Zhen Yu1, Dong Li1, Xiu-li Ju2. 1. Department of Pediatrics, Qilu Hospital, Shandong University, 107 Wen Hua Xi Road, Jinan, Shandong, 250012, People's Republic of China. 2. Department of Pediatrics, Qilu Hospital, Shandong University, 107 Wen Hua Xi Road, Jinan, Shandong, 250012, People's Republic of China. jxiuli2015@163.com.
Abstract
BACKGROUND: The abnormality of bone marrow-derived mesenchymal stem cells (BM-MSCs) has been reported to contribute to the pathogenesis of acute myeloid leukemia (AML). T cell immunodeficiencies play important roles in the progression of leukemia. This study investigated the effect of CD4+ T cells from AML patients on the proliferation of BM-MSCs. METHODS: The growth rate of BM-MSCs from AML patients and healthy donor was compared. CD4+ T cells were separated and identified from AML patients. Through co-culturing CD4+ T cells from AML patients and BM-MSCs from healthy, we detected the proliferation of BM-MSCs from healthy by MTT assay. qRT-PCR was performed to examine the expression of miR-10a. Luciferase reporter assay was used to analyze the regulation of miR-10a on the expression of BCL6. RESULTS: Here, we observed that BM-MSC from AML patients grew slower than that from healthy. CD4+ T cells from AML patients inhibited the proliferation of BM-MSCs through secreting miR-10a. In addition, miR-10a was found to target BCL6 and regulated its expression in transcription and translation levels. Correlation analysis revealed that the level of miR-10a in serum of AML patients was negatively correlated with BCL6 in BM-MSC. CONCLUSION: This study provides evidence that CD4+ T cells from AML patients suppress the proliferation of BM-MSCs via secreting miR-10a.
BACKGROUND: The abnormality of bone marrow-derived mesenchymal stem cells (BM-MSCs) has been reported to contribute to the pathogenesis of acute myeloid leukemia (AML). T cell immunodeficiencies play important roles in the progression of leukemia. This study investigated the effect of CD4+ T cells from AMLpatients on the proliferation of BM-MSCs. METHODS: The growth rate of BM-MSCs from AMLpatients and healthy donor was compared. CD4+ T cells were separated and identified from AMLpatients. Through co-culturing CD4+ T cells from AMLpatients and BM-MSCs from healthy, we detected the proliferation of BM-MSCs from healthy by MTT assay. qRT-PCR was performed to examine the expression of miR-10a. Luciferase reporter assay was used to analyze the regulation of miR-10a on the expression of BCL6. RESULTS: Here, we observed that BM-MSC from AMLpatients grew slower than that from healthy. CD4+ T cells from AMLpatients inhibited the proliferation of BM-MSCs through secreting miR-10a. In addition, miR-10a was found to target BCL6 and regulated its expression in transcription and translation levels. Correlation analysis revealed that the level of miR-10a in serum of AMLpatients was negatively correlated with BCL6 in BM-MSC. CONCLUSION: This study provides evidence that CD4+ T cells from AMLpatients suppress the proliferation of BM-MSCs via secreting miR-10a.
Entities:
Keywords:
Acute myeloid leukemia; BCL6; Bone marrow mesenchymal stromal cells; Proliferation; T cells; miR-10a
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