The effects of p-benzoquinone and hydroquinone on the RUNX2 gene expression and osteoblastic differentiation of human marrow derived mesenchymal stem cells

Authors
Fatemeh Zolghadr 1
Majid Sadeghizadeh 2
Majid Sadeghizadeh 2
Naser Amirizadeh 3
Mehrdad Behmanesh 4
Mehrdad Behmanesh 4
Saman Hosseinkhani 5
Maryam Amani 6
1 Ph.D. Student, Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University
2 Professor, Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University
3 Associated Professor, Research Center of Iranian Blood Transfusion Organization
4 Associated Professor, Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University
5 Associated Professor, Department of Biochemistry, Faculty of Biological Sciences, Tarbiat Modares University
6 Research Center of Iranian Blood Transfusion Organization
Abstract
Objective: Evaluating the effects of p-benzoquinone and hydroquinone on the RUNX2 expression and osteoblastic differentiation of human marrow derived mesenchymal stem cells (MSCs).
Materials and Methods: Bone marrow MSCs obtained by cultivating marrow mononuclear cells, were exposed to 10μM of either p-benzoquinone or hydroquinone. Following chemical treatment, RUNX2 gene expression was assessed by Real-time RT PCR 1, 6, 24 and 48 hours later and osteogenic differentiation was analyzed using alizarin red and alkaline phosphatase staining methods on days 7 and 14 after ostegenic induction.
Results: RUNX2 expression was significantly elevated (up to approximately 8 times) due to chemical exposure but the applied chemicals exert no considerable effect on MSCs osteogenic differentiation.
Conclusion: According to the literature, despite the necessity of RUNX2 overexpression on the induction of osteogenic differentiation, but it is not sufficient for osteogenesis to occure so increase in RUNX2 expression observed in our study is not the indicator of the induced osteogenic differentiation. Instead, this elevated expression could be the sign of increased activity of the canonical Wnt signaling pathway thereby its involvement in the development of AML due to exposure to benzene and its metabolites. Moreover, this augmented expression of RUNX2 in MSCs can indicate the
RUNX2 overexpression in myeloid progenitors as an expected similar effect of exposure to benzene and its metabolites to contribute in myeloid malignancies developed due to benzene exposure.

Keywords

Pathobiology Reserach
Volume 14, Issue 2
Spring 2011
Pages 25-35