CXCL16 regulates cisplatin-induced acute kidney injury. Academic Article uri icon

Overview

abstract

  • The pathogenesis of cisplatin-induced acute kidney injury (AKI) is characterized by tubular cell apoptosis and inflammation. However, the molecular mechanisms are not fully understood. We found that CXCL16 was induced in renal tubular epithelial cells in response to cisplatin-induced AKI. Therefore, we investigated whether CXCL16 played a role in cisplatin-induced tubular cell apoptosis and inflammation. Wild-type and CXCL16 knockout mice were administrated with vehicle or cisplatin at 20 mg/kg by intraperitoneal injection. CXCL16 knockout mice had lower blood urea nitrogen and less tubular damage following cisplatin-induced AKI as compared with wild-type mice. Genetic disruption of CXCL16 reduced tubular epithelial cell apoptosis and decreased caspase-3 activation. Furthermore, CXCL16 deficiency inhibited infiltration of macrophages and T cells into the kidneys following cisplatin treatment, which was associated with reduced expression of the proinflammatory cytokines in the kidneys. Taken together, our results indicate that CXCL16 plays a crucial role in the pathogenesis of cisplatin-induced AKI through regulation of apoptosis and inflammation and maybe a novel therapeutic target for cisplatin-induced AKI.

publication date

  • May 31, 2016

Research

keywords

  • Acute Kidney Injury
  • Apoptosis
  • Chemokine CXCL16
  • Cisplatin
  • Kidney

Identity

PubMed Central ID

  • PMC5077966

Scopus Document Identifier

  • 84973532318

Digital Object Identifier (DOI)

  • 10.18632/oncotarget.439

PubMed ID

  • 27191747

Additional Document Info

volume

  • 7

issue

  • 22