Screening and experimental study of potential biomarkers for ulcerative colitis based on weighted gene co-expression network analysis and machine learning

  • 0Department of Anorectal Surgery, LongHua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, China.

|

|

Summary

This summary is machine-generated.

Poly(ADP-ribose) polymerase family member 8 (PARP8) is identified as a potential biomarker for ulcerative colitis (UC). This finding, derived from integrated bioinformatics and machine learning, suggests PARP8 plays a role in UC pathogenesis through immune pathways.

Area Of Science

  • Immunology
  • Genomics
  • Bioinformatics

Background

  • Ulcerative colitis (UC) is a chronic inflammatory bowel disease with unclear pathogenesis.
  • It affects the intestinal mucosa and submucosa, causing continuous inflammation.

Purpose Of The Study

  • To identify novel ulcerative colitis (UC) biomarkers.
  • Integrate weighted gene co-expression network analysis (WGCNA) with machine learning for biomarker discovery.
  • Validate potential biomarkers in an experimental UC mouse model.

Main Methods

  • Systematic querying of the Gene Expression Omnibus database (GSE87466 dataset).
  • Identification of differentially expressed genes (DEGs) and enrichment analyses.
  • Application of WGCNA, LASSO, and SVM-RFE for biomarker screening.
  • Validation through in vivo animal experiments.

Main Results

  • 1,097 DEGs were identified; WGCNA highlighted a turquoise module strongly associated with UC.
  • Poly(ADP-ribose) polymerase family member 8 (PARP8) was identified as a key biomarker by LASSO and SVM-RFE.
  • PARP8 expression correlated with increased neutrophils, M1 macrophages, and activated CD4+ T cells in UC patients.
  • Elevated PARP8 expression was confirmed in a mouse model of UC.

Conclusions

  • PARP8 may contribute to ulcerative colitis (UC) pathogenesis via immune-related pathways.
  • PARP8 shows promise as a diagnostic and predictive biomarker for UC.
  • Further research into PARP8's role in immune dysregulation in UC is warranted.