ADAM10 mediates ectopic proximal tubule development and renal fibrosis through Notch signalling.

ABSTRACT: Disturbed intrauterine development increases the risk of renal disease. Various studies have reported that Notch signalling plays a significant role in kidney development and kidney diseases. A disintegrin and metalloproteinase domain 10 (ADAM10), an upstream protease of the Notch pathway, is also reportedly involved in renal fibrosis. However, how ADAM10 interacts with the Notch pathway and causes renal fibrosis is not fully understood. In this study, using a prenatal chlorpyrifos (CPF) exposure mouse model, we investigated the role of the ADAM10/Notch axis in kidney development and fibrosis. We found that prenatal CPF-exposure mice presented overexpression of Adam10, Notch1 and Notch2, and led to premature depletion of Six2⁺ nephron progenitors and ectopic formation of proxima

SUBMITTER: Li B 

PROVIDER: S-EPMC7702158 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature