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Increased endothelial calcium signals in cerebral vessels following traumatic brain injury
Author(s) -
Le Tran Tram,
VillalbaIsabel Nuria,
Nelson Mark T.,
Wellman George C.,
Freeman Kalev
Publication year - 2013
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.27.1_supplement.875.9
Subject(s) - traumatic brain injury , cerebral arteries , calcium signaling , medicine , nitric oxide , cerebral circulation , calcium , endocrinology , chemistry , neuroscience , anesthesia , biology , psychiatry
Traumatic brain injury (TBI) can cause impairment in cerebrovascular function. Endothelial cell (EC) Ca 2+ signals normally activate both nitric oxide (NO) and endothelium‐derived hyperpolarizing factor (EDHF) vasodilatory pathways in cerebral arteries. Little is currently known about the impact of brain injury on vascular endothelial Ca 2+ signaling. We studied the effects of TBI on EC and Ca 2+ signals in rat basilar arteries. Arteries were harvested 24h after fluid percussion injury or sham surgery. We measured EC Ca 2+ signals in slit‐opened basilar arteries from TBI and control animals using the Ca 2+ fluorophore Fluo2‐leakage resistant and confocal microscopy. We found that localized EC Ca 2+ signals were elevated in TBI animals. The optical waveforms of these events were consistent with two Ca 2+ signaling modalities: 1) Ca 2+ pulsars—mediated via endoplasmic reticulum Ca 2+ release through inositol trisphosphate receptors and 2) Ca 2+ sparklets—caused by Ca 2+ entry through Ca 2+ permeable channel (e.g. TRPV4 channels) in the EC plasma membrane. The frequency of both types of EC Ca 2+ signaling events were elevated after TBI. These data suggest that altered EC Ca 2+ signaling may play a role in abnormal cerebrovascular function after TBI.