Title of article :
Expression of hsa-MIR-204, RUNX2, PPARγ, and BCL2 in Bone Marrow Derived Mesenchymal Stem Cells from Multiple Myeloma Patients and Normal Individuals
Author/Authors :
Mansurabadi ، Raziyeh - Tarbiat Modares University , Abroun ، Saeid - Tarbiat Modares University , Hajifathali ، Abass - Shahid Beheshti University of Medical Sciences , Asri ، Amir - Tarbiat Modares University , Atashi ، Amir - Tarbiat Modares University , Haghighi ، Mansoureh - Isfahan University of Medical Sciences
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.
Keywords :
Multiple Myeloma , Mesenchymal Stem Cells , hsa , MIR , 204 , RUNX2
Journal title :
Cell Journal(Yakhteh)
Journal title :
Cell Journal(Yakhteh)