RGD Reference Report - Cerebrovascular connexin expression: effects of traumatic brain injury. - Rat Genome Database

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Cerebrovascular connexin expression: effects of traumatic brain injury.

Authors: Avila, MA  Sell, SL  Hawkins, BE  Hellmich, HL  Boone, DR  Crookshanks, JM  Prough, DS  DeWitt, DS 
Citation: Avila MA, etal., J Neurotrauma. 2011 Sep;28(9):1803-11. doi: 10.1089/neu.2011.1900. Epub 2011 Sep 6.
RGD ID: 7207391
Pubmed: PMID:21895483   (View Abstract at PubMed)
PMCID: PMC3172862   (View Article at PubMed Central)
DOI: DOI:10.1089/neu.2011.1900   (Journal Full-text)

Traumatic brain injury (TBI) results in dysfunction of the cerebrovasculature. Gap junctions coordinate vasomotor responses and evidence suggests that they are involved in cerebrovascular dysfunction after TBI. Gap junctions are comprised of connexin proteins (Cxs), of which Cx37, Cx40, Cx43, and Cx45 are expressed in vascular tissue. This study tests the hypothesis that TBI alters Cx mRNA and protein expression in cerebral vascular smooth muscle and endothelial cells. Anesthetized (1.5% isoflurane) male Sprague-Dawley rats received sham or fluid-percussion TBI. Two, 6, and 24 h after, cerebral arteries were harvested, fresh-frozen for RNA isolation, or homogenized for Western blot analysis. Cerebral vascular endothelial and smooth muscle cells were selected from frozen sections using laser capture microdissection. RNA was quantified by ribonuclease protection assay. The mRNA for all four Cx genes showed greater expression in the smooth muscle layer compared to the endothelial layer. Smooth muscle Cx43 mRNA expression was reduced 2 h and endothelial Cx45 mRNA expression was reduced 24 h after injury. Western blot analysis revealed that Cx40 protein expression increased, while Cx45 protein expression decreased 24 h after injury. These studies revealed significant changes in the mRNA and protein expression of specific vascular Cxs after TBI. This is the first demonstration of cell type-related differential expression of Cx mRNA in cerebral arteries, and is a first step in evaluating the effects of TBI on gap junction communication in the cerebrovasculature.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
GJA5HumanBrain Injuries  ISOGja5 (Rattus norvegicus)protein:increased expression:cerebral arteryRGD 
Gja5RatBrain Injuries  IEP protein:increased expression:cerebral arteryRGD 
Gja5MouseBrain Injuries  ISOGja5 (Rattus norvegicus)protein:increased expression:cerebral arteryRGD 

Objects Annotated

Genes (Rattus norvegicus)
Gja5  (gap junction protein, alpha 5)

Genes (Mus musculus)
Gja5  (gap junction protein, alpha 5)

Genes (Homo sapiens)
GJA5  (gap junction protein alpha 5)


Additional Information