Modulation of the Notch System in Response to Wnt Inhibition Induces Restoration of the Rat Luteal Function
- PMID: 32046463
- DOI: 10.1007/s43032-019-00043-2
Modulation of the Notch System in Response to Wnt Inhibition Induces Restoration of the Rat Luteal Function
Abstract
The aim of this study was to investigate whether the Notch pathway is modulated in response to the downregulation of the Wnt/Β-catenin system in corpora lutea (CLs) from superovulated rats. To this end, we analyzed the effect of in vitro CL Wnt/Β-catenin inhibition on the expression of Notch members and on luteal function. Mechanically isolated rat CLs were cultured with ICG-001, a Wnt/B-catenin inhibitor. In this system, Wnt/B-catenin inhibition reduced progesterone production and decreased StAR protein levels. Besides, Wnt/B-catenin inhibition stimulated the Notch system, evidenced by an increase in Hes1 expression, and promoted the expression of selected Notch family members. At long incubation times, StAR levels and progesterone concentration reached the control values, effects probably mediated by the Notch pathway. These results provide the first evidence of a compensatory mechanism between Wnt/B-catenin signaling and the Notch system, which contributes to the homeostasis of luteal cells.
Keywords: Corpus luteum; HES1; Notch; StAR; WNT/B-catenin.
References
-
- Stouffer RL. The function and regulation of cell populations comprising the corpus luteum during the ovarian cycle.: San Diego: Elsevier, Academic Press; 2004.
-
- Stocco C, Telleria C, Gibori G. The molecular control of corpus luteum formation, function, and regression. Endocr Rev. 2007;28(1):117–49. - DOI
-
- Stocco DM, Clark BJ. Regulation of the acute production of steroids in steroidogenic cells. Endocr Rev. 1996;17(3):221–44. - PubMed
-
- Artavanis-Tsakonas S, Rand MD, Lake RJ. Notch signaling: cell fate control and signal integration in development. Science. 1999;284(5415):770–6. - DOI
-
- Logan CY, Nusse R. The Wnt signaling pathway in development and disease. Annu Rev Cell Dev Biol. 2004;20:781–810. - DOI
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