TIPE2 Improves the immune tolerance of human amniotic mesenchymal stem cells

Abstract

Tumor necrosis factor-α induced protein 8 like 2 (TIPE2) is one of the newly discovered negative regulators for body’s immune balance. The present study aimed to investigate the effect of TIPE2 gene-modified human amniotic mesenchymal stem cells (hAD-MSCs) on immune tolerance. In this study, the TIPE2 over-expressed and the non-transfected hAD-MSCs were severally co-cultured with injured cardiomyocytes. Cell cycle and apoptosis were detected by flow cytometry. Cell viability was measured by MTT, and expressions of immune-related factors were detected by qRT-PCR and western blot. When compared with the empty vector-transfected hAD-MSCs, the TIPE2-overexpression hAD-MSCs co-cultured with injured cardiomyocytes show accelerated cell viability and declined apoptosis. After TIPE2 over-expression, the mRNA and protein levels of p38, extracellular signal-regulated kinases (ERK) and interferon-γ (INF-γ) notably decreased, whereas those of transforming growth factor-β (TGF-β) and interleukin-10 (IL-10) increased in a converse trend. This study suggested that TIPE2 may enhance the cellular immune tolerance in co-culture systems of hAD-MSCs and injured cardiomyocyte, providing a theoretical basis for the allogeneic heart transplantation.

KEYWORDS:

• TIPE2
• hAD-MSCs
• heart transplantation
• immune tolerance

Acknowledgements

This work was supported by the National Natural Science Foundation of China (# 81660074). FW and SP collected the data and wrote the manuscript. GY, YY, XM, GL and LY contributed to collecting data and reviewing the manuscript. YG conceived the study and contributed to reviewing/editing the manuscript. All authors have read and approved the final manuscript.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Ethical approval

The study complies with the Declaration of Helsinki and was approved by West China Hospital Ethics Committee.

Data availability statement

The data that support the findings of this study are openly available in https://share.weiyun.com/590ocgl

Additional information

Funding

This work was supported by the National Natural Science Foundation of China [#81660074].