ArticleAmerican journal of physiology. Lung cellular and molecular physiology2010
Increased degradation of MYPT1 contributes to the development of tolerance to nitric oxide in porcine pulmonary artery.
Article in American journal of physiology. Lung cellular and molecular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- MYPT1 reduction is a pathogenic factor of erectile dysfunction.Communications biology · 2022Article
- TIMAP inhibits endothelial myosin light chain phosphatase by competing with MYPT1 for the catalytic protein phosphatase 1 subunit PP1cβ.The Journal of biological chemistry · 2019Article
- Overexpression of Myosin Phosphatase Target Subunit 1 (MYPT1) Inhibits Tumor Progression and Metastasis of Gastric Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- A splice variant of the myosin phosphatase regulatory subunit tunes arterial reactivity and suppresses response to salt loading.American journal of physiology. Heart and circulatory physiology · 2016Article
- Preservation of nitric oxide-induced relaxation of porcine coronary artery: roles of the dimers of soluble guanylyl cyclase, phosphodiesterase type 5, and cGMP-dependent protein kinase.Pflugers Archiv : European journal of physiology · 2014Article
- Myosin phosphatase isoforms as determinants of smooth muscle contractile function and calcium sensitivity of force production.Microcirculation (New York, N.Y. : 1994) · 2014Review
- Sulfhydryl-dependent dimerization of soluble guanylyl cyclase modulates the relaxation of porcine pulmonary arteries to nitric oxide.Pflugers Archiv : European journal of physiology · 2013Article
- Altered reactivity of tertiary mesenteric arteries following acute myocardial ischemia.Journal of vascular research · 2013Article
- Heterogeneity in relaxation of different sized porcine coronary arteries to nitrovasodilators: role of PKG and MYPT1.Pflugers Archiv : European journal of physiology · 2012Article
- Phosphoproteomic analysis of lung tissue from patients with pulmonary arterial hypertension.Pulmonary circulationArticle
- Hypoxia modulates the expression of leucine zipper-positive MYPT1 and its interaction with protein kinase G and Rho kinases in pulmonary arterial smooth muscle cells.Pulmonary circulationArticle
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Myosin phosphatase target subunit 1 (MYPT1) is the regulatory subunit of myosin light chain phosphatase (MLCP). It plays a critical role in vasodilatation induced by cGMP-elevating agents such as nitric oxide (NO). The present study was performed to determine the role of MYPT1 in the development of tolerance of the pulmonary artery to NO. Incubation of isolated porcine pulmonary arteries for 24 or 48 h with DETA NONOate (DETA NO) significantly reduced protein levels of MYPT1 and the leucine zipper-positive (LZ+) isoform of MYPT1 but not that of PP1cdelta. The extent of reduction in total MYPT1 protein level was comparable to that of MYPT1 (LZ+). The decrease in MYPT1 protein caused by 48-h DETA NO incubation was prevented by ODQ, an inhibitor of guanylyl cyclase, and by inhibitors of proteasomes (MG-132 and lactacystin) but was not affected by the inhibitor of protein synthesis, cycloheximide. A reduction in MYPT1 protein was also obtained with 8-bromo-cGMP, but this was prevented by Rp-8-bromo-PET-cGMP [inhibitor of cGMP-dependent protein kinase (PKG)]. Incubation for 48 h with DETA NO also reduced dephosphorylation of myosin light chain and relaxation of the artery in response to DETA NO, which was prevented by MG-132. These results suggest that the reduction in MYPT1 protein contributes to the development of tolerance of pulmonary arteries to NO. This may result from increased degradation of MYPT1 after prolonged PKG activation.
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