Ischemia-reperfusion decreases protein tyrosine phosphorylation and p38 mitogen-activated protein kinase phosphorylation in rat lung transplants.

作者: Shoji Sakiyama , Marc dePerrot , Bing Han , Thomas K Waddell , Shaf Keshavjee

DOI: 10.1016/S1053-2498(02)00553-3

关键词:

摘要: Abstract Background: Dramatic alterations of protein tyrosine phosphorylation have been found during the ischemia–reperfusion (IR) period human lung transplantation. IR also induces activation p38 mitogen-activated kinase (p38) in heart and kidney. The objective present study was to determine whether these changes exist a rat single-lung transplant model for further mechanistic investigations. Methods: Isogeneic transplantation performed from Lewis (LEW) LEW rats, whereas allogeneic Brown Norway (BN) rats. Blood gases peak airway pressure were monitored. Lung tissues collected after 6 hours cold ischemic preservation, 30 minutes warm ischemia implantation, 2 reperfusion. Protein (PTK) phosphatase (PTP) activities measured. phosphorylation, Src PTK expression examined by western blotting. Results: In both iso- allografts, function transplants very well preserved. PTP decreased significantly level reduced Conclusions: During early transplantation, may be involved apoptosis other biologic changes. lack suggests that activity pathways setting different processes.

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