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Tissue kallikrein protects cortical neurons against hypoxia/reoxygenation injury via the ERK1/2 pathway.

Abstract
Systemic or local delivery of human tissue kallikrein gene (hTK) has been shown to be an effective strategy to alleviate cerebral ischemia/reperfusion (I/R) injury, and tissue kallikrein (TK) administration can suppress glutamate- or acidosis-mediated neurotoxicity in vitro. In the present study, the role of TK in hypoxia/reoxygenation (H/R) induced neuronal cell death was investigated. We found that TK administration could remarkably alleviate H/R-induced neuronal injury by reduction of LDH release and promotion of neuron viability. The protective effects of TK could be counteracted by bradykinin B2 receptor (B2R) antagonist HOE140, which could suppress up-regulation of TK on the ERK signal pathway under H/R condition. These results indicate that TK plays an important role in preventing neurons from H/R damage at least partially through the TK-B2R-ERK1/2 pathway.
AuthorsLing Liu, Haibo Liu, Fang Yang, Guanghui Chen, Houguang Zhou, Min Tang, Renliang Zhang, Qiang Dong
JournalBiochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 407 Issue 2 Pg. 283-7 (Apr 08 2011) ISSN: 1090-2104 [Electronic] United States
PMID21376701 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2011 Elsevier Inc. All rights reserved.
Chemical References
  • Bradykinin Receptor Antagonists
  • icatibant
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3
  • Tissue Kallikreins
  • Bradykinin
Topics
  • Animals
  • Bradykinin (analogs & derivatives, pharmacology)
  • Bradykinin Receptor Antagonists
  • Brain Ischemia (enzymology, pathology)
  • Cells, Cultured
  • Cerebral Cortex (enzymology, pathology)
  • Cytoprotection
  • Humans
  • Mitogen-Activated Protein Kinase 1 (metabolism)
  • Mitogen-Activated Protein Kinase 3 (metabolism)
  • Neurons (enzymology, pathology)
  • Rats
  • Reperfusion Injury (enzymology, pathology)
  • Tissue Kallikreins (genetics, pharmacology, physiology)

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