Transient receptor potential melastatin subfamily member 2 cation channel regulates detrimental immune cell invasion in ischemic stroke. – ScienceOpen
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      Transient receptor potential melastatin subfamily member 2 cation channel regulates detrimental immune cell invasion in ischemic stroke.

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          Abstract

          Brain injury during stroke results in oxidative stress and the release of factors that include extracellular Ca(2+), hydrogen peroxide, adenosine diphosphate ribose, and nicotinic acid adenine dinucleotide phosphate. These alterations of the extracellular milieu change the activity of transient receptor potential melastatin subfamily member 2 (TRPM2), a nonselective cation channel expressed in the central nervous system and the immune system. Our goal was to evaluate the contribution of TRPM2 to the tissue damage after stroke.

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          Author and article information

          Journal
          Stroke
          Stroke; a journal of cerebral circulation
          1524-4628
          0039-2499
          Nov 2014
          : 45
          : 11
          Affiliations
          [1 ] From the Department of Neurology (M. Gelderblom, P.A., C.G., T.M.), Institute of Neuroimmunology and Multiple Sclerosis (B.S., F.U., M.A.F.), and Institute of Neuropathology (C.B., M. Glatzel), University Medical Center Hamburg-Eppendorf, Hamburg, Germany; Department of Neurology, University of Muenster, Muenster, Germany (N.M., G.H., S.B., A.M.H., S.G.M.); and Department of Neurology, University Clinics Wuerzburg, Wuerzburg, Germany (E.G., C.K.).
          [2 ] From the Department of Neurology (M. Gelderblom, P.A., C.G., T.M.), Institute of Neuroimmunology and Multiple Sclerosis (B.S., F.U., M.A.F.), and Institute of Neuropathology (C.B., M. Glatzel), University Medical Center Hamburg-Eppendorf, Hamburg, Germany; Department of Neurology, University of Muenster, Muenster, Germany (N.M., G.H., S.B., A.M.H., S.G.M.); and Department of Neurology, University Clinics Wuerzburg, Wuerzburg, Germany (E.G., C.K.). t.magnus@uke.de manuel.friese@zmnh.uni-hamburg.de.
          Article
          STROKEAHA.114.005836
          10.1161/STROKEAHA.114.005836
          25236871
          c6d429b6-8c63-4079-bdbf-ba18be2c685e
          © 2014 American Heart Association, Inc.
          History

          inflammation,ion channels,neutrophils,stroke
          inflammation, ion channels, neutrophils, stroke

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