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Related Experiment Video

Updated: May 22, 2026

Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice
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Published on: October 19, 2013

Glc-6-PD and PKG contribute to hypoxia-induced decrease in smooth muscle cell contractile phenotype proteins in

Sukrutha Chettimada1, Dhwajbahadur K Rawat, Nupur Dey

  • 1Department of Biochemistry & Molecular Biology, College of Medicine, University of South Alabama, Mobile, AL 36688, USA.

American Journal of Physiology. Lung Cellular and Molecular Physiology
|May 15, 2012
PubMed
Summary

Hypoxia activates glucose-6-phosphate dehydrogenase (Glc-6-PD) in pulmonary arteries, causing pulmonary hypertension. Inhibiting Glc-6-PD reduces this vasoconstriction by affecting smooth muscle cell proteins.

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Published on: January 14, 2014

Area of Science:

  • Cardiovascular Biology
  • Pulmonary Medicine
  • Metabolic Regulation

Background:

  • Persistent hypoxic pulmonary vasoconstriction (HPV) is a key factor in pulmonary hypertension development.
  • Hypoxia-induced glucose-6-phosphate dehydrogenase (Glc-6-PD) activation in pulmonary artery smooth muscle links metabolic shifts to HPV.
  • Previous studies indicated Glc-6-PD inhibition reduces acute HPV.

Purpose of the Study:

  • To investigate the role of Glc-6-PD in hypoxia-induced changes in pulmonary artery smooth muscle cell phenotype and HPV.
  • To explore the molecular mechanisms linking Glc-6-PD activity, protein kinase G (PKG), and smooth muscle cell markers under hypoxia.
  • To determine the effect of modulating Glc-6-PD and PKG activity on HPV and associated protein expression.

Main Methods:

  • Pulmonary arterial rings were exposed to hypoxia (20-30 Torr) for 12 hours in vitro.
  • Measurements included SM22α and smooth muscle myosin heavy chain expression, Glc-6-PD activity, and HPV.
  • Pharmacological inhibition of Glc-6-PD and modulation of PKG activity were employed; protein complex formation and VASP phosphorylation (p-VASP) were assessed.

Main Results:

  • Hypoxia significantly reduced SM22α and smooth muscle myosin heavy chain expression and induced HPV.
  • Glc-6-PD activity was elevated in hypoxic pulmonary arteries; its inhibition prevented SM22α reduction and largely inhibited HPV.
  • Glc-6-PD inhibition increased PKG activity, evidenced by increased p-VASP, which upregulated SM22α and attenuated HPV.

Conclusions:

  • Increased Glc-6-PD activity under hypoxia contributes to pulmonary hypertension by altering smooth muscle cell phenotype.
  • Glc-6-PD interacts with PKG, influencing downstream signaling pathways that regulate pulmonary artery contractility and remodeling.
  • Targeting Glc-6-PD activity represents a potential therapeutic strategy for managing pulmonary hypertension.