Strathprints logo
Strathprints Home | Open Access | Browse | Search | User area | Copyright | Help | Library Home | SUPrimo

Regulation of store-operated Ca2+ entry in pulmonary artery smooth muscle cells

McElroy, S.P. and Drummond, R.M. and Gurney, A.M. (2009) Regulation of store-operated Ca2+ entry in pulmonary artery smooth muscle cells. Cell Calcium, 46 (2). pp. 99-106. ISSN 0143-4160

Full text not available in this repository. (Request a copy from the Strathclyde author)

Abstract

Store-operated Ca2+ entry (SOCE) is an important mechanism for Ca2+ influx in smooth muscle cells; however the activation and regulation of this influx pathway are incompletely understood. In the present study we have examined the effect of several protein kinases in regulating SOCE in pulmonary artery smooth muscle cells (PASMCs) of the rat. Inhibition of protein kinase C with chelerythrine (3 μM) potentiated SOCE by 47 ± 2%, while the tyrosine kinase inhibitors genistein (100 μM) and tyrphostin 23 (100 μM) caused a significant reduction in SOCE of 55 ± 9% and 43 ± 7%, respectively. It has been proposed that Ca2+-insensitive phospholipase A2 (iPLA2) is involved in the activation of SOCE in many different cell types. The iPLA2 inhibitor, bromoenol lactone had no effect on SOCE, suggesting that this mechanism was not involved in the activation of the pathway. The calmodulin antagonists, calmidazolium (CMZ) (10 μM) and W-7 (10 μM) appeared to potentiate SOCE in PASMCs. Further investigation established that CMZ was actually activating a Ca2+ influx pathway that was independent of the filling state of the sarcoplasmic reticulum. The CMZ-activated Ca2+ influx was blocked by Gd3+ (10 μM), but unaffected by 2-APB (75 μM), indicating a pharmacological profile distinct from the classical SOCE pathway.

Item type: Article
ID code: 12992
Keywords: pulmonary artery, smooth muscle, store-operated Ca2+ entry, protein kinase C, tyrosine kinase, calmodulin, Ca2+ independent phospholipase A(2), ca2+-independent phospholipase a(2), protein-kinase-c, capacitative calcium-entry, inositol 1, 4, 5-trisphosphate receptors, portal-vein myocytes, bromoenol lactone, trpc channels, crac channel, intravenous anesthetics, Therapeutics. Pharmacology, Pharmacy and materia medica, Microbiology, Cell Biology, Molecular Biology, Physiology
Subjects: Medicine > Therapeutics. Pharmacology
Medicine > Pharmacy and materia medica
Science > Microbiology
Department: Faculty of Science > Strathclyde Institute of Pharmacy and Biomedical Sciences
Related URLs:
    Depositing user: Ms Ann Barker-Myles
    Date Deposited: 31 Aug 2009 14:23
    Last modified: 04 Sep 2014 23:21
    URI: http://strathprints.strath.ac.uk/id/eprint/12992

    Actions (login required)

    View Item