Actin cytoskeleton derangement induces apoptosis in renal ischemia/reperfusion

HL-1 mouse cardiomyocyte injury and death after simulated ischemia and reperfusion: roles of pH, Ca2+-independent phospholipase A2, and Na+/H+ exchange

“…Simulated ischemia was associated with a marked disruption of F-actin and cortactin organization, which was largely reversible upon reperfusion, in accordance with previous reports of SI/R-mediated F-actin disruption in the heart (25,39) and other tissues (14). Caspase-3 and calpain are known to cleave F-actin (62) and cortactin (44), respectively; however, at least caspase-3 was not cleaved during SI per se, and hence, the mechanism of cytoskeletal disruption during SI remains to be elucidated.…”

Depletion of PtdIns(4,5)P2 underlies retinal degeneration in Drosophila trp mutants

“…Moesin depletion has been reported to trigger apoptosis in Drosophila epithelial cells via upregulation of RhoA and activation of the JNK pathway (Neisch et al, 2010). Both actin depolymerisation and microvillar breakdown due to loss of membrane associated ERM have also been shown to trigger cell death processes in several independent mammalian studies (Genescà et al, 2006;Kondo et al, 1997;Martin and Leder, 2001;Suria et al, 1999). Whether these events are sufficient to trigger trp degeneration or whether the degeneration pathway in these mutants involves other parallel pathways needs further investigation.…”

Oxidants as important determinants of renal apoptosis during pneumoperitoneum: a study in an isolated perfused rat kidney model

“…In intact kidney, there are various protective mechanisms, so that when the kidney is kept perfused, the phenomenon of apoptosis may not be noticed macroscopically. Also, apoptosis is programmed during reperfusion following warm ischemia, and administration of stabilizing agents was shown to reverse apoptosis in kidneys that had previously undergone warm ischemia [36]. Early administration of compounds accelerating recovery from ischemic injury following near-normothermic acellular perfusion, as could be considered the herein used tungstate, has been shown to trigger pathways for new synthesis, leading to cellular recovery rather than cell death [37].…”