Volume 78, Issue 2 (May 2020)                   Tehran Univ Med J 2020, 78(2): 93-98 | Back to browse issues page

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Abtahi S H, Mohammadi M H, Allahbakhshian Farsani M. Alterations of adiponectin gene expression in bone marrow of acute myeloid leukemia. Tehran Univ Med J 2020; 78 (2) :93-98
URL: http://tumj.tums.ac.ir/article-1-10380-en.html
1- Department of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
2- HSCT Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
3- HSCT Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. , allahbakhshian@sbmu.ac.ir
Abstract:   (1943 Views)
Background: Acute myeloid leukemia (AML) is characterized by the proliferation of myeloid precursors and abnormal differentiation of hematopoietic stem cells, which results in the accumulation of immature cells in the bone marrow (BM). The accumulation of these cells in the bone marrow causes molecular and cellular changes in the microenvironment of the bone marrow. The adiponectin hormone originates from adipose tissue of the bone marrow, which in addition to effective functions in cellular metabolism, suppresses cancer through various mechanisms, including inhibition of metastasis, angiogenesis, and proliferation. In the bone marrow sample, patients with acute myeloid leukemia are associated with different subtypes of the disease.
Methods: In this basic-fundamental research, a total of 40 BM samples from de novo AML patients and 15 BM samples from healthy volunteers as the healthy group referred to the Stem Cell Transplantation Laboratory and Cell Therapy of Taleghani Hospital and with assisting the Research Center, Shahid Beheshti University of Medical Sciences, Tehran, from March 2015 to February 2017, were entered into the study. Then used the Real-time polymerase chain reaction (RT-PCR) method for diagnosis level of adiponectin gene expression in BM samples patients and the healthy group.
Results: The results of the present study showed that the level of adiponectin gene expression in the BM sample of patients was significantly decreased in comparison with the healthy group (P=0.002). While, there was no significant difference (P<0.05) in adiponectin gene expression in AML subtypes myeloblastic, promyelocytic, and myelomonocytic/monocytic.
Conclusion: The results of this study indicate that there was a decrease in adiponectin gene expression in the bone marrow of acute myeloid leukemia patients compared to healthy controls. This decrease in adiponectin expression may be due to myeloid hyperplasia and a decrease in bone marrow adipocytes. In fact, The nutritional, metabolic, and mechanical stresses associated with myeloid cells accumulation cause alterations in bone marrow microenvironment structure and destruction of bone marrow adipose tissue. Therefore, reduced adiponectin gene expression in AML patients is one of the key indicators of bone ‎marrow microenvironmental changes in AML patients.‎‎
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