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HIV‐1 p55‐gag protein induces senescence of human bone marrow mesenchymal stem cells and reduces their capacity to support expansion of hematopoietic stem cells in vitro
Author(s) -
Yuan Yahong,
Zhao Shanshan,
Wang Xiaoli,
Teng Zhiping,
Li Dongsheng,
Zeng Yi
Publication year - 2017
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10791
Subject(s) - haematopoiesis , cd34 , bone marrow , senescence , mesenchymal stem cell , progenitor cell , stem cell , biology , microbiology and biotechnology , cord blood , immunology
Patients with human immunodeficiency virus‐1 (HIV‐1) infection often present with hematopoietic failure. As the important hematopoietic support cells in the bone marrow (BM), the BM mesenchymal stem cells (BMSCs) can be impacted by HIV proteins that are released by infected cells within BM. In this study, we tested whether HIV protein p55‐gag could induce senescence of BMSCs and reduce their capacity to support expansion of hematopoietic stem cells in vitro. BMSCs were chronically treated with p55‐gag (BMSC gag ) for up to 20 days, and their proliferative activity and senescence makers were compared to nontreated cells (BMSC con ). Then, we analyzed the hematopoietic support function of BMSC con and BMSC gag by determining cellular proliferation, colony‐forming ability, and primitive hematopoietic populations of hematopoietic progenitors grown on the BMSCs. In addition, we compared the gene expression patterns for supporting hematopoiesis of BMSC con and BMSC gag. The results show that when compared to BMSC con , BMSC gag reduced their proliferative activity and underwent senescence. The ability of BMSC gag to support the expansion of committed hematopoietic progenitors from umbilical cord blood‐derived CD34 + cells may be impaired, while the expression of genes associated with maintaining and enhancing hematopoiesis appeared to be decreased in treated BMSCs compared to control BMSCs. In conclusion, senescence induced by p55‐gag resulted in decreased hematopoietic support function of BMSCs through reducing a series of hematopoietic cytokine expression.