Effect of Differentially Expressed LBX1 in Adolescent Idiopathic Scoliosis Paraspinal Muscle Phenotypes via Modulating Myoblasts
Refereed conference paper presented and published in conference proceedings


摘要Introduction: LBX1 is the most reported AIS predisposing gene, however, its biological function in AIS remains unclear. In this study, we hypothesized LBX1 is differentially expressed in the concave and convex sides of AIS apical paraspinal muscles and affect muscle phenotypes via modulating the myogenic differentiation activity of myoblast.
Materials and Methods: Paraspinal muscle biopsies were taken intraoperatively from concave and convex side of the apex of the major curve in AIS and age- and curve severity-matched congenital scoliosis (CS) patients undergoing surgery. qPCR analysis was examined to validate LBX1 and myogenic markers expression. Muscle fiber types distribution analysis was conducted as well. Human skeletal muscle myoblast cell (HSMM) was used in a gain- and loss-of-function cellular study to elucidate the effect of LBX1 on myogenic differentiation and myosin heavy chain isoforms expression.
Results: The results (24 AIS Vs 9 CS) showed significantly differential pattern of muscle fiber types distribution, expression of LBX1 and myogenic markers between the concave and convex sides of the apical paraspinal muscle in AIS which was not observed in CS. In vitro study showed that elevated expression of LBX1 inhibited myogenic differentiation and affected myosin heavy chain type I/II ratio.
Discussion and conclusion: This is the first study demonstrated that unlike in CS patients, LBX1 expresses differentially in concave and convex apical paraspinal muscles in AIS, and the modulating effect of LBX1 on myoblasts suggests its novel pathological role underlying the imbalanced paraspinal muscles in AIS.
著者Yujia Wang, Ka-lo Cheng, Tsz-ping Lam, Alec LH Hung, Jack CY Cheng, Wayne YW Lee
會議名稱Hong Kong Orthopaedic Association 39th Annual Congress 2019 (HKOA 2019)
會議地點Hong Kong
出版地Hong Kong

上次更新時間 2020-29-05 於 11:23