بررسي الگوي بروز (ERK1/2)Extracellular regulated kinases1/2 و فرم فعال آنها P-ERK1/2در روند استخوان سازي درزهاي فوقاني جمجمه اي در مراحل مختلف جنيني و نوزادي موش سوري

Background: The normal growth and morphogenesis of calvarial sutures id dependent upon a balance between proliferations of osteogenic precursors within the sutural mesenchyme and differentiation to osteoblast at the osteogenic front. Reports have shown that, in a variety of cell types, processes such as proliferation, differentiation and apoptosis require a Extracellular regulated kinases1/2 (ERK1/2). The present study focused on Evaluation of expression Pattern of Extracellular regulated kinases1/2(ERK1/2) and its active form in osteogenesis of superior sutures of calvarial during different stages of embryonic and neonatal of mice. Material and method: Formalin –fixed paraffin –embedded upper part of skull of E12,E15,E18,F1 and F7days of mice samples were obtained. Samples were immune-stained with monoclonal antibody against ERK1/2 and its active form. ABC staining method was applied. ERK1/2 and its active form expression pattern was scaled by HSCORE method. Result: Immunoreactivity was assessed in coronal and lambdoid sutures ERK1/2 in coronal and lambdoid sutures in E12and E15 day is up-regulated but in E18,F1and F7day showed down regulation of ERK1/2. Activated form of ERK1/2 express only in E12 and showed down regulation in coronal and lambdoid sutures. Active form of ERK1/2 express only in the coronal and lambdoid E12 day. This study has shown that ossification ERK1/2 expression is stage-dependent during different stages of embryonic and neonatal of mice. Conclusion: Enhanced expression of ERK1/2 during embryo stages in ossification of coronal and lambdoid sutures may be responsible for proliferation and differentiation of sutural mesenchyme to osteoblast cell. Down regulation of ERK1/2 during neonatal mice may be facilitate apoptosis and calcification of osteoblast cells. Down expression of active form of ERK1/2 may be responsible for primitive proliferation of sutural mesenchyme cells. It appears that ERK1/2 as key kinas plays a critical role in ossification and it is time-dependent cellular processes.