From Humans to Experimental Models: The Cytoprotective Role of Clusterin in the KidneyQiunong Guan, Hatem A Alnasser, Christopher YC Nguan and Caigan Du*
Department of Urologic Sciences, University of British Columbia, Vancouver, BC V6H 3Z6, Canada
- *Corresponding Author:
- Caigan Du, PhD
Jack Bell Research Centre
2660 Oak Street, Vancouver, BC, Canada V6H 3Z6
Tel: 604-875-4111, ext 63793
E-mail: [email protected]
Received date : April 21, 2014; Accepted date : May 24, 2014; Published date : May 29, 2014
Citation: Guan Q, Alnasser HA, Nguan CYC, Du C (2014) From Humans to Experimental Models: The Cytoprotective Role of Clusterin in the Kidney. Med Surg Urol 3:134. doi:10.4172/2168-9857.1000134
Copyright: © 2014 Guan Q, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Clusterin (CLU) is a chaperone-like protein and has been discovered more than thirty years ago; however, its biological significance is still not fully understood. This review aims to summarize the principal observations of CLU roles related to the kidney. In humans, three or more mRNA isoforms of CLU could be expressed due to different translation start sites, but only two forms of CLU protein, secreted (sCLU, isoform 2) and nuclear (nCLU, isoform 1), have been well characterized, whereas there is only sCLU form in mice. In the biopsies of renal tissue from patients, up regulated CLU expression has been found in rejecting kidney transplants or diseased kidneys, and a lower level of serum CLU is correlated with many types of kidney disease in patients. In mice, a deficiency in CLU expression specifically leads to the phenotype of age-dependent chronic glomerular injury - moderate to severe accumulation of the mesangial matrix, becomes more susceptible to ischemia-reperfusion injury (IRI), negatively impacts renal repair after IRI and worsens renal fibrosis after ureteral obstruction. All these observations may imply the biological significance of CLU for the maintenance of the tissue homeostasis in adult kidneys. However, how CLU protects the kidney from injury or by which extracellular and intracellular pathways mediate the cyto-protection of CLU in the kidney has not been well investigated. Understanding of the cyto-protective activities of CLU in the kidney could lead to the development of novel therapeutic strategies for the prevention and/or treatment of kidney injury or diseases.