Asymmetric Expression of Wnt/B-catenin Pathway in AIS: Primary or Secondary to the Curve?

Abstract

Study Design.A prospective case-control study.Objectives.To investigate whether the asymmetric changes are primary or secondary to spinal deformity.Summary of Background Data.Previous study reported significantly decreased expression of Wnt/B-catenin pathway in adolescent idiopathic scoliosis (AIS) patients. To date, there is a lack of study investigating the relationship between differentially expressed Wnt/B-catenin pathway and the onset of the curve.Methods.Paraspinal muscles were collected from 40 female AIS patients and 20 age-matched congenital scoliosis (CS) patients. For CS patients, the samples were collected from the concave side and the convex side at the apical region. For AIS patients, the samples were collected from the proximal bilateral sides of the spine in addition to the apical region. qPCR and western blot were used to determine the expression of LBX1, B-catenin, and PAX3, all of which are regulated by the Wnt/B-catenin pathway. The relative mRNA expression level between the concave and the convex side was performed with the Student t test. Pearson correlation analysis was used to determine the relationship between gene expression and the curve magnitude.Results.AIS patients were found to have remarkably lower mRNA and protein expression of B-catenin, LBX1, and PAX3 in the concave side than in the convex side at the apical region. By contrast, at the proximal region, the mRNA expression of these three genes was comparable. Moreover, no significant difference regarding mRNA expression was found between the concave side and the convex side of CS patients. There was no remarkable correlation between the mRNA expression of the three genes and Cobb angle.Conclusion.There exists remar kably asymmetric expression of Wnt/B-catenin pathway at the apical region of AIS, which however was comparable at the apical region of CS patients. Further investigation of Wnt/B-catenin signaling pathway may help reveal the etiology of AIS in future study.Level of Evidence: 4.