Vasopressin V1a Receptors Regulate Cerebral Aquaporin 1 after Traumatic Brain Injury.
Vasopressin V1a Receptors Regulate Cerebral Aquaporin 1 after Traumatic Brain Injury.
复制标题
加压素 V1a 受体在创伤性脑损伤后调节大脑水通道蛋白 1。
DOI：
10.1089/neu.2019.6653
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发表时间：
2020
影响因子：
4.2
通讯作者：
Plesnila,Nikolaus
中科院分区：
文献类型：
--
作者：
Rauen,Katrin;Pop,Viorela;Trabold,Raimund;Badaut,Jerome;Plesnila,Nikolaus
Brain edema formation contributes to secondary brain damage and unfavorable outcome after 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. Because vasopressin receptors are involved in AQP-mediated water transport in the kidney and inhibition of V1areceptors reduces post-trauma brain edema formation, we hypothesize that cerebral AQPs may be regulated by V1areceptors. CerebralAqp1andAqp4messenger ribonucleic acid (mRNA) and AQP1 and AQP4 protein levels were quantified in wild-type and V1areceptor knockout(V1a-/-)mice before and 15 min, 1, 3, 6, 12, or 24 h after 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 onAqp4mRNA or AQP4 protein expression, but increasedAqp1mRNA (p< 0.05) and AQP1 protein expression (p< 0.05) in both hemispheres. TheAqp1mRNA and AQP1 protein regulation was blunted in V1areceptor knockout mice. The V1areceptors regulate cerebral AQP1 expression after experimental TBI, thereby unraveling the molecular mechanism by which these receptors may mediate brain edema formation after TBI.
