Alpha-Smooth Muscle Actin (a-SMA) Gene, a Possible Derive of Myofibroblasts in Bone Marrow Fibrosis

Document Type : Original Article

Authors

1 Clinical Pathology department, Benha Faculty of Medicine, Benha University, Egypt

2 Department of Clinical and Chemical Pathology, Cairo Faculty of medicine, Cairo University

3 Department of Clinical and Chemical Pathology, Benha Faculty Of Medicine, Benha university

4 Department of Clinical and Chemical Pathology, Benha Faculty Of Medicine, Benha university,

Abstract

Background: Alpha-smooth muscle actin (α-SMA) is used as a marker for a subset of activated fibrogenic cells, myofibroblasts, which are regarded as important effector cells of tissue fibrogenesis. Purpose: We addressed whether ASMA gene (actin alpha 2 gene or ACTA2) expression is up regulated in cases with BM fibrosis compared to those with no bone marrow (BM) fibrosis in order to evaluate its role in the pathogenesis of BM fibrosis. Subjects and methods: ASMA expression was detected by quantitative RT-PCR in formalin fixed paraffin embedded (FFPE) bone marrow trephine biopsy samples of cases with neoplastic bone marrow diseases as well as reactive bone marrow disorders cases. Both groups included cases with and without bone marrow fibrosis. Results: Results indicated that there was no statistically significant difference in ASMA (ACTA2) gene expression between neoplastic fibrotic and non-fibrotic cases as well as between reactive fibrotic and non-fibrotic cases. Also the level of α-SMA expression does not correlate positively with the grade of bone marrow fibrosis. Conclusion: We conclude that α-SMA is not a functional marker of fibrogenic cells in bone marrow fibrosis.  Exploration of other related genetic pathway is recommended.

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