Bcl-2 is associated with the outer mitochondrial membrane of viable cells and prevents Bax from perforating the outer mitochondrial membrane, causing cytochrome c to leak out. When cytochrome c enters the cytoplasm, it binds to apoptotic protease-activating factor 1 leading to activation of caspase 9 and subsequently apoptosis. However, recently it has become evident that the function of the members of the Bcl-2 family is not limited to the regulation of apoptosis, but that they also play a role in the regulation of mitochondrial fusion and fission, and thereby in morphogenesis. The kidney is a critical organ for filtering the plasma and is constitutively reabsorbing selected parts of the glomerular filtrate, which is an energy consuming process, located especially to the proximal and distal tubules. Therefore, the epithelial cells in these two tubule segments are rich in mitochondria. Kidney development is a complex process including basic morphogenesis of the collecting duct system and nephrons, involving interactions between the epithelium of ureteric buds and the metanephric mesenchyme. These processes are rigorously controlled in order to ensure that events happen at the right time and in the right sequence in order to build and maintain the various cell populations Sennidin-B present in the different structures. Thus, excessive or insufficient apoptosis during kidney development may cause anormogenesis. The expression of the Bcl-2 and caspase family members has been investigated in vivo and in vitro in order to explore their apoptotic and non-apoptotic function during kidney morphogenesis. Furthermore, it has been suggested that members of the Bcl-2 and caspase families also are involved in cell adhesion, migration, Qingyangshengenin-B differentiation, survival, and proliferation by interaction with other factors during kidney development. However, the analysis of the apoptotic or non apoptotic roles of Bcl-2 and Bax during kidney development requires knowledge about the precise localization of their expression, which has not been available in previous studies in mice. When inspecting the cells in e.g. a developing proximal tubule, the cells in one region may appear almost mature, arranged in one layer, and with a complete brush border, whereas the cells in the adjacent segment of the same tubule appears small and premature, and are arranged in cellular clusters.
Therefore the epithelial cells in these two tubule segments are rich in mitochondria
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