Changes in Bone Marrow Stromal Progenitor Cells in Patients with Hematoblastosis at the Onset of the Disease
| Autor: | N A, Petinati, I N, Shipounova, E A, Fastova, A U, Magomedova, S K, Kravchenko, E Yu, Chelysheva, O A, Shukhov, A G, Turkina, N V, Sats, N I, Drize, E N, Parovichnikova, V G, Savchenko |
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| Rok vydání: | 2021 |
| Předmět: |
Adult
Male Time Factors Stem Cells Bone Marrow Cells Cell Count Cell Differentiation Mesenchymal Stem Cells Middle Aged Precursor Cell Lymphoblastic Leukemia-Lymphoma Hematopoiesis Cohort Studies Leukemia Myeloid Acute Young Adult Bone Marrow Case-Control Studies Hematologic Neoplasms Leukemia Myelogenous Chronic BCR-ABL Positive Humans Female Lymphoma Large B-Cell Diffuse |
| Zdroj: | Bulletin of experimental biology and medicine. 171(4) |
| ISSN: | 1573-8221 |
| Popis: | Multipotent mesenchymal stromal cells (MSC) are the key regulators of hematopoiesis. We studied changes in MSC characteristics in patients with myeloid leukemia and patients with lymphoproliferative diseases. MSC were obtained from the bone marrow of patients at the time of diagnostic puncture using a standard technique. Their proliferative potential and expression of genes associated with differentiation and regulation of hematopoiesis were studied. The total cell production of MSC in patients with leukemia at the onset of the disease did not differ from that in the group of healthy donors. The relative expression of the IL6, TGFb1 and TGFb2, PPARG genes was similar in all patients. The relative expression of the JAG1, LIF, IGF1, CSF1, IL1b, and IL1bR1 genes in MSC of patients with leukemia was enhanced and the relative expression of SDF1 was unchanged in comparison with MSC from donors. MSC from patients with leukemia were characterized by enhanced relative expression of PDGFRA and PDGFRB, and reduced expression of SOX9. Changes functions of the stromal microenvironment in patients with hemoblastoses attested to the role of stromal cells in the maintenance and spread of tumor cells. |
| Databáze: | OpenAIRE |
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