2005年12月
Activation of mitogen-activated protein kinases during human lung transplantation
JOURNAL OF HEART AND LUNG TRANSPLANTATION
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- 巻
- 24
- 号
- 12
- 開始ページ
- 2079
- 終了ページ
- 2085
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1016/j.healun.2005.04.011
- 出版者・発行元
- ELSEVIER SCIENCE INC
Background: Ischemia-reperfusion is one of the unavoidable steps in lung transplantation; it is associated with acute inflammatory responses and cell death. The intracellular signal transduction mechanisms of these events are largely unknown. We hypothesize that activation of mitogen-activated protein kinases (MAPKs) is one of the important signaling events during human lung transplantation.
Methods: Lung tissue biopsies were performed on 15 patients undergoing transplantation: after cold ischemic preservation; after warm, ischemia (implantation); and after 1- or 2-hour reperfusion. The phosphorylation status of MAPK isoforms (ERK, p38-MAPK and JNK) was examined by Western blotting.
Results: Phosphorylation of ERK was dramatically increased during the first 2 hours of reperfusion. Phosphorylation of JNK also significantly increased at lower levels. In contrast, phosphorylation of p38 showed no significant changes.
Conclusions: We speculate that the rapid and sustained activation of ERK and JNK during the early reperfusion period may contribute to acute inflammatory responses and cell death of lung grafts.
Methods: Lung tissue biopsies were performed on 15 patients undergoing transplantation: after cold ischemic preservation; after warm, ischemia (implantation); and after 1- or 2-hour reperfusion. The phosphorylation status of MAPK isoforms (ERK, p38-MAPK and JNK) was examined by Western blotting.
Results: Phosphorylation of ERK was dramatically increased during the first 2 hours of reperfusion. Phosphorylation of JNK also significantly increased at lower levels. In contrast, phosphorylation of p38 showed no significant changes.
Conclusions: We speculate that the rapid and sustained activation of ERK and JNK during the early reperfusion period may contribute to acute inflammatory responses and cell death of lung grafts.
- リンク情報
- ID情報
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- DOI : 10.1016/j.healun.2005.04.011
- ISSN : 1053-2498
- Web of Science ID : WOS:000234308700012