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CaMKII regulates intracellular calcium stores of native endothelial cells from mesenteric arteries
Author(s) -
Toussaint Fanny,
Charbel Chimène,
Blanchette Alexandre,
Villeneuve Louis R.,
Ledoux Jonathan
Publication year - 2012
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.26.1_supplement.1129.22
Subject(s) - ionomycin , homeostasis , intracellular , microbiology and biotechnology , extracellular , mesenteric arteries , chemistry , endoplasmic reticulum , medicine , endocrinology , calcium , endothelium , calcium in biology , biology , artery
Ca 2+ homeostasis is crucial for endothelial function and the regulation of vascular tone. The Ca 2+ ‐dependent kinase CaMKII is activated by Ca 2+ pulsars and might play an important role in endothelial Ca 2+ homeostasis. Thus, the involvement of endothelial CaMKII in the regulation of intracellular Ca 2+ dynamics has been investigated in native endothelial cells of mesenteric arteries. Acute exposure to KN‐93 (10 μM), a CaMKII inhibitor, has little if any effect on Ca 2+ pulsars frequency or amplitude. However, CaMKII inhibition induces pulsar sites recruitment as more pulsars sites are active in the presence of KN‐93 compared to control (25%). Interestingly, in absence of extracellular Ca 2+ , KN‐93 appears to empty intracellular Ca 2+ stores. Indeed, exposure to ionomycin, to empty endoplasmic reticulum in absence of extrallular Ca 2+ , provoked a large and transient intracellular Ca 2+ increase. However, preincubation with KN‐93 abolished the ionomycin‐induced Ca 2+ transient. These results suggest that CaMKII might inhibit IP 3 R receptors and/or phosphorylates phospholamban to regulate ER Ca 2+ content. Confocal microscopy revealed that CaMKIIα & β are colocalized with IP 3 R1 in native endothelium. Our data suggest that CaMKII is an important regulator of endothelial Ca 2+ homeostasis and may represent a novel target for the treatment of pathologies like hypertension. Supported by FRSQ, CFI, CIHR and HSFC.