Integrated bioinformatic analysis of the shared mechanisms in endochondral ossification Between ossification of the ligamentum flavum (OLF) and ankylosing spondylitis (AS)

Author:

Yishan Liu1,Li Yang2,Liu Yixuan3,Gao Zhongya2,Zhang Jianjun4,Qiu Youcai2,Wang Can4,Lu Xuhua2,Yang Jiandong5

Affiliation:

1. Yangzhou University

2. Changzheng Hospital, Naval Medical University

3. Dalian Medical University

4. North Sichuan Medical College

5. Subei People's Hospital, Yangzhou University Affiliated Hospital

Abstract

Abstract Ossification of the ligamentum flavum (OLF) and ankylosing spondylitis (AS) are complex maladies characterized by the progressive process of endochondral ossification. This study aims to elucidate shared biomarkers related to ectopic ossification and the potential molecular regulatory mechanism. Microarray and RNA-seq datasets, obtained from the Gene Expression Omnibus (GEO) database, were utilized to discern differentially expressed genes (DEGs) in the OLF and AS datasets. Weighted gene co-expression network analysis (WGCNA) was conducted to identify co-expression modules associated with OLF and AS. Furthermore, the central hub genes were thoughtfully selected through the application of the least absolute shrinkage and selection operator (LASSO) regression, and three pivotal hub genes (MAB21L2, MEGF10, ISLR) were screened. Among these, ROC analysis demonstrated the exceptional diagnostic potential of MAB21L2. Finally, an examination of immune infiltration patterns unveiled activated CD8 T cells as shared differential immune infiltrating cells, significantly linked to MAB21L2 in both pathogeneses. This study represents the first instance of identifying MAB21L2 as a prospective diagnostic marker for patients contending with OLF complicated by AS. Results suggest a plausible association with the extracellular matrix (ECM)-receptor interaction in both pathogeneses, thereby offering valuable insights into the pathogenesis of spinal ligament ossification and unveiling promising therapeutic targets.

Publisher

Research Square Platform LLC

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