Protective Effects of Growth Arrest-Specific Protein 6 (Gas6) on Sepsis-Induced Acute Kidney Injury

Inflammation. 2016 Apr;39(2):575-82. doi: 10.1007/s10753-015-0282-2.

Abstract

Acute kidney injury (AKI) is a serious complication of sepsis, which has a high mortality rate. Growth arrest-specific protein 6 (Gas6), the protein product of the growth arrest specific gene 6, has been shown to have an anti-apoptotic effect as well as pro-survival capability. Here, we investigated the effects of Gas6 on sepsis-associated AKI in mice subjected to cecal ligation and puncture (CLP). We found that the administration of rmGas6 significantly reduced serum urea nitrogen and creatinine and improved the survival of septic mice. Furthermore, the renal pathological damage induced by CLP was attenuated by rmGas6 treatment. Finally, rmGas6 reduced the renal tissue apoptotic index and the expression of Bax, while it upregulated the expression of Bcl-2. The data suggest that rmGas6 might be used as a potential therapeutic agent for sepsis-induced AKI.

Keywords: acute kidney injury; apoptosis; gas6; sepsis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Kidney Injury / drug therapy*
  • Acute Kidney Injury / pathology
  • Animals
  • Apoptosis / drug effects*
  • Blood Urea Nitrogen*
  • Cecum / surgery
  • Creatinine / blood*
  • Intercellular Signaling Peptides and Proteins / therapeutic use*
  • Kidney / pathology
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Proto-Oncogene Proteins c-bcl-2 / biosynthesis
  • Sepsis / pathology*
  • bcl-2-Associated X Protein / biosynthesis

Substances

  • Bax protein, mouse
  • Intercellular Signaling Peptides and Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • bcl-2-Associated X Protein
  • growth arrest-specific protein 6
  • Creatinine