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Expression of Hsa-Mir-204, Runx2, Pparγ, and Bcl2 in Bone Marrow Derived Mesenchymal Stem Cells From Publisher



Mansurabadi R1 ; Abroun S1 ; Hajifathali A2 ; Asri A1 ; Atashi A1 ; Haghighi M3
Authors
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Authors Affiliations
  1. 1. Department of Hematology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
  2. 2. Bone Marrow Transplantation Center, Taleghani Hospital, Shahid Beheshti University of Medical Sciences, P.O.Box: 14115-331, Tehran, Iran
  3. 3. Department of Clinical Biochemistry, Faculty of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Iran

Source: Cell Journal Published:2017


Abstract

Objective: Multiple Myeloma (MM) is a heterogeneous cytogenetic disorder in which clonal plasma cells proliferate in the bone marrow (BM) and cause bone destruction. The BM microenvironment plays a crucial role in pathogenesis of this disease, and mesenchymal stem cells (MSCs) are one of the key players. Herein, we propose to investigate the expressions of hsa-MIR-204, runt-related transcription factor 2 (RUNX2), peroxisome proliferator-Activated receptor gamma (PPARγ), and B-cell lymphoma 2 (BCL2) as factors involved in osteogenesis, adipogenesis, and MSC survival in BM-MSCs from MM patients and normal individuals. Materials and Methods: In this experimental study, we isolated MSCs from BM aspirates of MM patients and healthy donors. Total RNA were extracted before and after co-culture with L363 myeloma cells. Gene expressions of RUNX2, PPARγ, BCL2, and hsa-MIR-204 were assessed by quantitive real time polymerase chain reaction (qRT-PCR). Results: Higher levels of RUNX2, PPARγ, and hsa-MIR-204 expressions existed in MM-MSCs compared to normally derived (ND)-MSCs. BCL2 expression decreased in MM-MSCs. We observed different results in the co-culture model. Conclusion: In general, the MM-MSCs gene expression profile differed compared to ND-MSCs. Upregulation of RUNX2, PPARγ, and hsa-MIR-204 in MM-MSCs compared to ND-MSCs would result in formation of bone defects. Downregulation of BCL2 would lead to MM-MSC cell death.
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