APOL1 renal risk variants exacerbate podocyte injury by increasing inflammatory stress.

ABSTRACT:

Background

Apolipoprotein L1, APOL1, is a trypanosome lytic factor present in human and certain other primates. APOL1 gene variants, present in individuals of recent sub-Saharan African descent, increase risk for glomerular disease and associate with the disease progression, but the molecular mechanisms have not been defined.

Objectives

We focus on the mechanism how APOL1 variant proteins enhance podocyte injury in the stressed kidney.

Methods

First, we investigated the expression of APOL1 protein isoform and the localization of APOL1 protein in the kidney. Next, we examined the role of APOL1 in the podocyte stress and the inflammatory signaling in the kidney after hemi-nephrectomy.

Results

We identified a novel RNA variant that lacks a secretory pathway signal

SUBMITTER: Wakashin H 

PROVIDER: S-EPMC7450955 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature