ADAM10-Mediated Ectodomain Shedding Is an Essential Driver of Podocyte Damage.

ABSTRACT:

Background

Podocytes embrace the glomerular capillaries with foot processes, which are interconnected by a specialized adherens junction to ultimately form the filtration barrier. Altered adhesion and loss are common features of podocyte injury, which could be mediated by shedding of cell-adhesion molecules through the regulated activity of cell surface-expressed proteases. A Disintegrin and Metalloproteinase 10 (ADAM10) is such a protease known to mediate ectodomain shedding of adhesion molecules, among others. Here we evaluate the involvement of ADAM10 in the process of antibody-induced podocyte injury.

Methods

Membrane proteomics, immunoblotting, high-resolution microscopy, and immunogold electron microscopy were used to analyze human and murine podocyte ADAM10 expression

SUBMITTER: Sachs M 

PROVIDER: S-EPMC8259650 | biostudies-literature | 2021 Jun

REPOSITORIES: biostudies-literature