MAPK/ERK Signaling Pathway Analysis in Primary Osteoblasts from Patients with Non-Syndromic Sagittal Craniosynostosis
Abstract
Objective The MAPK/ERK signaling pathway has been implicated in several craniosynostosis syndromes and represents a plausible target for therapeutic management of craniosynostosis. The causes of sagittal nonsyndromic craniosynostosis (sNSC) have not been well understood and the role that MAPK/ERK signaling cascade plays in this condition warrants an investigation. We hypothesized that MAPK-signaling is misregulated in calvarial osteoblasts derived from patients with sNSC. Methods In order to analyze if the MAPK/ERK pathway is perturbed in sNSC, we established primary calvarial osteoblast cell lines from patients undergoing surgery for correction of this congenital anomaly. Appropriate negative and positive control cell lines were used for comparison, and we examined the levels of phosphorylated ERK by immunoblotting. Results Primary osteoblasts from patients with sNSC showed no difference in ERK1/2 phosphorylation with or without FGF2 stimulation as compared with control osteoblasts. Conclusion Under the described test conditions, we did not observe convincing evidence that MAPK/ERK signaling contributes to the development of sNSC.
Read the paper
Related studies
- Irisin Enhances Osteoblast DifferentiationIn Vitro
- Glucocorticoids suppress Wnt16 expression in osteoblasts in vitro and in vivo
- Interaction between Schwann Cells and Osteoblasts In Vitro
- Administration of cinnamaldehyde promotes osteogenesis in ovariectomized rats and differentiation of osteoblast in vitro
- The Effect of the Major Components of Fructus Cnidii on Osteoblasts In Vitro
- Estrogen depletion alters osteogenic differentiation and matrix production by osteoblasts in vitro
Go deeper in Evidence Hub
Evidence Hub adds a study data sheet (design, sample size, evidence level, key numbers), an AI summary and a chat grounded in the paper's text.