Kir6.2, the pore-forming subunit of ATP-sensitive K+ channels, is overexpressed in human post-traumatic brain contusions.

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Kir6.2, the pore-forming subunit of ATP-sensitive K+ channels, is overexpressed in human post-traumatic brain contusions.

J Neurotrauma. 2018 May 08;:

Authors: Castro L, Noelia M, Vidal-Jorge M, Sanchez-Ortiz D, Gándara D, Martínez-Saez E, Cicuendez M, Poca MA, Simard JM, Sahuquillo J

Abstract
Brain contusions (BCs) are one of the most frequent lesions in patients with moderate and severe traumatic brain injury (TBI). BCs increase their volume due to perilesional edema formation and/or hemorrhagic transformation. This may have deleterious consequences and its mechanisms are still poorly understood. We previously identified de novo upregulation SUR1, the regulatory subunit of KATP and other channels, in human BCs. Our aim here was to study the expression of the pore-forming subunit of KATP, Kir6.2, in human BCs, and identify its localization in different cell types. Protein levels of Kir6.2 were detected by western blot (WB) from 33 contusion specimens obtained from 32 TBI patients aged 14-74 years. The evaluation of Kir6.2 expression in different cell types was performed by immunofluorescence in 29 contusion samples obtained from 28 patients with a median age of 42 years. Control samples were obtained from limited brain resections performed to access extra-axial skull base tumors or intraventricular lesions. Contusion specimens showed an increase of Kir6.2 expression in comparison with controls. Regarding cellular location of Kir6.2, there was no expression of this channel subunit in blood vessels, either in control samples or in contusions. The expression of Kir6.2 in neurons and microglia was also analyzed, but the observed differences were not statistically significant. However, a significant increase of Kir6.2 was found in GFAP positive cells in contusion specimens. Our data suggest that further research on SUR1-regulated ionic channels may lead to a better understanding of key mechanisms involved in the pathogenesis of BCs, and may identify novel targeted therapeutic strategies.

PMID: 29737232 [PubMed - as supplied by publisher]

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