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Hypothermia attenuates ischemia/reperfusion‐induced endothelial cell apoptosis via alterations in apoptotic pathways and JNK signaling
Author(s) -
Yang Dan,
Guo Shubin,
Zhang Tianpeng,
Li Huihua
Publication year - 2009
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2009.07.006
Subject(s) - apoptosis , signal transduction , hypothermia , ischemia , microbiology and biotechnology , reperfusion injury , chemistry , medicine , biology , biochemistry
Hypothermia is the most effective means of protecting the brain, heart and other organs during ischemia/reperfusion (I/R) injury. However, the precise mechanisms for hypothermia to inhibit I/R‐induced endothelial cell apoptosis are not fully understood. In the present study, human umbilical endothelial cells (HUVECs) were exposed to ischemia followed by reperfusion under normothermia (37 °C) or hypothermia (33 °C). Our results showed that hypothermia markedly reduced I/R‐induced endothelial cell apoptosis, the expression of cleaved caspase‐3 and PARP. Moreover, hypothermia markedly reversed I/R‐induced activation of Fas/caspase‐8, the increase of Bax and decrease of Bcl‐2. Furthermore, hypothermia inhibited JNK1/2 activation via MKP‐1 induction. Together, these data demonstrate that hypothermia represses I/R‐induced endothelial cell apoptosis by inhibiting both extrinsic‐ and intrinsic‐dependent apoptotic pathways and activation of JNK1/2.