The Study of LPL Gene Expression during Differentiation of Human BM-MSC into Adipocytes

• Main Authors: Seied Rasoul Razavi babaheidari, Kamran Mousavi Hosseini, Amir Atashi, Arezou Oodi, Shadi Esmaeili
• Format: Article
• Language: English
• Published: Tehran University of Medical Sciences 2014-01-01
• Series: Basic & Clinical Cancer Research
• Subjects: Mesenchymal stem cell; Differentiation; Adipocyte; Lipoprotein lipase
• Online Access: https://bccr.tums.ac.ir/index.php/bccrj/article/view/132

Background: Many types of cancer cells require a supply of fatty acids (FA) for growth and survival, LPL, in the presence of triglyceride-rich lipoproteins, accelerates the growth of these cells. Recent evidence shows that LPL plays important roles in inflammation and obesity, implies that it is an appropriate general target for chemo preventive and chemotherapeutic agents. Thus, we reported LPL expression before and after BM-MSCs differentiation into adipocytes. Methods: In this study, we isolated mesenchymal stem cells from human bone marrow by Ficoll - gradient and then their surface markers by flow cytometry confirmed and osteoblastic and adipocytes differentiation by Dexamethasone protocol were done and confirmed by staining .Then qualitative expression of LPL gene by RT-PCR before and after of differentiation into adipocytes .Statistical analysis was performed by paired t test and by using Pfaffl and graph pad software. Results: After 14 days, analysis of morphology with invert microscopy indicated that BM-MSCs have ability of differentiation capacities into adipocytes. Investigations of expression of LPL showed BM-MSC that served as negative control have not expression of LPL while in BM-MSCs derived- adipocyte have found significant expression of LPL. Conclusions: BM-MSCs can differentiate into either adipocytes or osteoblastic cells that in decision between the two lineages, LPL has the important role through activation inhibiting osteoblastic in favor of adipogenic differentiation. LPL could be an effective agent on tumor suppressing with catalyzes the hydrolysis of plasma TG.  LPL gene deficiency, such as due to chromosome 8p22 loss, LPL gene polymorphism, and epigenetic changes increases cancer risk, especially in the prostate.