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Age-Related Impaired Efficacy of Bone Marrow Cell Therapy for Myocardial Infarction Reflects a Decrease in B

Songtao An1, Xiaoyin Wang2, Melissa A Ruck3

  • 1Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA 94143, USA; Division of Cardiology, Henan Provincial People's Hospital, Zhengzhou University, Zhengzhou, Henan 450003, China.

Molecular Therapy : the Journal of the American Society of Gene Therapy
|June 20, 2018
PubMed
Summary

Bone marrow cells (BMCs) from older or heart attack donors are less effective for treating myocardial infarction (MI). B lymphocytes within BMCs are crucial for effective cardiac repair after MI.

Keywords:
B lymphocyteadvanced ageagedbone marrowcell therapyejection fractioninfarct sizemyocardial infarctionparacrine

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Area of Science:

  • Cardiology
  • Immunology
  • Regenerative Medicine

Background:

  • Bone marrow cell (BMC) therapy shows promise for treating myocardial infarction (MI) in rodents, but clinical results are less effective.
  • Rodent studies often use young, healthy donors, unlike older patients undergoing autologous cell therapy post-MI.
  • Previous work indicated impaired therapeutic function of BMCs from aged or post-MI donors, with reduced B lymphocytes.

Purpose of the Study:

  • To investigate the role of B lymphocytes in the reduced therapeutic efficacy of BMCs from aged and post-MI donors.
  • To determine if B cell alterations in bone marrow contribute to the diminished therapeutic potential of BMCs.

Main Methods:

  • Administered BMCs from progressively aged donor mice to assess cardiac function and infarct size.
  • Utilized flow cytometry to analyze B cell populations in aged donor bone marrow.
  • Depleted B cells from young, healthy donor BMCs to evaluate their therapeutic efficacy.
  • Compared the effects of implanting intact or lysed B cells versus T cells.

Main Results:

  • Increasing donor age correlated with poorer cardiac function and larger infarct size post-MI.
  • Aged donor bone marrow exhibited significantly fewer B cells.
  • Depletion of B cells from BMCs reduced their therapeutic benefit.
  • Intact or lysed B cells significantly improved cardiac function, while T cells offered minimal benefit.

Conclusions:

  • B cells play a critical paracrine role in the therapeutic efficacy of BMCs for myocardial infarction.
  • Reduced B cell levels in bone marrow due to aging or MI may explain the discrepancy between preclinical rodent findings and clinical outcomes.
  • Targeting or augmenting B cell populations could enhance BMC therapy for MI.