Mechanism of TauT in protecting against cisplatin-induced kidney injury (AKI)

Adv Exp Med Biol. 2009:643:105-12. doi: 10.1007/978-0-387-75681-3_11.

Abstract

Acute renal failure (ARF) results from ischemic or toxic renal injury and is a common disorder with an overall mortality rate of about 50%. Despite the advent of dialysis and increasing knowledge regarding the causes and the effects of ARF, this trend has hardly changed for several decades. Cisplatin is a broadly used anticancer drug and is widely known to induce acute renal failure as a result of renal tubular injury. In this study, we have demonstrated that: (1) TauT is down-regulated by the p53 tumor suppressor gene in renal proximal tubule LLC-PK1 cells; (2) cisplatin down-regulates the expression of TauT in renal proximal tubule cells through, at least in part, a p53-dependent pathway; and (3) forced overexpression of TauT can attenuate cisplatin-induced apoptosis of renal proximal tubule cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Kidney Injury / chemically induced*
  • Animals
  • Antineoplastic Agents / toxicity*
  • Apoptosis / drug effects
  • Base Sequence
  • Blotting, Western
  • Cisplatin / toxicity*
  • DNA Primers
  • Genes, p53
  • LLC-PK1 Cells
  • Membrane Glycoproteins / genetics
  • Membrane Glycoproteins / physiology*
  • Membrane Transport Proteins / genetics
  • Membrane Transport Proteins / physiology*
  • Swine

Substances

  • Antineoplastic Agents
  • DNA Primers
  • Membrane Glycoproteins
  • Membrane Transport Proteins
  • taurine transporter
  • Cisplatin