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| Content Provider | Springer Nature : BioMed Central |
|---|---|
| Author | Liu, Jing Cao, Bin Li, Yu-xia Wu, Xiao-qiu Wang, Yan-ling |
| Abstract | Background Matrix metalloproteinase-26 (MMP-26), one of the main mediators of extracellular matrix (ECM) degradation, has been shown to exist in trophoblasts of human placenta and to play a role in trophoblast cell invasion. However, little is known about the regulation of MMP-26 expression in human trophoblasts. Recently, gonadotropin-releasing hormone I (GnRH I) and GnRH II have been shown to regulate the expression of MMP-2, MMP-9/tissue inhibitor of metalloproteinases 1 (TIMP-1), and urokinase plasminogen activator (uPA)/plasminogen activator inhibitor (PAI) in human trophoblasts, suggesting that these two hormones may work as paracrine and/or autocrine regulators in modulating the activities of various protease systems at the feto-maternal interface. In this study, we determined the regulatory effects of GnRH I and GnRH II on the expression of MMP-26 in human immortalized cytotrophoblast-like cell line, B6Tert-1. Methods Real-time PCR was used to quantify mRNA levels of MMP-26 in human trophoblast-like cell line, B6Tert-1 and primary cultured cytotrophoblasts. Western blotting was used to characterize the expression of MMP-26 and the phosphorylation of c-Jun NH2-terminal kinase (JNK) and extracellular signal-regulated kinase 1/2 (ERK1/2) in B6Tert-1 cells after treatment with GnRH I and GnRH II. Results We found that GnRH I increased MMP-26 expression in B6Tert-1 cells after 12 h of treatment at both the mRNA and protein level, while GnRH II increased MMP-26 expression beginning at 3 h of treatment. Treatment of GnRH I at 1 nM resulted in maximal increase of MMP-26 mRNA and protein levels, whereas GnRH II treatment at a concentration of 100 nM was required to induce maximal increase in MMP-26 expression. In addition, we demonstrated that the activation of JNK, but not ERK1/2, was required for GnRH I and II-stimulated MMP-26 production in B6Tert-1 cells and primary cytotrophoblasts. Conclusions These novel findings indicated that GnRH I and II could up-regulate MMP-26 expression through the JNK signaling pathway in human trophoblast-like/trophoblast cells. |
| Related Links | https://rbej.biomedcentral.com/counter/pdf/10.1186/1477-7827-8-5.pdf |
| Ending Page | 10 |
| Page Count | 10 |
| Starting Page | 1 |
| File Format | HTM / HTML |
| ISSN | 14777827 |
| DOI | 10.1186/1477-7827-8-5 |
| Journal | Reproductive Biology and Endocrinology |
| Issue Number | 1 |
| Volume Number | 8 |
| Language | English |
| Publisher | BioMed Central |
| Publisher Date | 2010-01-15 |
| Access Restriction | Open |
| Subject Keyword | Reproductive Medicine Endocrinology Trophoblast Cell GnRH Receptor Human Trophoblast Human Trophoblast Cell GnRHR Gene |
| Content Type | Text |
| Resource Type | Article |
| Subject | Endocrinology Obstetrics and Gynecology Developmental Biology Reproductive Medicine |
| Journal Impact Factor | 4.2/2023 |
| 5-Year Journal Impact Factor | 5.3/2023 |
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