Vasopressin V1a receptors regulate cerebral aquaporin 1 after traumatic brain injury.
J Neurotrauma. 2019 Sep 24. doi: 10.1089/neu.2019.6653. [Epub ahead of print]
| Authors/Editors: | Rauen K, Pop V, Trabold R, Badaut J, Plesnila N. |
|---|---|
| Publication Date: | 2019 |
Abstract
Brain edema formation contributes to secondary brain damage and unfavorable outcome following traumatic brain injury (TBI). Aquaporins (AQP), highly selective water channels, are involved in the formation of post-trauma brain edema, however, their regulation is largely unknown. Since vasopressin receptors are involved in aquaporin-mediated water transport in the kidney and inhibition of V<sub>1a</sub> receptors reduces post-trauma brain edema formation, we hypothesize that cerebral aquaporins may be regulated by V<sub>1a</sub> receptors. Cerebral <i>Aqp1</i> and <i>Aqp4</i> mRNA and AQP1 and AQP4 protein levels were quantified in wild-type (WT) and V<sub>1a</sub> receptor knock-out <i>(V<sub>1a</sub><sup>-/-</sup>)</i> mice before and 15 min, 1, 3, 6, 12 or 24 hours following experimental TBI by controlled cortical impact. In non-traumatized mice, we found AQP1 and AQP4 expression in cortical neurons and astrocytes, respectively. Experimental TBI had no effect on <i>Aqp4</i> mRNA or AQP4 protein expression, but increased <i>Aqp1</i> mRNA (p<0.05) and AQP1 protein expression (p<0.05) in both hemispheres. <i>Aqp1</i> mRNA and AQP1 protein regulation was blunted in V<sub>1a</sub> receptor knock-out mice. V<sub>1a</sub> receptors regulate cerebral AQP1 expression following experimental TBI thereby unraveling the molecular mechanism by which these receptors may mediate brain edema formation following TBI. Keywords Cerebral aquaporin; arginine vasopressin; brain edema; vasopressin V1a receptor knock-out mouse; traumatic brain injury.
