ArticleScientific reports2024
Platelet activation through CD62P and the formation of platelet-monocyte complexes are associated with the exacerbation of mucosal inflammation in patients with ulcerative colitis.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Circulating cell adhesion molecules as biomarkers in inflammatory bowel disease: a systematic review and meta-analysis.Frontiers in immunology · 2025Pooled it
- Diagnostic efficacy of pan-immune inflammation value for ulcerative colitis activity: a study based on multi-indicator comparison and diagnostic grey zone validation.BMC gastroenterology · 2026Article
- Effect of the atherogenic index of plasma on the expression of platelet CD36 and CD62P in patients with acute ischemic stroke: a retrospective study from Tianjin, China.BMC neurology · 2026Article
- NPHR, FPR, and PLT as predictors of ulcerative colitis severity: a single-center retrospective study in China.Frontiers in medicine · 2026Article
- P-Selectin and Platelet-Monocyte Interaction in Inflammation: Mechanisms, Hypothesis, and Open Questions.Journal of inflammation research · 2026Review
- Analysis of Platelet Membrane Glycoproteins and The Specific Antibodies in MYH9-Related Diseases.International journal of general medicine · 2026Article
- Article
- Platelet activation stimulates macrophages to enhance ulcerative colitis through PF4/CXCR3 signaling.International journal of molecular medicine · 2025Article
- Pazopanib-associated remodeling of platelet-immune cell crosstalk and immune suppressive platelet-derived extracellular vesicles in metastatic RCC.Frontiers in immunology · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
Ulcerative colitis (UC) is a refractory, chronic inflammatory bowel disease of unknown etiology. Although platelets are activated in UC, their relevance in pathophysiology remains unclear. We analyzed the correlation of platelet activation and platelet-monocyte complexes (PMCs) with severity of mucosal inflammation using the Mayo endoscopic subscore (MES). Platelet activation marker, CD62P was upregulated in patients with UC compared with that in healthy controls (P < 0.05). CD62P expression was significantly higher in patients with MES3 (severe inflammation) than in those with MES ≤ 2 (endoscopic remission to moderate inflammation) (P < 0.001). The concentration of sCD62P in patients with MES0 (endoscopic remission) was significantly higher than in those with MES ≥ 1 (P < 0.01). The expression of CD40L, CD63, PAC-1, annexin V, and CD36, and the concentrations of sCD40L, PF4, and RANTES did not correlate with MES. The proportion of PMCs in patients with MES3 was higher than in those with MES ≤ 2 (P < 0.05). CD16 expression on monocytes with platelets was significantly higher than in monocytes without platelets (P < 0.001). Patients with complete remission after treatment showed significant reduction in PMCs 3 months after treatment (P < 0.05) but had no change in CD62P and sCD62P. Our data suggest that platelet activation via the CD62P-PMC axis is involved in UC pathophysiology.
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