z-logo
open-access-imgOpen Access
Somatostatin and somatostatin analogues reduce PDGF-induced endometrial cell proliferation and motility
Author(s) -
Marta Annunziata,
Raúl M. Luque,
Mario DuránPrado,
Alessandra Baragli,
Cristina Grande,
Marco Volante,
Manuel D. Gahete,
Francesco Deltetto,
Marco Camanni,
Ezio Ghigo,
Justo P. Castaño,
Riccarda Granata
Publication year - 2012
Publication title -
human reproduction
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.446
H-Index - 226
eISSN - 1460-2350
pISSN - 0268-1161
DOI - 10.1093/humrep/des144
Subject(s) - platelet derived growth factor receptor , cell growth , biology , somatostatin , stromal cell , motility , cancer research , growth factor , microbiology and biotechnology , endocrinology , receptor , biochemistry
Endometriosis is characterized by ectopic implantation of endometrial cells, which show increased proliferation and migration. Somatostatin (SST) and its analogues inhibit normal and cancer cell growth and motility through the SST receptors, sst1-5. Cortistatin (CST), which displays high structural and functional homology with SST, binds all ssts, as well as MrgX2. Our objective was to investigate the gene expression of the SST/CST system and to determine the effect of SST and its analogues on platelet-derived growth factor (PDGF)-induced proliferation and motility in telomerase-immortalized human endometrial stromal cell (T HESC) line and in primary endometrial stromal cell (ESCs) isolated from human endometriotic tissues.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom