Tubular cell loss in early inv/nphp2 mutant kidneys represents a possible homeostatic mechanism in cortical tubular formation.

ABSTRACT: Inversion of embryonic turning (inv) cystic mice develop multiple renal cysts and are a model for type II nephronophthisis (NPHP2). The defect of planar cell polarity (PCP) by oriented cell division was proposed as the underlying cellular phenotype, while abnormal cell proliferation and apoptosis occur in some polycystic kidney disease models. However, how these cystogenic phenotypes are linked and what is most critical for cystogenesis remain largely unknown. In particular, in early cortical cytogenesis in the inv mutant cystic model, it remains uncertain whether the increased proliferation index results from changes in cell cycle length or cell fate determination. To address tubular cell kinetics, doubling time and total number of tubular cells, as well as amount of genomic DNA (gDNA), w

SUBMITTER: Shigeta M 

PROVIDER: S-EPMC5995398 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature