ArticleVascular health and risk management2010
Urotensin II-induced signaling involved in proliferation of vascular smooth muscle cells.
Article in Vascular health and risk management, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 20 citations in OpenAlex.
- Urotensin-II-Targeted Liposomes as a New Drug Delivery System towards Prostate and Colon Cancer Cells.Journal of oncology · 2019Article
- Urotensin II promotes aldosterone expression in rat aortic adventitial fibroblasts.Molecular medicine reports · 2018Article
- The G Protein-Coupled Receptor UT of the Neuropeptide Urotensin II Displays Structural and Functional Chemokine Features.Frontiers in endocrinology · 2017Review
- The role of urotensin II and atherosclerotic risk factors in patients with slow coronary flow.Interventional medicine & applied science · 2016Review
- Up-regulation of urotensin II and its receptor contributes to human hepatocellular carcinoma growth via activation of the PKC, ERK1/2, and p38 MAPK signaling pathways.Molecules (Basel, Switzerland) · 2014Article
- Urotensin-II promotes vascular smooth muscle cell proliferation through store-operated calcium entry and EGFR transactivation.Cardiovascular research · 2013Article
- A closer look at the role of urotensin II in the metabolic syndrome.Frontiers in endocrinology · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The urotensin II receptor, bound by the ligand urotensin II, generates second messengers, ie, inositol triphosphate and diacylglycerol, which stimulate the subsequent release of calcium (Ca(2+)) in vascular smooth muscle cells. Ca(2+) influx leads to the activation of Ca(2+)-dependent kinases (CaMK) via calmodulin binding, resulting in cellular proliferation. We hypothesize that urotensin II signaling in pulmonary arterial vascular smooth muscle cells (Pac1) and primary aortic vascular smooth muscle cells (PAVSMC) results in phosphorylation of Ca(2+)/calmodulin-dependent kinases leading to cellular proliferation. Exposure of Pac1 cultures to urotensin II increased intracellular Ca(2+), subsequently activating Ca(2+)/calmodulin-dependent kinase kinase (CaMKK), and Ca(2+)/calmodulin-dependent kinase Type I (CaMKI), extracellular signal-regulated kinase (ERK 1/2), and protein kinase D. Treatment of Pac1 and PAVSMC with urotensin II increased proliferation as measured by (3)H-thymidine uptake. The urotensin II-induced increase in (3)H-thymidine incorporation was inhibited by a CaMKK inhibitor. Taken together, our results demonstrate that urotensin II stimulation of smooth muscle cells leads to a Ca(2+)/calmodulin-dependent kinase-mediated increase in cellular proliferation.
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