A role for p21ras in the angiotensin II AT2 receptor transduction pathway

Endocr Res. 1998 Aug-Nov;24(3-4):409-12. doi: 10.3109/07435809809032623.

Abstract

We have previously shown that the activation of the AT2 receptor of Ang II induced neurite outgrowth in NG108-15 cells. We also found that stimulation of NG108-15 cells with Ang II induced a rapid decrease in GTP-bound p21ras. In order to investigate the possible role of p21ras in Ang II-induced neuronal differentiation, we have established NG108-15 sublines which inducibly express a dominant inhibitory form of p21ras (p21N17Ras). We observed that IPTG-induced expression of p21N17Ras in these NG108-15 sublines induced the same morphological changes as does Ang II in control untransfected cells. Immunofluorescence labeling of beta-tubulin showed that expression of p21N17Ras induced neurite outgrowth and elongation. These observations were supported by Western blot analysis of the level of polymerized tubulin. These results strongly support the hypothesis that AT2 receptor-induced neuronal differentiation in NG108-15 cells is mediated by the inhibition of p21ras.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Isopropyl Thiogalactoside / pharmacology
  • Microscopy, Phase-Contrast
  • Polymers / metabolism
  • Proto-Oncogene Proteins p21(ras) / genetics
  • Proto-Oncogene Proteins p21(ras) / physiology*
  • RNA, Messenger / metabolism
  • Receptor, Angiotensin, Type 2
  • Receptors, Angiotensin / genetics*
  • Transcription, Genetic / physiology
  • Transduction, Genetic / physiology*
  • Transfection / physiology
  • Tubulin / metabolism
  • Tumor Cells, Cultured / drug effects
  • Tumor Cells, Cultured / pathology

Substances

  • Polymers
  • RNA, Messenger
  • Receptor, Angiotensin, Type 2
  • Receptors, Angiotensin
  • Tubulin
  • Isopropyl Thiogalactoside
  • Proto-Oncogene Proteins p21(ras)