H(2)O (2)-stimulated Ca(2+) influx via TRPM2 is not the sole determinant of subsequent cell death.

H(2)O (2)-stimulated Ca(2+) influx via TRPM2 is not the sole determinant of subsequent cell death. Research Abstract Details 

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H(2)O (2)-stimulated Ca(2+) influx via TRPM2 is not the sole determinant of subsequent cell death. Abstract Text:

Jenny A Wilkinson,Jason L Scragg,John P Boyle,Bernd Nilius,Chris Peers,

Activation of transient receptor potential melastatin 2 (TRPM2), a non-selective, Ca(2+)-permeable cation channel, is implicated in cell death. Channel opening is stimulated by oxidative stress, a feature of numerous disease states. The wide expression profile of TRPM2 renders it a potentially significant therapeutic target in a variety of pathological settings including cardiovascular and neurodegenerative diseases. HEK293 cells transfected with human TRPM2 (HEK293/hTRPM2) were more vulnerable to H(2)O(2)-mediated cell death than untransfected controls in which H(2)O(2)-stimulated Ca(2+) influx was absent. Flufenamic acid partially reduced Ca(2+) influx in response to H(2)O(2) but had no effect on viability. N-(p-Amylcinnamoyl) anthranilic acid substantially attenuated Ca(2+) influx but did not alter viability. Poly(adenosine diphosphate ribose) polymerase inhibitors (N-(6-oxo-5,6-dihydro-phenanthridin-2-yl)-N,N-dimethylacetamide, 3,4-dihydro-5-[4-(1-piperidinyl)butoxy]-1(2H)-isoquinolinone and nicotinamide) reduced Ca(2+) influx and provided a degree of protection but also had some protective effects in untransfected controls. These data suggest H(2)O(2) triggers cell death in HEK293/hTRPM2 cells by a mechanism that is in part Ca(2+) independent, as blockade of channel opening (evidenced by suppression of Ca(2+) influx) did not correlate well with protection from cell death. Determining the underlying mechanisms of TRPM2 activation is pertinent in elucidating the relevance of this channel as a therapeutic target in neurodegenerative diseases and other pathologies associated with Ca(2+) dysregulation and oxidative stress.

H(2)O (2)-stimulated Ca(2+) influx via TRPM2 is not the sole determinant of subsequent cell death. Publishing Authors By Initials

JA Wilkinson,JL Scragg,JP Boyle,B Nilius,C Peers,

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H(2)O (2)-stimulated Ca(2+) influx via TRPM2 is not the sole determinant of subsequent cell death. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Pflügers Archiv : European journal of physiology

VOLUME: 455

Page Numbers: 1141-51

Journal Abbreviation: Pflugers Arch.

ISSN: 0031-6768

DAY: 28

MONTH: 11

YEAR: 2007

H(2)O (2)-stimulated Ca(2+) influx via TRPM2 is not the sole determinant of subsequent cell death. Information

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LANGUAGE: eng

NlmUniqueID: 154720

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Grant and Affiliation Information for H(2)O (2)-stimulated Ca(2+) influx via TRPM2 is not the sole determinant of subsequent cell death.

AFFILIATION: School of Medicine, University of Leeds, Leeds, LS2 9JT, UK.

Country: Germany

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MEDLINETA: Pflugers Arch

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