Bioinformatics Analysis and Verification of Aging-Related Genes of Bone Marrow Mesenchymal Stem Cells in Patients with Acute Myeloid Leukemia.
10.19746/j.cnki.issn.1009-2137.2019.02.001
- Author:
Shi-Qi LIU
1
;
Jing-Ying CHENG
1
;
Ya-Jing JIANG
1
;
Ying LI
1
;
Qing-Hua LI
1
;
Tian-Xiang PANG
2
Author Information
1. State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin 300020, China.
2. State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin 300020, China,E-mail: pang@ihcams.ac.cn.
- Publication Type:Journal Article
- MeSH:
Bone Marrow Cells;
Cell Proliferation;
Cells, Cultured;
Computational Biology;
Humans;
Leukemia, Myeloid, Acute;
Mesenchymal Stem Cells
- From:
Journal of Experimental Hematology
2019;27(2):311-317
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To screen and verify the differentially expressed genes related with aging of bone marrow mesenchymal stem cells (BM-MSCs) in acute myeloid leukemia (AML) patients by bioinformatics, so as to provide new molecular markers for the research and clinical treatment of AML.
METHODS:The gene expression profiling chip related with BM-MSCs in AML patients in our hospital and the gene chip GSE84881 selected from NCBI database GEO were used for data analysis and exploration. The DAVID analysis software was used to perform gene ontology (GO) enrichment analysis and KEGG pathway enrichment analysis. Furthermore, the differentially expressed genes related with aging of BM-MSCs in AML patients were identified. Bone marrow samples were collected and MSCs were amplified in vitro, and RT-PCR was used to verify the differentially expressed genes, which should be further identified with senescence-associated β-galactosidase staining and MTT cell proliferation assays.
RESULTS:A total of 247 differentially expressed genes were screened out by bioinformatics methods, including genes of 132 up-regulated expression and 115 down-regulated expression. Six differentially expressed genes related with aging of BM-MSCs in AML patients were screened out, including the genes of up-regulated expression, COL3A1 (P<0.05), CRYAB (P<0.01), DCN (P<0.05), and the genes of down-regulated expression, including CCL2 (P<0.05), CTSC (P<0.01) and IL6 (P<0.05). These 6 differentially expressed genes were consistent with data from chip assays, and which was significantly correlated with aging of BM-MSCs in AML patients. Meanwhile, the positive rate of senescence-associated β-galactosidase staining in BM-MSCs of AML patients was significantly different from that of healthy donors (P<0.01). MTT cell proliferation assay showed that BM-MSCs in AML patients had proliferative ability lower than the healthy donors' BM-MSCs.
CONCLUSION:The data here suggest novel clues for the clinical research and treatment of BM-MSCs aging in AML patients.
