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Updated: Jul 1, 2025
A Modified Cuff Technique for Mouse Cervical Heterotopic Heart Transplantation Model
Published on: February 7, 2022
Human amniotic mesenchymal stem cells inhibit immune rejection injury from allogeneic mouse heart transplantation: A
Haoyuan Wang1, Xin Mao2, Yue Zhong3
1Department of Cardiothoracic Surgery, The Second Affiliated Hospital of Zunyi Medical University, Zunyi 563006, Guizhou, China; The Second Clinical Institute, Zunyi Medical University, Zunyi 563006, Guizhou, China; Key Laboratory of Cell Engineering of Guizhou Province, Affiliated Hospital of Zunyi Medical University, Zunyi 563003, Guizhou, China.
Background:
Mesenchymal stem cell therapy is a new treatment for immune rejection in heart transplantation. The aim of this paper is to investigate the effect of human amniotic mesenchymal stem cells (hAMSCs) on alleviating immune rejection of allogeneic heart transplantation in mice and its possible underlying mechanism.
Methods:
We injected hAMSCs into cervical ectopic heart transplantation model mice via tail vein to observe the survival time, the pathological changes of donor myocardium, and the fluorescent distribution of hAMSCs after the transplantation. MicroRNAs (miRs) with significantly differential expression were obtained by RNA sequencing and bioinformatic analysis, and a dual luciferase reporter gene assay together with real-time quantitative PCR (qRT-PCR) was performed to verify the relationship between miRs and their targeting genes.
Results:
The intervention of hAMSCs prolonged the graft survival time and alleviated the pathological damage of the donor heart. The injected hAMSCs were distributed mainly in the liver, spleen, and kidney, only a very small portion in the donor and recipient hearts. In the allogeneic transplantation models, the expression of miR-34b-5p significantly increased after hAMSC treatment. MiR-34b-5p showed a knockdown effect on gene Fc gamma receptor 2B (FCGR2B).
Conclusions:
hAMSCs can reduce the immune rejection injury after allogeneic heart transplantation. This effect may be associated with the upregulation of miR-34b-5p expression to knock down its targeting gene FCGR2B.
