Differential Expression of Insulin Growth Factor 1 (IGF-1) Isoforms in Different Types of Endometriosis: Preliminary Results of a Single-Center Study

Biomolecules. 2023 Dec 20;14(1):7. doi: 10.3390/biom14010007.

Abstract

Endometriosis is a benign, estrogen-dependent gynecological condition with an uncertain exact pathogenetic mechanism. The aim of this study was to evaluate the potential differential expression of Insulin Growth Factor 1 (IGF-1) isoforms in deeply infiltrating endometriotic (DIE) lesions, in ovarian endometriomas, and in the eutopic endometrium of the same endometriosis patients and to compare their expression with that in the eutopic endometrium of women without endometriosis. A total of 39 patients were included: 28 with endometriosis, of whom 15 had endometriomas only, 7 had DIE nodules only, and 6 had both DIE and endometriomas, and 11 without endometriosis served as controls. We noticed a similar pattern of expression between IGF-1Ea and IGF-1Ec, which differed from that of the IGF-1Eb isoform, possibly implying differential biological actions of different isoforms in DIE subtypes. We observed a tendency of lower expression of IGF-1Ea and IGF-1Ec in endometriomas without DIE compared to endometriomas with concurrent DIE or in DIE nodules. In conclusion, differential expression of IGF-1 isoforms may indicate that DIE with its associated ovarian lesions and simple ovarian endometriosis should be considered as two forms of the disease developing under different molecular pathways.

Keywords: endometriosis; endometriotic nodules; insulin growth factor 1 isoforms.

MeSH terms

  • Endometriosis* / metabolism
  • Female
  • Humans
  • Insulin
  • Insulin-Like Growth Factor I / genetics
  • Intercellular Signaling Peptides and Proteins
  • Ovarian Cysts*
  • Ovarian Neoplasms*
  • Protein Isoforms / genetics

Substances

  • Insulin-Like Growth Factor I
  • Insulin
  • Protein Isoforms
  • Intercellular Signaling Peptides and Proteins

Grants and funding

This research received no external funding.