Traumatic brain injury in vivo and in vitro contributes to cerebral vascular dysfunction through impaired gap junction communication between vascular smooth muscle cells

Guang-Xiang Yu; Martin Mueller; Bridget E Hawkins; Babu P Mathew; Margaret A Parsley; Leoncio A Vergara; Helen L Hellmich; Donald S Prough; Douglas S Dewitt

doi:10.1089/neu.2013.3187

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Traumatic brain injury in vivo and in vitro contributes to cerebral vascular dysfunction through impaired gap junction communication between vascular smooth muscle cells

Journal article

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Peer reviewed

Traumatic brain injury in vivo and in vitro contributes to cerebral vascular dysfunction through impaired gap junction communication between vascular smooth muscle cells

Guang-Xiang Yu, Martin Mueller, Bridget E Hawkins, Babu P Mathew, Margaret A Parsley, Leoncio A Vergara, Helen L Hellmich, Donald S Prough and Douglas S Dewitt

Journal of neurotrauma, Vol.31(8), pp.739-748

04/15/2014

DOI: 10.1089/neu.2013.3187

PMCID: PMC4047850

PMID: 24341563

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Abstract

Gap junctions (GJs) contribute to cerebral vasodilation, vasoconstriction, and, perhaps, to vascular compensatory mechanisms, such as autoregulation. To explore the effects of traumatic brain injury (TBI) on vascular GJ communication, we assessed GJ coupling in A7r5 vascular smooth muscle (VSM) cells subjected to rapid stretch injury (RSI) in vitro and VSM in middle cerebral arteries (MCAs) harvested from rats subjected to fluid percussion TBI in vivo. Intercellular communication was evaluated by measuring fluorescence recovery after photobleaching (FRAP). In VSM cells in vitro, FRAP increased significantly (p<0.05 vs. sham RSI) after mild RSI, but decreased significantly (p<0.05 vs. sham RSI) after moderate or severe RSI. FRAP decreased significantly (p<0.05 vs. sham RSI) 30 min and 2 h, but increased significantly (p<0.05 vs. sham RSI) 24 h after RSI. In MCAs harvested from rats 30 min after moderate TBI in vivo, FRAP was reduced significantly (p<0.05), compared to MCAs from rats after sham TBI. In VSM cells in vitro, pretreatment with the peroxynitrite (ONOO(-)) scavenger, 5,10,15,20-tetrakis(4-sulfonatophenyl)prophyrinato iron[III], prevented RSI-induced reductions in FRAP. In isolated MCAs from rats treated with the ONOO(-) scavenger, penicillamine, GJ coupling was not impaired by fluid percussion TBI. In addition, penicillamine treatment improved vasodilatory responses to reduced intravascular pressure in MCAs harvested from rats subjected to moderate fluid percussion TBI. These results indicate that TBI reduced GJ coupling in VSM cells in vitro and in vivo through mechanisms related to generation of the potent oxidant, ONOO(-).

Brain - blood supply

Gap Junctions - pathology

Animals

Cerebrovascular Circulation - physiology

Brain - physiopathology

Rats

Cell Communication - physiology

Male

Brain Injuries - physiopathology

Muscle, Smooth, Vascular - physiopathology

Rats, Sprague-Dawley

Disease Models, Animal

Details

Title: Subtitle: Traumatic brain injury in vivo and in vitro contributes to cerebral vascular dysfunction through impaired gap junction communication between vascular smooth muscle cells
Creators: Guang-Xiang Yu - Charles R. Allen Research Laboratories, Department of Anesthesiology, University of Texas Medical Branch , Galveston, Texas
Martin Mueller
Bridget E Hawkins
Babu P Mathew
Margaret A Parsley
Leoncio A Vergara
Helen L Hellmich
Donald S Prough
Douglas S Dewitt
Resource Type: Journal article
Publication Details: Journal of neurotrauma, Vol.31(8), pp.739-748
DOI: 10.1089/neu.2013.3187
PMID: 24341563
PMCID: PMC4047850
NLM abbreviation: J Neurotrauma
ISSN: 0897-7151
eISSN: 1557-9042
Publisher: United States
Grant note: NS19355 / NINDS NIH HHS
Language: English
Date published: 04/15/2014
Academic Unit: Stead Family Department of Pediatrics; Anesthesia
Record Identifier: 9984007285002771

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