WISP-2 modulates the induction of inflammatory mediators and cartilage catabolism in chondrocytes

Ruiz-Fernández, Clara; González-Rodríguez, María; Abella, Vanessa; Francisco, Vera; Cordero-Barreal, Alfonso; Eldjoudi, Djedjiga Ait; Farrag, Yousof; Pino, Jesús; Conde, Javier; Varela, A. Mera; Mobasheri, Ali; García‐Caballero, Lucía; Gándara-Cortés, Marina; Lago, Francisca; Scotece, Morena; Gualillo, Oreste

doi:10.1038/s41374-022-00793-9

Cited by 3 publications

(3 citation statements)

References 30 publications

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“…7), were detected in MCAO, indicating a critical role of in ammation in IRI. WISP2, potentially pro-in ammatory, might in uence pyroptosis post-IRI considering its link to the immune microenvironment [30]. Moreover, the in ltration of dendritic cells and natural killer cells were positively correlated with SDF2L1 expression in high and low IRI risk groups, respectively.…”

Section: Discussionmentioning

confidence: 97%

“…Employing logistic modeling and SVM analyses, we strategically focused on four hub genes-WISP2, MELK, SDF2L1, and AURKB-as central players orchestrating the expression landscape of MCAO. WISP2, an adipokine known for its role in pro-in ammatory responses, emerged as a central player in modulating the in ammatory cascade in pyroptosis (30). Importantly, its anti-in ammatory properties align seamlessly with pathways governing immune responses and tissue repair (31).…”

Section: Discussionmentioning

confidence: 99%

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Unveiling Pyroptosis-Related Hub Genes in Ischemic Stroke Provides Insights for Enhanced Risk Assessment

Ye,

Liangbin,

Can

et al. 2024

Preprint

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Background: Stroke is the second-leading global cause of death. The immune storm triggered by ischemia-reperfusion injury after stroke is a crucial damaging factor. This study analyzed the expression of key pyroptosis genes in stroke and their correlation with immune infiltration. Methods: Middle Cerebral Artery Occlusion datasets were obtained and pyroptosis-related genes were identified. Differential expression and functional analyses of pyroptosis-related genes were performed. Differences in functional enrichment between high-risk and low-risk groups were determined. After selecting pyroptosis-related genes with differential expression, a MCAO diagnostic model was constructed and validated. High and low-risk MCAO groups were constructed for expression and immune cell correlation analysis with pyroptosis-related hub genes. A regulatory network between pyroptosis-related hub genes and miRNA was built, and protein domains were predicted. The expression of key pyroptosis genes was validated in the MCAO rat model. Results: Twenty-five pyroptosis genes showed differential expression, including four hub genes (WISP2, MELK, SDF2L1, and AURKB). The high- and low-risk groups showed significant expression differences for WISP2, MELK and SDF2L1. In immune infiltration analysis, 12 immune cells exhibited expression differences in MCAO samples. Further analysis demonstrated significant positive correlations between the pyroptosis-related hub gene SDF2L1 and immune cell-activated dendritic cells in the high-risk group and immune cell natural killer cells in the low-risk group. Conclusion: This study identified four pyroptosis-related hub genes, with elevated WISP2, MELK, and SDF2L1 expression closely associated with the high-risk group. Analysis of inflammatory cell types in immune infiltration provides a theoretical basis for predicting ischemic stroke risk levels and treatment.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Unveiling Pyroptosis-Related Hub Genes in Ischemic Stroke Provides Insights for Enhanced Risk Assessment

Ye,

Liangbin,

Can

et al. 2024

Preprint

View full text Add to dashboard Cite

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“…This evidence speaks to the positive role for CCN5 in diabetes. Recent work from Ruiz‐Fernández et al (2022) on OA revealed that CCN5 may act as a WNT agonist able to partially counteract the catabolic effects of IL‐1β, one of the main mediators of inflammatory response in cartilage. Thus CCN5 might function as a significant antagonist of inflammation.…”

Section: Introductionmentioning

confidence: 99%

CCN proteins: opportunities for clinical studies—a personal perspective

Yeger

2023

J. Cell Commun. Signal.

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The diverse members of the CCN family now designated as CCN1(CYR61), CCN2 (CTGF), CCN3(NOV), CCN4(WISP1), CCN5(WISP2), CCN6(WISP3) are a conserved matricellular family of proteins exhibiting a spectrum of functional properties throughout all organs in the body. Interaction with cell membrane receptors such as integrins trigger intracellular signaling pathways. Proteolytically cleaved fragments (constituting the active domains) can be transported to the nucleus and perform transcriptional relevant functional activities. Notably, as also found in other protein families some members act opposite to others creating a system of functionally relevant checks and balances. It has become apparent that these proteins are secreted into the circulation, are quantifiable, and can serve as disease biomarkers. How they might also serve as homeostatic regulators is just becoming appreciated. In this review I have attempted to highlight the most recent evidence under the subcategories of cancer and non‐cancer relevant that could lead to potential therapeutic approaches or ideas that can be factored into clinical advances. I have added my own personal perspective on feasibility.

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Ceria-vesicle nanohybrid therapeutic for modulation of innate and adaptive immunity in a collagen-induced arthritis model

Koo,

Sohn,

Kim

et al. 2023

Nat. Nanotechnol.

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WISP-2 modulates the induction of inflammatory mediators and cartilage catabolism in chondrocytes

Cited by 3 publications

References 30 publications

Unveiling Pyroptosis-Related Hub Genes in Ischemic Stroke Provides Insights for Enhanced Risk Assessment

Unveiling Pyroptosis-Related Hub Genes in Ischemic Stroke Provides Insights for Enhanced Risk Assessment

CCN proteins: opportunities for clinical studies—a personal perspective

Ceria-vesicle nanohybrid therapeutic for modulation of innate and adaptive immunity in a collagen-induced arthritis model

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