Department of Infectious Disease, Renmin Hospital (J.Y.) and Department of Microbiology, School of Basic Medical Science (J.Y., J.Z.), Hubei University of Medicine, Shiyan, China.

Circulation Research
|October 13, 2017
PubMed
Summary
This summary is machine-generated.

Lactate promotes vascular smooth muscle cell (vSMC) transition to a synthetic phenotype, increasing proliferation and migration. This finding links glucose metabolism to cardiovascular disease pathogenesis and treatment.

Keywords:
induced pluripotent stem cellsmonocarboxylic acid transportersmyocardial infarctionphenotypeswine

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Area of Science:

  • Cardiovascular Biology
  • Cellular Phenotyping
  • Metabolic Regulation

Background:

  • Vascular smooth muscle cell (vSMC) phenotypes exist on a continuum from contractile to synthetic.
  • The mechanisms driving vSMC phenotypic switching, especially after ischemic injury, are not well understood.

Purpose of the Study:

  • To investigate if lactate, elevated during ischemia, induces a synthetic phenotype in vSMCs.
  • To explore the role of monocarboxylic acid transporters and NDRG in lactate-mediated vSMC changes.

Main Methods:

  • Differentiated human induced pluripotent stem cells into vSMCs and cultured in lactate-enriched or standard media.
  • Utilized cell culture, gene silencing (iRNA for NDRG), transporter blockade, proteomics, and a swine myocardial infarction model.
  • Assessed vSMC marker expression, proliferation, migration, and apoptosis.

Main Results:

  • Lactate-enriched medium significantly increased synthetic vSMC markers, proliferation, and migration while decreasing contractile and apoptotic markers.
  • These effects were linked to increased monocarboxylic acid transporter expression and were partially reversed by transporter blockade or NDRG silencing.
  • Hypoxia mimicked lactate effects, and elevated lactate, LDH, vSMC proliferation, and NDRG were observed in the ischemic zone of myocardial infarction models.

Conclusions:

  • Lactate directly promotes a synthetic vSMC phenotype in a lactate-rich microenvironment.
  • These findings highlight the link between glucose metabolism, vSMC phenotypic switching, and cardiovascular disease development.