Inflammatory EC Activation
Gene co-expression module in Endothelial
| Category | ECM remodeling |
|---|---|
| Genes | 13 |
| Annotation certainty | 3 of 5 |
| Annotation consistency | 8 of 13 genes have a known function matching the annotation |
Why this annotation
This module has the largest inflammation delta in the batch (1.767 UC, 1.591 CD) with strong remission reversal (-1.200 UC), indicating a highly inflammation-specific program. Hub genes: PMP22 (expressed in ECs as a growth arrest/differentiation gene), COL6A2/COL6A1 (collagen VI, ECM structural component upregulated in IBD fibrosis), TGM2 (transglutaminase 2, crosslinks ECM proteins, activated in inflammation), OAF (out at first homolog, poorly characterized), CD200 (immune checkpoint ligand expressed on ECs to suppress inflammation), NT5E/CD73 (ecto-5'-nucleotidase, generates immunosuppressive adenosine, marker of anti-inflammatory EC phenotype), LAMP3 (lysosomal membrane protein, also DC maturation marker — possible contamination signal but uniform expression argues against), IGFBP5 (IGF binding protein, ECM-associated, upregulated in fibrosis), CAPG (actin-capping protein, macrophage marker but also expressed in ECs during remodeling), PTPRE (receptor tyrosine phosphatase). The combination of COL6A1/2, TGM2, IGFBP5 points to ECM remodeling/fibrotic response; CD200 and NT5E suggest an immunomodulatory activated EC state. This likely represents an inflammation-activated EC phenotype with concurrent ECM remodeling — consistent with venular high endothelial or activated stromal-like EC state in IBD. Distinguished from neighbors by ECM content and much stronger inflammation response.
Genes
C4orf48, CAPG, CD200, COL6A1, COL6A2, IGFBP5, LAMP3, NT5E, OAF, PMP22, PTPRE, SH3TC1, TGM2
Most correlated modules
- ER Protein Processing · correlation 0.86
- p53 Stress Response · correlation 0.85
- Redox Stress Response · correlation 0.85
- Actin Cytoskeletal Remodeling · correlation 0.83
- ECM Fibrotic Remodeling · correlation 0.77
- Inflammatory Endothelial Activation · correlation 0.76
Module annotations were drafted by a large language model from the module's genes, then reviewed and approved by a domain expert. See sources & licences.