Background Although hepatocyte transplantation is a therapeutic op tion

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Background Although hepatocyte transplantation is a therapeutic op tion

Post  jy9202 on Fri Nov 13, 2015 4:25 am

B6Tert 1 cells exhibit the characteristics of normal EVTs by producing various biomarkers includ ing CK8, HLA G, integrin a1 and integrin b1. They also exhibit the ability to invade matrix and express pro teinase genes including MMP 2, MMP 9, MMP 14, TIMP 1, TIMP 2 and TIMP 3, which are JNJ-7706621 important properties of EVTs. In this study, we further demonstrated that the expression of MMP 26 in B6Tert 1 cells was comparable to that in the primary CTB cells at early gestation. The invasiveness of B6Tert 1 cells was regulated by paracrine andor autocrine fac tors such as EGF and transforming growth factor b. Here we showed that the invasive ability of B6Tert 1 cells was increased by GnRH I and GnRH II. This observation is also consistent with our previous report that GnRH I and GnRH II stimulated the invasiveness of primary EVT cells.

Our data and other groups studies strongly suggest that the LDN193189 B6Tert 1 cell line is a valuable in vitro cellular model for the investigation of trophoblast liketrophoblast cell behaviors. In the present study, we utilized B6Tert 1 cells to deter mine the regulatory mechanism of GnRHs on MMP 26 expression in human trophoblast liketrophoblast cells. The classical mammalian GnRH is a deca peptide that is well known for its role in regulating the release of gonadotropins from the pituitary. Evi dence shows that in addition to its classical endocrine functions, GnRH I has direct regulatory actions on the development and function of gonads and other repro ductive tissues such as the ovary, endometrium and pla centa.

A distinct gene encoding a second form of GnRH, termed GnRH II, that is expressed in human extrapituitary tissues, has been LY2157299 溶解度 shown to imitate the paracrineautocrine function of GnRH I in extrapituitary compartments. Recent stu dies demonstrated that GnRH I and GnRH II promoted the invasive capacity of human trophoblasts by regulat ing MMP 2, MMP 9TIMP 1 and uPAPAI protease systems. Consistent with these findings, our present work indicated that both GnRH I and GnRH II were capable of increasing the mRNA and protein levels of MMP 26 in trophoblast liketrophoblast cells. In addition to its direct proteolytic action on ECM sub strates, MMP 26 has also been reported to be an activa tor of proMMP 9 in prostate cancer cells and correlated to MMP 9 activity in esophageal carcinoma.

Considering the similar expression patterns between MMP 26 and MMP 9 in trophoblasts during early gestation, GnRH induced MMP 26 production may, at least in part, participate in proteolysis of the ECM through activating the latent form of MMP 9. The coordinate induction of MMP 2, MMP 9 and MMP 26 by GnRHs suggests that these enzymes possibly elicit their functions as components of a proteolytic cascade in trophoblasts. Although GnRH II is capable of mimicking the biolo gical actions of GnRH I in extrapituitary tissues, evi dence shows differential effects of these two hormones. For instance, GnRH II exhibited more potent anti prolif erative effects than an equimolar dose of GnRH I in human endometrial and ovarian cancer cells. In human placenta, GnRH I was more effective than GnRH II on hCG synthesis and secretion, while GnRH II appeared to be more potent than GnRH I in stimulating leptin secretion.


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