Meprin β expression modulates the interleukin-6 mediated JAK2-STAT3 signaling pathway in ischemia/reperfusion-induced kidney injury.

ABSTRACT: Meprin metalloproteinases have been implicated in the pathophysiology of ischemia/reperfusion (IR)-induced kidney injury. Previous in vitro data showed that meprin β proteolytically processes interleukin-6 (IL-6) resulting in its inactivation. Recently, meprin-β was also shown to cleave the IL-6 receptor. The goal of this study was to determine how meprin β expression impacts IL-6 and downstream modulators of the JAK2-STAT3-mediated signaling pathway in IR-induced kidney injury. IR was induced in 12-week-old male wild-type (WT) and meprin β knockout (βKO) mice and kidneys obtained at 24 h post-IR. Real-time PCR, western blot, and immunostaining/microscopy approaches were used to quantify mRNA and protein levels respectively, and immunofluorescence counterstaining with proximal tubule (PT)

SUBMITTER: Abousaad S 

PROVIDER: S-EPMC9483619 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature