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Proliferative and survival effects of PUMA promote angiogenesis

Fan Zhang1, Yang Li, Zhongshu Tang

  • 1National Eye Institute, National Institutes of Health, Rockville, MD 20852, USA.

Cell Reports
|November 6, 2012
PubMed

Insights

The p53 upregulated modulator of apoptosis (PUMA) surprisingly promotes new blood vessel growth (angiogenesis) and cell survival. PUMA deficiency inhibits angiogenesis and reduces microglia, suggesting therapeutic potential.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • The p53 upregulated modulator of apoptosis (PUMA) is a key inducer of apoptosis.
  • Its role in cell proliferation and survival has been less understood.

Purpose of the Study:

  • To investigate the role of PUMA in angiogenesis and cell survival.
  • To elucidate the underlying molecular mechanisms.

Main Methods:

  • Genetic deletion and small hairpin RNA (shRNA) knockdown of Puma in vivo.
  • Puma gene delivery.
  • Analysis of angiogenesis, microglia numbers, cell survival, Erk activation, and intracellular calcium levels.

Main Results:

  • Puma deficiency inhibited developmental and pathological angiogenesis and reduced microglia numbers.
  • Puma gene delivery increased angiogenesis and cell survival.
  • PUMA regulates autophagy by modulating Erk activation and intracellular calcium.

Conclusions:

  • PUMA functions as a proangiogenic factor essential for vascular and microglia cell proliferation and survival.
  • PUMA's role in regulating autophagy offers potential therapeutic targets for cancer and degenerative diseases.

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