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Effect of Ang III on JNK mitogen activated protein (MAP) kinase in Wistar rat VSMCs
Author(s) -
Alanazi Ahmed Z.,
Clark Michelle A.
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.719.7
Subject(s) - mitogen activated protein kinase , phosphorylation , kinase , angiotensin ii , p38 mitogen activated protein kinases , vascular smooth muscle , protein kinase a , microbiology and biotechnology , medicine , chemistry , endocrinology , biology , blood pressure , smooth muscle
Objective We investigated whether angiotensin (Ang) III induces JNK mitogen activated protein (MAP) kinase protein phosphorylation in isolated rat vascular smooth muscle cells (VSMCs). Moreover, we compared its effect with Ang II. Background The molecular mechanisms by which Ang III induces various biological effects have not been fully investigated. Most studies have shown that MAP kinases mediate Ang II apoptosis and growth promoting effects in VSMCs. In addition, Ang II induces vascular remodeling in these cells leading to increases in blood pressure. MAP kinases regulate or induce two crucial actions in VSMCs, proliferation and migration, which are associated with atherosclerosis and restenosis. Methods Primary cultures of VSMCs were isolated from the thoracic aorta of adult Wistar rats by the explant technique. VSMCs were treated with Ang II and Ang III ranging in concentration from 0.1 nM to 1000 nM for 10 minutes or with 100 nM Ang II and Ang III for 1 minute to 60 minutes. Western blotting technique was used to determine the effects of both peptides on JNK MAP kinase protein phosphorylation. Results Concentration studies showed that Ang II and Ang III caused a dose‐dependent increase in JNK MAP kinase protein phosphorylation. The effects of the peptides on this MAP kinase phosphorylation were maximal between 10 nM and 100 nM. The peptides’ effects were rapid and significant, occurring within minutes of treatment and the maximal effects on MAP kinases phosphorylation was observed by 10 minutes. Conclusion These findings provide insight into the molecular nature of the actions of Ang III and offer possible mechanism by which Ang III physiological actions occur in VSMCs. Support or Funding Information Funding for this project was provided through: Nova Southeastern University Health Professions Division Grant & Saudi Arabian Cultural Mission.