Open AccessGonadotropin‐releasing hormone agonist induces downregulation of tensin 1 in women with endometriosis
Author(s) -
Rahmawati Endah,
Yang WeiChung V.,
Lei YenPing,
Maurya Pawan K.,
Chen HueiWen,
Tzeng ChiiRuey
Publication year - 2019
Publication title -
acta obstetricia et gynecologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.401
H-Index - 102
eISSN - 1600-0412
pISSN - 0001-6349
DOI - 10.1111/aogs.13481
Subject(s) - endometriosis , medicine , downregulation and upregulation , endocrinology , immunohistochemistry , stromal cell , gonadotropin releasing hormone , agonist , gonadotropin releasing hormone agonist , western blot , andrology , hormone , luteinizing hormone , receptor , biology , biochemistry , gene
Many cell migration‐related molecules are associated with endometriosis. Tensin 1 (TNS1), which has been implicated in cell migration, may play a role in endometriosis. The study goal was to evaluate the TNS1 expression in endometrial tissue and serum from women with endometriosis treated with gonadotropin‐releasing hormone agonist (GnRHa). Material and methods Tissue and serum samples were collected from women with endometriosis who were treated (n = 29) with GnRHa or untreated (n = 30). TNS1 mRNA was examined using quantitative PCR. TNS1 protein levels in tissue and serum samples were investigated using Western blot, immunohistochemistry and ELISA. Eleven women with endometriosis participated in a follow‐up investigation of serum TNS1 before and after GnRHa treatment. Results TNS1 mRNA ( P = 0.006) and protein ( P = 0.001) were significantly downregulated in endometriotic tissue from women with endometriosis who received GnRHa. Immunolocalization of TNS1 showed strong expression in the epithelial and stromal cells of endometriotic tissue from women untreated with GnRHa, whereas endometriotic tissue from GnRHa‐treated women showed low TNS1 expression. Follow‐up monitoring of serum TNS1 concentration in 11 women showed an average decrease in concentration of 53%, from 294.9 ± 66.69 to 140.3 ± 55.21 pg/mL, following GnRHa treatment ( P = 0.003). Conclusions GnRHa induces downregulation of TNS1 in tissue and serum in women with endometriosis. These results emphasize the importance TNS1 as a potential therapeutic molecular target for the treatment of endometriosis with GnRHa.