ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011
A role for zinc in regulating hypoxia-induced contractile events in pulmonary endothelium.
Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 41 citations in OpenAlex.
- Zinc, Soluble Epoxide Hydrolase, and the Pulmonary Vascular Paradox: Novel Insights into a Well-Known Phenomenon.American journal of respiratory and critical care medicine · 2025Article
- Serine/Threonine Protein Phosphatases 1 and 2A in Lung Endothelial Barrier Regulation.Biomedicines · 2023Review
- Effects of Zinc on the Right Cardiovascular Circuit in Long-Term Hypobaric Hypoxia in Wistar Rats.International journal of molecular sciences · 2023Article
- Article
- A Potential New Role for Zinc in Age-Related Macular Degeneration through Regulation of Endothelial Fenestration.International journal of molecular sciences · 2021Article
- Zinc-mediated activation of CREB pathway in proliferation of pulmonary artery smooth muscle cells in pulmonary hypertension.Cell communication and signaling : CCS · 2021Article
- Analysis of flow resistance in the pulmonary arterial circulation: implications for hypoxic pulmonary vasoconstriction.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- Characterization of Contractile Machinery of Vascular Smooth Muscles in Hypertension.Life (Basel, Switzerland) · 2021Review
- Quantum Blue Reduces the Severity of Woody Breast Myopathy via Modulation of Oxygen Homeostasis-Related Genes in Broiler Chickens.Frontiers in physiology · 2019Article
- Zn2+ chelation by serum albumin improves hexameric Zn2+-insulin dissociation into monomers after exocytosis.PloS one · 2017Article
- The zinc transporter ZIP12 regulates the pulmonary vascular response to chronic hypoxia.Nature · 2015Article
- Functional role of intracellular labile zinc in pulmonary endothelium.Pulmonary circulation · 2012Article
- A critical role for increased labile zinc in reducing sensitivity of cultured sheep pulmonary artery endothelial cells to LPS-induced apoptosis.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Zinc homeostasis and signaling in health and diseases: Zinc signaling.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2011Review
- Coding your way out of a problem.Nature methods · 2011Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
We previously reported that zinc thiolate signaling contributes to hypoxic contraction of small, nonmuscularized arteries of the lung. The present studies were designed to investigate mechanisms by which hypoxia-released zinc induces contraction in isolated pulmonary endothelial cells and to delineate the signaling pathways involved in zinc-mediated changes in the actin cytoskeleton. We used fluorescence-based imaging to show that hypoxia induced time-dependent increases in actin stress fibers that were reversed by the zinc chelator, N,N,N',N'-tetrakis-(2-pyridylmethyl)-ethylenediamine (TPEN). We further showed that hypoxia-induced phosphorylation of the contractile protein myosin light chain (MLC) and assembly of actin stress fibers were each TPEN sensitive. Hypoxia and zinc-induced inhibition of MLC phosphatase (MLCP) were independent of the regulatory subunit (MYPT1) of MLCP, and therefore hypoxia-released zinc likely inhibits MLCP at its catalytic (PP1) subunit. Inhibition of PKC by Ro-31-8220 and a dominant-negative construct of PKC-ε attenuated hypoxia-induced contraction of isolated pulmonary endothelial cells. Furthermore, zinc-induced phosphorylation of MLC (secondary to inhibition of MLCP) was PKC dependent, and hypoxia-released zinc promoted the phosphorylation of the PKC substrate, CPI-17. Collectively, these data suggest a link between hypoxia, elevations in labile zinc, and activation of PKC, which in turn acts through CPI-17 to inhibit MLCP activity and promote MLC phosphorylation, ultimately inducing stress fiber formation and endothelial cell contraction.
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