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TNF-alpha modulates the migratory response of mesenchymal stem cells to TRAIL

Federica Corallini1, Paola Secchiero, Antonio Paolo Beltrami

  • 1Department of Morphology and Embryology, University of Ferrara, Ferrara, Italy.

Cellular and Molecular Life Sciences : CMLS
|January 12, 2010
PubMed

Insights

Lower circulating mesenchymal stem cells (MSC) and higher tumor necrosis factor-alpha (TNF-alpha) and osteoprotegerin (OPG) levels were observed in acute myocardial infarction (AMI) patients who developed heart failure (HF). TNF-alpha

Area of Science:

  • Cardiovascular Biology
  • Stem Cell Biology
  • Immunology

Background:

  • Mesenchymal stem cells (MSCs) play a crucial role in cardiac repair after myocardial infarction (MI).
  • Reduced MSC levels post-MI are associated with adverse outcomes like heart failure (HF).
  • Circulating factors influencing MSC behavior after MI require further investigation.

Purpose of the Study:

  • To investigate the relationship between circulating MSCs, TNF-alpha, OPG, and the development of HF after acute myocardial infarction (AMI).
  • To elucidate the in vitro effects of TNF-alpha and OPG on MSC migration in the context of AMI.

Main Methods:

  • Analysis of circulating MSC counts, TNF-alpha, and OPG levels in AMI patients with and without subsequent HF.
  • In vitro experiments assessing MSC migration in response to TNF-related apoptosis-inducing ligand (TRAIL) under varying conditions of TNF-alpha and OPG exposure.
  • Assessment of OPG release from endothelial cells upon TNF-alpha stimulation.

Main Results:

  • AMI patients who developed HF had significantly lower circulating MSC counts compared to those who did not develop HF.
  • Elevated circulating levels of TNF-alpha and OPG were found in AMI patients who subsequently developed HF.
  • In vitro, TNF-alpha enhanced MSC migration induced by TRAIL but also increased OPG release from endothelial cells.
  • OPG dose-dependently inhibited the pro-migratory effect of TRAIL on MSCs.

Conclusions:

  • TNF-alpha has dual, opposing effects on MSC migration post-AMI: it can enhance migration directly but also inhibit it indirectly via OPG induction.
  • Elevated OPG levels, induced by TNF-alpha, may counteract the beneficial pro-migratory effects of TRAIL, leading to suboptimal MSC recruitment.
  • This complex interplay may contribute to the reduced MSC recruitment observed in AMI patients who develop HF.

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