scholarly journals Endometrial stromal cells regulate epithelial cell growth in vitro: a new co-culture model

2001 ◽  
Vol 16 (5) ◽  
pp. 836-845 ◽  
Author(s):  
Julia T. Arnold ◽  
David G. Kaufman ◽  
Markku Seppälä ◽  
Bruce A. Lessey
Keyword(s):  
Cell Growth ◽  
Epithelial Cell ◽  
Stromal Cells ◽  
Endometrial Stromal Cells ◽  
Culture Model

Impact of growth hormone-releasing hormone (GHRH) antagonist on Decidual stromal cell growth and apoptosis in vitro

2021 ◽  
Author(s):  
Hsien-Ming Wu ◽  
Liang-Hsuan Chen ◽  
Andrew V Schally ◽  
Hong-Yuan Huang ◽  
Yung-Kuei Soong ◽  
...  
Keyword(s):  
Cell Growth ◽  
Stromal Cells ◽  
Stromal Cell ◽  
Molecular Mechanisms ◽  
Antitumor Agents ◽  
Gynecological Cancer ◽  
Dependent Manner ◽  
Endometrial Stromal Cells ◽  
The Impact

Abstract Endometrial stromal cells remodeling is critical during human pregnancy. GHRH and its functional receptor have been shown to be expressed in gynecological cancer cells and eutopic endometrial stromal cells. Recent studies have demonstrated the potential clinical uses of antagonists of GHRH as effective antitumor agents because of its directly antagonistic effect on the locally produced GHRH in gynecological tumors. However, the impact of GHRH antagonists on normal endometrial stromal cell growth remained to be elucidated. The aim of this study was to investigate the effect of a GHRH antagonist (JMR-132) on cell proliferation and apoptosis of human decidual stromal cells and the underlying molecular mechanisms. Our results showed that GHRH and the splice variant 1 (SV1) of GHRH receptor (GHRH-R SV1) are expressed in human decidual stromal cells isolated from the decidual tissues of early pregnant women receiving surgical abortion. In addition, treatment of stroma cells with JMR-132 induced cell apoptosis with increasing cleaved caspase-3 and caspase-9 activities, and decrease cell viability in a time- and dose-dependent manner. Using a dual inhibition approach (pharmacological inhibitors and siRNA-mediated knockdown), we showed that JMR-132-induced activation of apoptotic signals are mediated by the activation of ERK1/2 and JNK signaling pathways and the subsequent upregulation of GADD45α. Taken together, JMR-132 suppresses cell survival of decidual stromal cells by inducing apoptosis through the activation of ERK1/2- and JNK-mediated upregulation of GADD45α in human endometrial stromal cells. Our findings provide new insights into the potential impact of GHRH antagonist on the decidual programming in humans.

Establishment of a Primary Culture Model of Mouse Uterine and Vaginal Stroma for Studying In Vitro Estrogen Effects

2006 ◽  
Vol 231 (3) ◽  
pp. 303-310 ◽  
Author(s):  
Keiko Inada ◽  
Shinji Hayashi ◽  
Taisen Iguchi ◽  
Tomomi Sato
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Primary Culture ◽  
Stromal Cells ◽  
Renal Capsule ◽  
Epithelial Cell Proliferation ◽  
Culture Model ◽  
Brdu Labeling

Effects of 17β-estradiol (E2) on uterine and vaginal epithelial cell proliferation could be mediated by stromal cell-derived paracrine factors. To study the epithelial-stromal interactions in mice, an in vitro model of uterine and vaginal stromal cells of immature mice is essential. Therefore, we established a primary culture model of stromal cells both from uterus and vagina and examined the effect of E2 on proliferation of cultured stromal cells. We found that E2 stimulated proliferation of stromal cells from both organs in vitro, showing an increase in the number of cells and the percentage of 5-bromo-2'-deoxyurldine (BrdU)-labeled cells. Interestingly, vaginal stromal cells responded to lower E2 than uterine stromal cells in proliferation (10−12 M vs. 10−8 M) and BrdU labeling (10−14 -10−10 M vs. 10−10 - 10−6 M). To examine the effect of E2 in vivo, cells were grafted into the subrenal capsule of the host mice and grown for 2 weeks. The BrdU labeling in cultured stromal cells was increased by E2 in vivo. To examine the effect of cultured stromal cells on epithelial cell proliferation, uterine and vaginal epithelium of adult mice were separated, recombined with the cultured stromal cells, and grafted under the renal capsule of hosts for 3 weeks. Epithelial cells recombined with cultured stromal cells showed simple columnar morphology in uterine grafts and stratified and keratinized morphology in vaginal grafts under the influence of the hormonal environment of the hosts. The BrdU labeling in epithelial cells was increased by E2, suggesting that cultured stromal cells can stimulate epithelial cell proliferation. In conclusion, we established a primary culture model of uterine and vaginal stromal cells, which can be mitogenically stimulated by E2 in vitro and in vivo after being grafted under the renal capsule. This culture system will be useful for investigating the underlying molecular mechanisms of uterine and vaginal epithelial-stromal interactions.

scholarly journals Endometrial regeneration with endometrial epithelium: homologous orchestration with endometrial stroma as a feeder

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Ryo Yokomizo ◽  
Yukiko Fujiki ◽  
Harue Kishigami ◽  
Hiroshi Kishi ◽  
Tohru Kiyono ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Stromal Cells ◽  
Therapeutic Option ◽  
Three Dimensional ◽  
Fertility Treatment ◽  
Feeder Cells ◽  
Endometrial Stromal Cells ◽  
Thin Endometrium ◽  
Endometrial Epithelial Cells

Abstract Background Thin endometrium adversely affects reproductive success rates with fertility treatment. Autologous transplantation of exogenously prepared endometrium can be a promising therapeutic option for thin endometrium; however, endometrial epithelial cells have limited expansion potential, which needs to be overcome in order to make regenerative medicine a therapeutic strategy for refractory thin endometrium. Here, we aimed to perform long-term culture of endometrial epithelial cells in vitro. Methods We prepared primary human endometrial epithelial cells and endometrial stromal cells and investigated whether endometrial stromal cells and human embryonic stem cell-derived feeder cells could support proliferation of endometrial epithelial cells. We also investigated whether three-dimensional culture can be achieved using thawed endometrial epithelial cells and endometrial stromal cells. Results Co-cultivation with the feeder cells dramatically increased the proliferation rate of the endometrial epithelial cells. We serially passaged the endometrial epithelial cells on mouse embryonic fibroblasts up to passage 6 for 4 months. Among the human-derived feeder cells, endometrial stromal cells exhibited the best feeder activity for proliferation of the endometrial epithelial cells. We continued to propagate the endometrial epithelial cells on endometrial stromal cells up to passage 5 for 81 days. Furthermore, endometrial epithelium and stroma, after the freeze-thaw procedure and sequential culture, were able to establish an endometrial three-dimensional model. Conclusions We herein established a model of in vitro cultured endometrium as a potential therapeutic option for refractory thin endometrium. The three-dimensional culture model with endometrial epithelial and stromal cell orchestration via cytokines, membrane-bound molecules, extracellular matrices, and gap junction will provide a new framework for exploring the mechanisms underlying the phenomenon of implantation. Additionally, modified embryo culture, so-called “in vitro implantation”, will be possible therapeutic approaches in fertility treatment.

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