WISP2 downregulation inhibits the osteogenic differentiation of BMSCs in congenital scoliosis by regulating Wnt/β-catenin pathway.

Yang Zheng Panyang Shen Mengsha Tong Hangchao Li Conglin Ren Fengqing Wu Hanyu Li Huan Yang Bingbing Cai Weibin Du Xing Zhao Shasha Yao Renfu Quan

Biochim Biophys Acta Mol Basis Dis

Zhejiang Chinese Medical University, Hangzhou, China; Department of Orthopedics, Xiaoshan Traditional Chinese Medical Hospital, Hangzhou, China; Research Institute of Orthopedics, The Affiliated Jiangnan Hospital of Zhejiang Chinese Medical University, Hangzhou, China. Electronic address:

Published: October 2023

BMSCs play a crucial role in bone development and homeostasis, yet their effects on congenital scoliosis (CS) are not well understood.
The study compares BMSCs from CS patients (CS-BMSCs) to those from healthy donors (NC-BMSCs), revealing that CS-BMSCs exhibit reduced osteogenic differentiation abilities.
Findings suggest that WISP2 regulates osteogenic differentiation through the Wnt/β-catenin pathway, with its knockdown inhibiting and overexpression enhancing this process in CS-BMSCs, offering new insights into the causes of CS.

Objectives: Bone marrow mesenchymal stem cells (BMSCs) are instrumental in bone development, metabolism, and marrow microenvironment homeostasis. Despite this, the relevant effects and mechanisms of BMSCs on congenital scoliosis (CS) remain undefined. Herein, it becomes our focus to reveal the corresponding effects and mechanisms implicated.

Methods: BMSCs from CS patients (hereafter referred as CS-BMSCs) and healthy donors (NC-BMSCs) were observed and identified. Differentially expressed genes in BMSCs were analyzed utilizing scRNA-seq and RNA-seq profiles. The multi-differentiation potential of BMSCs following the transfection or infection was evaluated. The expression levels of factors related to osteogenic differentiation and Wnt/β-catenin pathway were further determined as appropriate.

Results: A decreased osteogenic differentiation ability was shown in CS-BMSCs. Both the proportion of LEPR BMSCs and the expression level of WNT1-inducible-signaling pathway protein 2 (WISP2) were decreased in CS-BMSCs. WISP2 knockdown suppressed the osteogenic differentiation of NC-BMSCs, while WISP2 overexpression facilitated the osteogenesis of CS-BMSCs via acting on the Wnt/β-catenin pathway.

Conclusions: Our study collectively indicates WISP2 knockdown blocks the osteogenic differentiation of BMSCs in CS by regulating Wnt/β-catenin signaling, thus providing new insights into the aetiology of CS.

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http://dx.doi.org/10.1016/j.bbadis.2023.166783	DOI Listing

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