Somatostatin and somatostatin analogues reduce PDGF-induced endometrial cell proliferation and motility

Marta Annunziata1, Raul M Luque, Mario Durán-Prado

  • 1Laboratory of Molecular and Cellular Endocrinology, Department of Internal Medicine, University of Turin, Corso Dogliotti 14, 10126 Turin, Italy.

Abstract

Insights

The somatostatin/cortistatin (SST/CST) system is present in endometriosis. SST and its analogues inhibit the proliferation and migration of endometrial stromal cells, suggesting potential therapeutic applications for endometriosis treatment.

Area of Science:

  • Reproductive biology
  • Endocrinology
  • Molecular biology

Background:

  • Endometriosis involves ectopic endometrial cell implantation, characterized by increased proliferation and migration.
  • Somatostatin (SST) and Cortistatin (CST) are peptides that regulate cell growth and motility via SST receptors.
  • The SST/CST system's role in endometriosis requires further investigation.

Purpose of the Study:

  • To investigate the gene expression of the SST/CST system in endometriotic tissues and cells.
  • To determine the effect of SST and its analogues on platelet-derived growth factor (PDGF)-induced proliferation and motility in endometrial stromal cells (ESCs).

Main Methods:

  • Analysis of gene and protein expression of the SST/CST system in human endometriotic tissues, primary ESCs, and T HESCs.
  • Assessment of cell proliferation using the Alamar blue assay.
  • Evaluation of cell motility via wound healing assays and Western blotting for signaling pathway activation (ERK1/2, Akt).

Main Results:

  • SST, CST, and their receptors were expressed in endometriotic tissues, primary ESCs, and T HESCs.
  • SST, SOM230, octreotide, and CST inhibited PDGF-induced proliferation and migration in both cell types.
  • SST reduced vascular endothelial growth factor and metalloprotease-2 mRNA expression and inhibited ERK1/2 phosphorylation.

Conclusions:

  • The SST/CST system is expressed in endometriotic tissues and cells.
  • SST and its analogues demonstrate inhibitory effects on endometrial stromal cell proliferation and motility.
  • These findings suggest the SST/CST system as a potential therapeutic target for endometriosis.

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