Pkd2 deletion during embryo development does not alter mesonephric programmed cell senescence.

Pkd2 deletion during embryo development does not alter mesonephric programmed cell senescence. Int J Dev Biol. 2018;62(9-10):637-640 Authors: Da Silva-Álvarez S, Lamas-González O, Ferreirós A, González P, Gómez M, García-Caballero T, González Barcia M, García-González MA, Collado M Abstract Programmed cell senescence during embryo development is a recently described process that opens a new perspective to understand the senescence response and that adds a new player whose contribution to development needs to be addressed. Identifying developmental syndromes with a root in deregulated programmed cell senescence will undoubtedly reinforce our view of senescence and could provide a new angle to confront disease. One of the structures that was initially reported to undergo cellular senescence is the mesonephros. During E12.5-E14.5, before regression, mesonephric tubules are positive for the most widely used marker of cell senescence, SAβG, and negative for proliferation marker, Ki67, in a p21Cip1-dependent manner. PKD2 is one of the genes defective in autosomal dominant polycystic kidney disease (ADPKD). Inherited mutations in this gene result in cyst formation in adults after a secondary hit. Polycystin-2 (PC2) protein, the product of PKD2 gene expression, inhibits cell cycle progression by inducing p21Cip1, whereas mutated PKD2 results in increased proliferation and defective differentiation of kidney epithelial cells. Here, ...
Source: International Journal of Developmental Biology - Category: Biology Tags: Int J Dev Biol Source Type: research