ArticleScientific reports2025
The YAP/TEAD4 transcriptional complex in intestinal macrophages promotes M2 polarization and alleviates DSS-induced colitis via the regulation of C/EBPβ.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Loss of tumor suppressor NF2 mediates resistance to CAR T cell and anti-PD-1 therapy: Strategies to restore immunotherapy sensitivity.Med (New York, N.Y.) · 2026Article
- HIRA promotes osteogenic differentiation of BMSCs and ameliorates osteoporosis by mediating M2 polarization of macrophages through the YAP1/β-catenin pathway.Molecular and cellular biochemistry · 2026Article
- CCAAT/enhancer binding protein β and its role in autoimmune diseases: a promising therapeutic target.Journal of translational medicine · 2026Review
- TEAD4 and RXRA Regulate the Function of Nucleus Pulposus Cells in Intervertebral Disc Degeneration Via the TNF-α/NF-κB Pathway: An Integrated Analysis of Single-Cell RNA-Seq, Bulk RNA-Seq, and In Vitro Validation.Applied biochemistry and biotechnology · 2026Article
- Macrophage pyroptosis in inflammatory bowel disease: mechanistic insights, pathological roles and treatment strategies.Frontiers in immunology · 2026Review
- Tumor Development in Ulcerative Colitis: Perspectives From Biomechanical Characteristics.Development, growth & differentiation · 2025Review
- M2 macrophage polarization in allogeneic skin transplantation: from intrinsic mechanisms to clinical prospects for immune tolerance.Molecular biology reports · 2025Review
- Mechanisms and therapeutic strategies of macrophages and neutrophils inducing ulcerative colitis progression.Frontiers in immunology · 2025Review
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Authors and funding
6 authors.
Funding
Abstract
Suppressing inflammation and promoting intestinal epithelial regeneration are the keys to mucosal healing in individuals with ulcerative colitis (UC). The upregulation of epithelial YAP and the induction of macrophages to polarize to the M2 phenotype in the mucosa can promote intestinal epithelial regeneration and alleviate ulcerative colitis. However, the role of YAP in macrophage polarization remains unclear. Here, we explored the effects of YAP on macrophage polarization and its biological role in a mouse DSS-induced colitis model. The results showed that YAP upregulation in macrophages could induce M2 polarization and increase the levels of anti-inflammatory cytokines such as IL-10 and IL-13. In addition, when mice were infused with YAP-overexpressing and empty vector-transfected macrophages, compared with control mice, YAP-overexpressing mice presented slower weight loss, a longer colon length, less intestinal inflammation, and a better arrangement of crypts. Moreover, macrophages in the lamina propria of the mouse colonic mucosa presented mainly the M2 phenotype in YAP-overexpressing macrophage-infused DSS-treated mice. Mechanistically, knockdown of the expression of the transcription factor TEAD4 in YAP-overexpressing macrophages inhibited macrophage M2 polarization and decreased anti-inflammatory cytokine expression, accompanied by the downregulated expression of C/EBPβ. Furthermore, silencing C/EBPβ following YAP overexpression suppressed M2 polarization. Chromatin immunoprecipitation revealed that TEAD4 was enriched at the C/EBPβ promoter region in YAP-overexpressing macrophages. Thus, YAP in macrophages regulates C/EBPβ expression through the transcription factor TEAD4, which mediates macrophage M2 polarization and inhibits the expression of inflammatory cytokines, thereby exerting inhibitory effects on intestinal inflammation and promoting mucosal healing in a colitis model.
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