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Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
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Adiponectinemia controls pro-angiogenic cell therapy.

Philippe Eren1, Stéphane Camus, Gianfranco Matrone

  • 1Institut National de la Santé et de la Recherche Médicale U.689, Cardiovascular Research Center Lariboisière, Hôpital Lariboisière, et Université Paris 7, F-75010 Paris, France.

Stem Cells (Dayton, Ohio)
|September 29, 2009
PubMed
Summary
This summary is machine-generated.

Adiponectin, a hormone, is crucial for cell therapy to promote blood vessel growth in ischemic tissues. High adiponectin levels in patients receiving cell therapy are essential for successful revascularization.

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Area of Science:

  • Cardiovascular Research
  • Regenerative Medicine
  • Endocrinology

Background:

  • Angiogenic cell therapy using endothelial progenitor cells (EPC) or bone marrow mononuclear cells (BM-MNC) aims to revascularize ischemic tissues.
  • Adiponectin, an adipocyte-secreted hormone, promotes physiological angiogenesis.
  • Patients with cardiovascular disease risk factors often have low adiponectin levels, potentially impacting cell therapy efficacy.

Purpose of the Study:

  • To investigate the role of adiponectin in the pro-angiogenic function of transplanted cells.
  • To determine if adiponectin levels in the cell donor or recipient influence the success of angiogenic cell therapy.

Main Methods:

  • In vitro studies using adipocyte-conditioned media and purified adiponectin to assess effects on BM-MNC and EPC.
  • In vivo experiments transplanting BM-MNC into ischemic hindlimbs of wild-type and adiponectin-deficient (apM1-/-) mice.

Main Results:

  • Adiponectin enhanced BM-MNC survival and proliferation and stimulated EPC differentiation in vitro.
  • While donor BM-MNC origin (wild-type vs. apM1-/-) did not affect angiogenesis in wild-type recipients, wild-type BM-MNC showed diminished effects in apM1-/- recipients.
  • Recipient adiponectinemia was essential for the pro-angiogenic benefits of cell therapy.

Conclusions:

  • Adiponectin significantly enhances the survival, proliferation, and differentiation of cells used in angiogenic therapy.
  • Recipient adiponectin levels are critical for the therapeutic success of progenitor cell transplantation in promoting angiogenesis.
  • The efficacy of cell therapy for revascularization may be limited to patients with sufficient adiponectin levels.