Interleukin-33 promotes intrauterine adhesion formation in mice through the mitogen-activated protein kinase signaling pathway

Commun Biol. 2024 Aug 20;7(1):1022. doi: 10.1038/s42003-024-06709-1.

Abstract

IL-33 belongs to the inflammatory factor family and is closely associated with the inflammatory response. However, its role in the development of intrauterine adhesions (IUAs) remains unclear. In this study, the role of IL-33 in the formation of IUAs after endometrial injury was identified via RNA sequencing after mouse endometrial organoids were transplanted into an IUA mouse model. Major pathological changes in the mouse uterus, consistent with the expression of fibrotic markers, such as TGF-β, were observed in response to treatment with IL-33. This finding may be attributed to activation of the phosphorylation of downstream MAPK signaling pathway components, which are activated by the release of IL-33 in macrophages. Our study provides a novel mechanism for elucidating IUA formation, suggesting a new therapeutic strategy for the prevention and clinical treatment of IUAs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Disease Models, Animal
  • Endometrium / metabolism
  • Endometrium / pathology
  • Female
  • Interleukin-33* / genetics
  • Interleukin-33* / metabolism
  • MAP Kinase Signaling System*
  • Mice
  • Mice, Inbred C57BL
  • Mitogen-Activated Protein Kinases / genetics
  • Mitogen-Activated Protein Kinases / metabolism
  • Signal Transduction
  • Tissue Adhesions / metabolism
  • Tissue Adhesions / pathology
  • Uterine Diseases / genetics
  • Uterine Diseases / metabolism
  • Uterine Diseases / pathology
  • Uterus / metabolism
  • Uterus / pathology

Substances

  • Interleukin-33
  • Il33 protein, mouse
  • Mitogen-Activated Protein Kinases