4.5 Article

Transplantation of human villous trophoblasts preserves cardiac function in mice with acute myocardial infarction

Journal

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
Volume 21, Issue 10, Pages 2432-2440

Publisher

WILEY
DOI: 10.1111/jcmm.13165

Keywords

Human villous trophoblasts; myocardial infarction; cell therapy; paracrine effects

Funding

  1. National Natural Science Foundation of China [81370216, 81671485, 81570457, 81301844, 31500636]
  2. Natural Science Foundation of Jiangsu Province [BK20150319]
  3. Priority Academic Program Development of Jiangsu Higher Education Institutes

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Over the past decade, cell therapies have provided promising strategies for the treatment of ischaemic cardiomyopathy. Particularly, the beneficial effects of stem cells, including bone marrow stem cells (BMSCs), endothelial progenitor cells (EPCs), mesenchymal stem cells (MSCs), embryonic stem cells (ESCs), and induced pluripotent stem cells (iPSCs), have been demonstrated by substantial preclinical and clinical studies. Nevertheless stem cell therapy is not always safe and effective. Hence, there is an urgent need for alternative sources of cells to promote cardiac regeneration. Human villous trophoblasts (HVTs) play key roles in embryonic implantation and placentation. In this study, we show that HVTs can promote tube formation of human umbilical vein endothelial cells (HUVECs) on Matrigel and enhance the resistance of neonatal rat cardiomyocytes (NRCMs) to oxidative stress in vitro. Delivery of HVTs to ischaemic area of heart preserved cardiac function and reduced fibrosis in a mouse model of acute myocardial infarction (AMI). Histological analysis revealed that transplantation of HVTs promoted angiogenesis in AMI mouse hearts. In addition, our data indicate that HVTs exert their therapeutic benefit through paracrine mechanisms. Meanwhile, injection of HVTs to mouse hearts did not elicit severe immune response. Taken together, our study demonstrates HVT may be used as a source for cell therapy or a tool to study cell-derived soluble factors for AMI treatment.

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