Wnt and Smad signaling pathways synergistically regulated the osteogenic differentiation of fibroblasts in ankylosing spondylitis

Zeng, Yong; Wang, Taiping; Liu, Yong; Luo, Ting; Li, Qing; Fang, Miao; He, Rui

doi:10.1016/j.tice.2022.101852

Cited by 2 publications

(2 citation statements)

References 33 publications

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“…Thus, identifying target molecules that prevent fibroblasts from diffusing into osteoblasts could serve as a theoretical foundation for the therapy of AS, which is extremely crucial for enhancing the prognosis of AS patients. Numerous studies have concentrated on the various signaling pathways engaged in the ectopic ossification of AS ( 37 ), but there have been relatively few investigations on peptideomics evaluation in relation to this process. This study further screened out 3 up‐regulated peptides from these differentially expressed peptides, according to activity fraction of peptide ranker, difference multiple, and P‐value.…”

Section: Discussionmentioning

confidence: 99%

Peptidomics analysis of plasma in patients with ankylosing spondylitis

Guo-ning

Xu²,

Jin³

2023

Front. Immunol.

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BackgroundThis study aimed to explore the differential expression of peptides associated with ankylosing spondylitis (AS) patients, enabling identification of potential functional peptides to provide the basis for the novel intervention targets for AS.Material and Methods3 AS patients and 3 healthy volunteers were enrolled in this study. The expression profiles for peptides present in the plasma of AS patients and the healthy individual were analyzed by liquid chromatography-tandem mass spectrometry (LC‐MS/MS). The physicochemical properties and biological functions of identified peptides were further analyzed by bioinformatics. The results of peptide identification were verified by cell viability analysis, using CCK8 and Edu staining assay, and the differential peptides relevant to the disease were screened.Results52 differential peptides were successfully identified using mass spectrometry. 44 peptides were up-regulated, while eight were down-regulated. FGA-peptide (sequences: DSGEGDFLAEGGGVRGPR), C4A-peptide (sequences: NGFKSHAL), and TUBB-peptide (sequences: ISEQFTAMFR) were screened out that could significantly promote the proliferation of fibroblasts in AS patients. Bioinformatics analysis showed these differentially expressed peptides might be associated with “MHC class I protein binding” and “pathogenic Escherichia coli infection” pathways, which might further affect the progression of AS.ConclusionThis pilot study shows 3 differentially expressed peptides may have the potential function for the occurrence and development of AS, may provide novel insights into the underlying molecular mechanisms of AS based on peptide omics.

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Section: Discussionmentioning

confidence: 99%

Peptidomics analysis of plasma in patients with ankylosing spondylitis

Guo-ning

Xu²,

Jin³

2023

Front. Immunol.

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“…Numerous studies have shown that fibroblasts are the starting point for AS ligament ossification. 32,33 Moreover, Joos et al confirmed IL-1β is significantly negatively correlated with TUBB, and participates in regulating various cytoskeleton components in human chondrocytes, and is related to the pathogenesis of osteoarthritis. 34 We have also mentioned that pro-inflammatory cytokines (such as TNF-α) can affect the expression of various kynurenine pathway enzymes, leading to metabolic changes and affecting inflammatory response and immunity.…”

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confidence: 99%

Identification of a Novel Gene Expression Signature Associated with Amino Acid Metabolism (AAM) in Ankylosing Spondylitis (AS)

Liu,

Peng

2024

IJGM

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Background: Studies have proven that amino acid metabolism (AAM) plays an important role in ankylosing spondylitis (AS). Therefore, this study identified key AAM-related genes (AAMRGs) for the diagnosis and prediction of AS. Methods: Firstly, the differentially expressed genes (DEGs) were identified between AS and normal groups in the GSE25101 and GSE73754 datasets downloaded from the Gene Expression Omnibus (GEO) database, and they were intersected to get common DEGs (Co-DEGs). Weighted Gene Co-expression Network Analysis (WGCNA) was used to identify AS and AAM score-related genes (AS-AAMSRGs). Then, AAM related DEGs (AAMR DEGs) were acquired by intersection of Co-DEGs and AS-AAMSRGs. Moreover, the least absolute shrinkage and selection operator (LASSO) was implemented on AAMR DEGs to identify diagnostic genes, and Gene Set Enrichment Analysis (GSEA) was used to explore the functional pathways of diagnostic genes. By screening differential immune cells, the correlation between differential immune cells and diagnostic genes was further analyzed. Finally, miRNA-mRNA networks were constructed and drug prediction analysis was performed. Results: By overlapping to obtain three AAMR DEGs (TP53INP1, TUBB and RBM47). The results of nomogram and decision curve analysis (DCA) suggested that three AAMR DEGs had diagnostic value for AS and significantly enriched to neutrophil activation, neutrophil degranulation. The proportion of eight kinds of immune cells in AS and normal groups was significantly different, such as activated dendritic cell, CD56 bright natural killer cell, effector memory CD4 T cell. In the miRNA-mRNA regulatory networks, three miRNAs (has-miR-429, has-miR-200c-3p, has-miR-200b-3p) could regulate TP53INP1 and TUBB. There was only one miRNA (has-miR-122-5p) could regulate RBM47. Finally, 51 target drugs (such as colchicine, vinblastine, vincristine) were associated with TUBB. Conclusion: TP53INP1, TUBB and RBM47 might play key roles in AS and could be used as potential biomarkers of AS.

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Wnt and Smad signaling pathways synergistically regulated the osteogenic differentiation of fibroblasts in ankylosing spondylitis

Cited by 2 publications

References 33 publications

Peptidomics analysis of plasma in patients with ankylosing spondylitis

Peptidomics analysis of plasma in patients with ankylosing spondylitis

Identification of a Novel Gene Expression Signature Associated with Amino Acid Metabolism (AAM) in Ankylosing Spondylitis (AS)

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