Hypothermia attenuates ischemia/reperfusion‐induced endothelial cell apoptosis via alterations in apoptotic pathways and JNK signaling | Zendy

Yang Dan | Zendy; Guo Shubin | Zendy; Zhang Tianpeng | Zendy; Li Huihua | Zendy

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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 , hypothermia , endothelial stem cell , ischemia , reperfusion injury , microbiology and biotechnology , signal transduction , pharmacology , chemistry , biology , medicine , anesthesia , biochemistry , in vitro

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.

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