NPR-C protects embryonic stem cells from apoptosis by regulating p53 levels

Stem Cells Dev. 2012 May 20;21(8):1264-71. doi: 10.1089/scd.2011.0239. Epub 2011 Sep 29.

Abstract

The identification of intrinsic factors required for propagation of self-renewing embryonic stem (ES) cells is important to improve the efficiency of expansion of ES cells for therapeutic purposes. Here, we report a novel role for natriuretic peptide receptor-C (NPR-C) in the survival of murine ES cells. We found that NPR-C was highly expressed in ES cells and was downregulated during ES cell differentiation. Knockdown of NPR-C in ES cells by using a small-interfering RNA resulted in apoptotic cell death, and the induction of p53 protein expression. Conversely, chemical inhibition of p53 by α-pifithrin significantly reduced apoptosis in NPR-C-deficient cells. cANF((4-23)), a selective NPR-C agonist, protected ES cells against oxidative stress-induced apoptosis, and blocked activation of p53 and Nanog suppression in the presence of DNA-damaging agents. Thus, NPR-C is required to control DNA damage-induced p53 levels to maintain ES cell self-renewal.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis* / drug effects
  • Blastocyst / cytology
  • Blastocyst / drug effects
  • Blastocyst / metabolism
  • Cell Line
  • Cell Survival / drug effects
  • Cytoprotection* / drug effects
  • Embryonic Stem Cells / cytology*
  • Embryonic Stem Cells / drug effects
  • Embryonic Stem Cells / metabolism*
  • Gene Expression Regulation / drug effects
  • Gene Knockdown Techniques
  • Hydrogen Peroxide / pharmacology
  • Mice
  • Receptors, Atrial Natriuretic Factor / antagonists & inhibitors
  • Receptors, Atrial Natriuretic Factor / genetics
  • Receptors, Atrial Natriuretic Factor / metabolism*
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • Tumor Suppressor Protein p53
  • Hydrogen Peroxide
  • Receptors, Atrial Natriuretic Factor
  • atrial natriuretic factor receptor C