Apoptotic microtubule network organization and maintenance depend on high cellular XXXX levels and energized mitochondria.

@entity1 @entity39 @entity1311 @entity1191 @entity9800 @entity460 @entity44753 @entity855
Microtubule cytoskeleton is reformed during apoptosis, forming a cortical structure beneath plasma membrane, which plays an important role in preserving cell morphology and plasma membrane integrity. However, the maintenance of the @entity44753 ( @entity44753 ) during apoptosis is not understood. In the present study, we examined apoptosis induced by @entity9800 ( @entity1191 ), a topoisomerase I inhibitor, in @entity1 @entity1 and porcine LLCPK-1a cells. We demonstrate that @entity44753 was organized in apoptotic cells with high @entity855 levels and hyperpolarized mitochondria and, on the contrary, was dismantled in apoptotic cells with low @entity855 levels and mitochondrial depolarization. @entity44753 disorganization after mitochondrial depolarization was associated with increased plasma membrane permeability assessed by enhancing LDH release and increased intracellular @entity460 levels. Living cell imaging monitoring of both, microtubule dynamics and mitochondrial membrane potential, showed that @entity44753 persists during apoptosis coinciding with cycles of mitochondrial hyperpolarization. Eventually, @entity44753 was disorganized when mitochondria suffered a large depolarization and cell underwent secondary @entity39 . @entity44753 stabilization by @entity1311 prevented LDH release and @entity460 influx even though mitochondria were depolarized, suggesting that @entity44753 is essential for plasma membrane integrity. Furthermore, high @entity855 levels and mitochondria polarization collapse after oligomycin treatment in apoptotic cells suggest that @entity855 synthase works in "reverse" mode during apoptosis. These data provide new explanations for the role of @entity44753 and mitochondria during apoptosis.
