alexa The Sur1-Trpm4 Channel in Spinal Cord Injury | OMICS International | Abstract
ISSN: 2165-7939

Journal of Spine
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Review Article

The Sur1-Trpm4 Channel in Spinal Cord Injury

J Marc Simard1-3*, Seung Kyoon Woo1, Bizhan Aarabi1 and Volodymyr Gerzanich1
1Department of Neurosurgery, University of Maryland School of Medicine, Baltimore, USA
2Department of Pathology, University of Maryland School of Medicine, Baltimore, USA
3Department of Physiology, University of Maryland School of Medicine, Baltimore, USA
Corresponding Author : Marc Simard J
Department of Neurosurgery
22 S. Greene St. Suite S12D
Baltimore, MD 21201-1595
Tel: 410-328-0850
Fax: 410-328-0124
E-mail: [email protected]
Received July 25, 2013; Accepted August 14, 2013; Published August 17, 2013
Citation: Simard JM, Woo SK, Aarabi B, Gerzanich V (2013) The Sur1-Trpm4 Channel in Spinal Cord Injury. J Spine S4:002. doi:10.4172/2165-7939.S4-002
Copyright: © 2013 Simard JM, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Spinal cord injury (SCI) is a major unsolved challenge in medicine. Impact trauma to the spinal cord shears blood vessels, causing an immediate ‘primary hemorrhage’. During the hours following trauma, the region of hemorrhage enlarges progressively, with delayed or ‘secondary hemorrhage’ adding to the primary hemorrhage, and effectively doubling its volume. The process responsible for the secondary hemorrhage that results in early expansion of the hemorrhagic lesion is termed ‘progressive hemorrhagic necrosis’ (PHN). PHN is a dynamic process of auto destruction whose molecular underpinnings are only now beginning to be elucidated. PHN results from the delayed, progressive, catastrophic failure of the structural integrity of capillaries. The resulting ‘capillary fragmentation’ is a unique, pathognomonic feature of PHN. Recent work has implicated the Sur1-Trpm4 channel that is newly upregulated in penumbral microvessels as being required for the development of PHN. Targeting the Sur1-Trpm4 channel by gene deletion, gene suppression, or pharmacological inhibition of either of the two channel subunits, Sur1 or Trpm4, yields exactly the same effects histologically and functionally, and exactly the same unique, pathognomonic phenotype – the prevention of capillary fragmentation. The potential advantage of inhibiting Sur1-Trpm4 channels using glibenclamide is a highly promising strategy for ameliorating the devastating sequelae of spinal cord trauma in humans.

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