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| Content Provider | Springer Nature Link |
|---|---|
| Author | Flacke, Jan Paul Kumar, Sanjeev Kostin, Sawa Reusch, H. Peter Ladilov, Yury |
| Copyright Year | 2008 |
| Abstract | To analyze the underlying cellular mechanisms of adaptation to ischemia-induced apoptosis through short acidic pretreatment, i.e. acidic preconditioning (APC), Wistar rat coronary endothelial cells (EC) were exposed for 40 min to acidosis (pH 6.4) followed by a 14 h recovery period (pH 7.4) and finally treated for 2 h with simulated in vitro ischemia (glucose-free anoxia at pH 6.4). APC led to a transient activation of p38 and Akt kinases, but not of JNK and ERK1/2 kinases, which was accompanied by significant reduction of the apoptotic cell number, caspase-12/-3 cleavage and Bcl-xL overexpression. These effects of APC were completely abolished by prevention of Akt- or p38-phosphorylation during APC. Furthermore, knock-down of Bcl-xL by siRNA-transfection also abolished the anti-apoptotic effect of APC. Therefore, APC leads to protection of EC against ischemic apoptosis by activation of Akt and p38 followed by overexpression of Bcl-xL, which is a key anti-apoptotic mechanism of APC. |
| Starting Page | 90 |
| Ending Page | 96 |
| Page Count | 7 |
| File Format | |
| ISSN | 13608185 |
| Journal | Apoptosis |
| Volume Number | 14 |
| Issue Number | 1 |
| e-ISSN | 1573675X |
| Language | English |
| Publisher | Springer US |
| Publisher Date | 2008-12-10 |
| Publisher Place | Boston |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Endothelial apoptosis Acidosis Preconditioning Bcl-xL Akt p38 Virology Biochemistry Oncology Cell Biology Cancer Research |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pharmaceutical Science Biochemistry (medical) Cell Biology Clinical Biochemistry Cancer Research Pharmacology |
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