Priority Research Papers:

CXCL16 regulates cisplatin-induced acute kidney injury

Hua Liang, Zhengmao Zhang, Liqun He and Yanlin Wang _

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Oncotarget. 2016; 7:31652-31662. https://doi.org/10.18632/oncotarget.9386

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Hua Liang1,2, Zhengmao Zhang1, Liqun He3 and Yanlin Wang1,4

1 Selzman Institute for Kidney Health and Section of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas, United States of America

2 Department of Anesthesiology, Affiliated Foshan Hospital of Sun Yat-Sen University, Foshan, China

3 Section of Nephrology, Department of Medicine, Shuguang Hospital, Shanghai, China

4 Center for Translational Research on Inflammatory Diseases and Renal Section, Michael E. DeBakey Veterans Affairs Medical Center, Houston, Texas, United States of America

Correspondence to:

Yanlin Wang, email:

Liqun He, email:

Keywords: acute kidney injury, cisplatin, chemokines, cytokines, apoptosis

Received: January 21, 2016 Accepted: May 04, 2016 Published: May 15, 2016


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.

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