Extracellular CIRP augments inflammation in acute kidney injury via NKG2D-positive macrophages.

ABSTRACT:

Introduction

The mechanism by which extracellular cold-inducible RNA-binding protein (eCIRP) aggravates renal ischemia/reperfusion (RIR) injury leading to acute kidney injury (AKI) is poorly understood. The natural killer group 2D (NKG2D) receptor and its ligand MULT-1 are key immunoregulatory mechanisms promoting responses to damaged and inflamed cells.

Methods

We subjected wild-type and CIRP^-/- mice to RIR. We then used immunohistochemistry (IHC), flow cytometry, and Western blotting to assess NKG2D and MULT-1 in kidney tissues, macrophages, and renal tubular epithelial cells (RTECs), and ELISA to assess TNFa and IL-6.

Results

The expression levels of NKG2D and its ligand MULT-1 were significantly elevated in wild-type mice subjected to RIR compared with

SUBMITTER: Zhang F 

PROVIDER: S-EPMC12823515 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature