Effect of gonadotropins on human endometrial stromal cell proliferation in vitro

2002 ◽  
Vol 266 (4) ◽  
pp. 223-228 ◽  
Author(s):  
Seung Yup Ku ◽  
Y. M. Choi ◽  
Chang Suk Suh ◽  
Seok Hyun Kim ◽  
Jung Gu Kim ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Stromal Cell ◽  
Endometrial Stromal Cell ◽  
Human Endometrial Stromal Cell ◽  
Proliferation In Vitro

Investigation into the effect of ovarian hormone to the thickness of human endometrial stromal cell sheets in vitro.

2020 ◽  
Vol 2020.28 (0) ◽  
pp. 512
Author(s):  
Mao FUJITA ◽  
Katsuhisa SAKAGUCHI ◽  
Goro KURAMOTO ◽  
Shinjiro UMEZU ◽  
Tatsuya SHIMIZU
Keyword(s):  
Stromal Cell ◽  
Ovarian Hormone ◽  
Endometrial Stromal Cell ◽  
Cell Sheets ◽  
Human Endometrial Stromal Cell

scholarly journals The characteristics of integrins expression in decidualized human endometrial stromal cell induced by 8-Br-cAMP in in vitro

2002 ◽  
Vol 34 (3) ◽  
pp. 194-200 ◽  
Author(s):  
Jung Hye Hwang ◽  
Moon Il Park ◽  
Youn Young Hwang ◽  
Hyung Jin Yoo ◽  
Helen J Mardon
Keyword(s):  
Stromal Cell ◽  
Endometrial Stromal Cell ◽  
Human Endometrial Stromal Cell

Uterus and endometrium: Inhibition of human endometrial stromal cell proliferation by interleukin 6

1995 ◽  
Vol 10 (9) ◽  
pp. 2395-2399 ◽  
Author(s):  
P. N. Zarmakoupis ◽  
S. E. Rier ◽  
G. B. Maroulis ◽  
J. L. Becker
Keyword(s):  
Cell Proliferation ◽  
Interleukin 6 ◽  
Stromal Cell ◽  
Endometrial Stromal Cell ◽  
Human Endometrial Stromal Cell

scholarly journals Interleukin-1β inhibits estrogen receptor-α, progesterone receptors A and B and biomarkers of human endometrial stromal cell differentiation: implications for endometriosis

2019 ◽  
Vol 25 (10) ◽  
pp. 625-637 ◽  
Author(s):  
Jie Yu ◽  
Sarah L Berga ◽  
Wei Zou ◽  
Robert N Taylor
Keyword(s):  
Estrogen Receptor ◽  
Cell Differentiation ◽  
Growth Factor ◽  
Stromal Cell ◽  
Time Course ◽  
Progesterone Receptors ◽  
Endometrial Stromal Cell ◽  
Human Endometrial Stromal Cell ◽  
Junction Protein

Abstract Human blastocyst nidation in the uterus and successful pregnancy require coordinated endometrial expression of estrogen receptor (ER)-α, progesterone receptors (PR)-A and -B and the gap junction protein, connexin (Cx)43. Our prior work established that inflammation associated with conditions of reduced fecundity, particularly endometriosis, can perturb eutopic decidual function. In the current studies, we have modeled endometrial decidualization in primary human endometrial stromal cell cultures derived from normal controls (NESC) and from the eutopic endometria of women with endometriosis (EESC) to test the hypothesis that a proinflammatory cytokine, interleukin (IL)-1β, can disrupt stromal cell differentiation. The cells were grown under a standard protocol with hormones (10 nM 17β-estradiol, 100 nM progesterone and 0.5 mM dibutyryl cAMP) for up to 7 days in the absence or presence of IL-1β. Time-course experiments showed that IL-1β compromised decidual function in both NESC and EESC, which was accompanied by rapid phosphorylation of ER-α, PR and Cx43 and their cellular depletion. Inhibition of the extracellular signal-regulated kinase (ERK)1/2 pathway by a selective pharmacological blocker (PD98059) or siRNA interference, or the addition of hormones themselves, blocked the phosphorylation of ERK mediators; increased the production of steroid receptors, Cx43, prolactin, insulin-like growth factor binding protein-1 (IGFBP)-1 and vascular endothelial growth factor (VEGF) and accelerated the differentiation. The results indicate that inhibition of IL-1β can enhance decidualization in NESC and EESC in vitro. Strategies to interfere with this pathway might be implemented as an in vivo approach to enhance fertility in women with endometriosis and, potentially, other inflammatory pathologies.

scholarly journals Calpain7 Negatively Regulates Human Endometrial Stromal Cell Decidualization in Endometriosis by Promoting FoxO1’s Phosphorylation and Nuclear Exclusion via Hydrolyzing AKT1

2021 ◽  
Author(s):  
Nannan Kang ◽  
Huizhi Shan ◽  
Junxia Wang ◽  
Jie Mei ◽  
Yue Jiang ◽  
...  
Keyword(s):  
Western Blotting ◽  
Stromal Cell ◽  
Endometrial Stromal Cell ◽  
Endometrial Stromal Cells ◽  
Forkhead Box ◽  
Human Endometrial Stromal Cell ◽  
Nuclear Exclusion ◽  
Potential Pest

Abstract Background Endometrial receptivity damage caused by impaired decidualization may be one of the mechanisms of infertility in endometriosis (EMs). Our previous study demonstrated that Calpain-7 (CAPN7) is abnormally overexpressed in EMs. Whether CAPN7 affects the regulation of decidualization and by what mechanism CAPN7 regulates decidualization remains to be determined. Methods Immunohistochemistry (IHC) was used to assess the CAPN7 expression in human endometria. Quantitative real-time PCR (qRT-PCR), western blotting, ELIFA and ELISA were applied to explore PRL and IGFBP-1 expressions in decidualized human endometrial stromal cells (HESC). Immunofluorescence analysis and the nuclear and cytoplasmic protein extract assay were employed to test CAPN7’s affection on FoxO1’s location in HESC. Western blotting was used to explore the regulatory mechanism of CAPN7 to AKT1/FoxO1 signalling pathway. Results In this study, we found CAPN7 expression decreased during human endometrial stromal cell (HESC) decidualization in vitro. CAPN7 negatively regulated decidualization in vitro and in vivo. We also identified one conserved potential PEST sequence in the AKT1 protein and found that CAPN7 was able to hydrolyse AKT1 and enhance AKT1’s phosphorylation. Correspondingly, CAPN7 notably promoted the phosphorylation of Forkhead Box O1 (FoxO1), the downstream of AKT1 protein, at Ser319, leading to increased FoxO1 exclusion from nuclei and attenuated FoxO1 transcriptional activity in decidualized HESC. In addition, we detected endometrium CAPN7, p-AKT1 and p-FoxO1 expressions were increased in EMs. Conclusions These data demonstrate that CAPN7 negatively regulates HESC decidualization in EMs probably by promoting FoxO1’s phosphorylation and FoxO1 nuclear exclusion via hydrolyzing AKT1. The dysregulation of CAPN7 may be a novel cause of EMs.

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