Acidic preconditioning protects endothelial cells against apoptosis through p38- and Akt-dependent Bcl-xL overexpression Export

@article{citeulike:3783481, abstract = {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.}, author = {Flacke, Jan-Paul and Kumar, Sanjeev and Kostin, Sawa and Reusch, H. and Ladilov, Yury}, citeulike-article-id = {3783481}, citeulike-linkout-0 = {http://dx.doi.org/10.1007/s10495-008-0287-5}, citeulike-linkout-1 = {http://www.springerlink.com/content/e2353h7jx720245g}, doi = {10.1007/s10495-008-0287-5}, journal = {Apoptosis}, keywords = {cell, cells, death, endothelial, flacke08pdf, inschemic}, posted-at = {2008-12-13 01:08:54}, priority = {2}, title = {Acidic preconditioning protects endothelial cells against apoptosis through p38- and Akt-dependent Bcl-xL overexpression}, url = {http://dx.doi.org/10.1007/s10495-008-0287-5} }

TY - JOUR ID - citeulike:3783481 L3 - citeulike-article-id:3783481 N2 - 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. JF - Apoptosis TI - Acidic preconditioning protects endothelial cells against apoptosis through p38- and Akt-dependent Bcl-xL overexpression KW - cell KW - cells KW - death KW - endothelial KW - flacke08pdf KW - inschemic AU - Flacke, Jan-Paul AU - Kumar, Sanjeev AU - Kostin, Sawa AU - Reusch, H AU - Ladilov, Yury UR - http://dx.doi.org/10.1007/s10495-008-0287-5 ER -