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Human pluripotent stem cell-derived cells endogenously expressing follicle-stimulating hormone receptors: modeling the function of an inactivating receptor mutation

ABSTRACT: Human pluripotent stem cell-derived cells endogenously expressing follicle-stimulating hormone receptors: modeling the function of an inactivating receptor mutation

PROVIDER: PRJNA764207 | ENA |

REPOSITORIES: ENA

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Human pluripotent stem cell-derived cells endogenously expressing follicle-stimulating hormone receptors: modeling the function of an inactivating receptor mutation

Project description:Follicle-stimulating hormone (FSH) is crucial in the development and regulation of reproductive functions. The actions of human FSH and its receptor (FSHR) and mutations therein have mainly been studied using in vivo models, primary cells, cancer cells and cell lines ectopically expressing the FSHR. To allow studies of endogenous FSHR function in vitro, we differentiated FSHR-expressing cells from human pluripotent stem cells. FSH stimulation of the wild-type (WT), but not the inactivating Finnish founder mutant (A189V) receptor, activated the canonical cAMP-dependent signaling pathway and downstream mediators. Interestingly, the WT and A189V mutant receptors activated distinct pathways in a G-protein-coupled receptor signaling assay. FSH stimulation of WT FSHR-expressing cells induced phosphorylation of PI3Kp85a/g, MAPKAPK2 and proteins involved in calcium-dependent signaling, among others, while in the A189V mutant cells FSH induced phosphorylation of e.g., P90RSK, ERK3, and focal adhesion kinase. Lastly, we expressed FSHR in HEK293 cells followed by affinity purification mass spectrometry analyses, to investigate protein-protein interaction partners of FSHR at resting state and upon FSH stimulation. We found 19 specific high-confidence interacting proteins for WT FSHR and 14 for A189V FSHR, several of which have been linked to infertility. In conclusion, our protocol allows detailed studies of FSH action and disease modeling in human cells endogenously expressing FSHR.

2022-05-01 | GSE184352 | GEO

RNA-Seq in porcine ovaries treated with recombinant pig follicle-stimulating hormone (rpFSH)

Project description:To identify the DE mRNA and lncRNA between the recombinant pig follicle-stimulating hormone traetment group and control grooup.

2022-02-21 | GSE192605 | GEO

Human pluripotent stem cell-derived cells endogenously expressing follicle-stimulating hormone receptors: modeling the function of an inactivating receptor mutation.

Project description: Not available

| S-EPMC9308958 | biostudies-literature

Intra-pituitary follicle-stimulating hormone signaling regulates hepatic lipid metabolism

Project description:Inter-organ communication is a major hallmark of health and is often orchestrated by hormones released by the anterior pituitary gland. Pituitary gonadotropes secrete follicle-stimulating hormone (FSH) and luteinizing hormone (LH) to regulate gonadal function and control fertility. Whether FSH and LH also act on organs other than the gonads is debated. Here, we found that gonadotrope depletion in adult female mice triggers profound hypogonadism, obesity, glucose intolerance, fatty liver, and bone loss. The absence of sex steroids precipitates these phenotypes, with the notable exception of fatty liver, which results from ovary-independent actions of FSH. We uncover paracrine FSH action on pituitary corticotropes as a novel mechanism to restrain the production of corticosterone and prevent hepatic steatosis. Our data demonstrate that functional communication of two distinct hormone-secreting cell populations in the pituitary regulates hepatic lipid metabolism.

2023-01-11 | GSE216096 | GEO

RNA-Seq in porcine ovaries treated with recombinant pig follicle-stimulating hormone (rpFSH)

Project description:RNA-Seq in porcine ovaries treated with recombinant pig follicle-stimulating hormone (rpFSH)

| PRJNA792332 | ENA

Leydig cells express follicle-stimulating hormone receptors in African catfish.

Project description: Not available

| S-EPMC2732288 | biostudies-literature

Follicle-Stimulating Hormone Glycobiology.

Project description: Not available

| S-EPMC6534497 | biostudies-literature

Melatonin, as a downstream molecule of follicle-stimulating hormone, improves nutrient accumulation and mitochondrial function in mammalian oocytes.

Project description:Background: Melatonin (MLT) supplementation has been shown to improve the quality of oocytes and embryos in vitro through its antioxidant mechanism. However, it is unclear whether endogenous MLT plays a role in oocyte quality control, casting doubt on the rationality of oral MLT in improving oocyte quality or fecundity. Methods:we measured the effects of PMSG on MLT synthesis in follicles, evaluated the effects of MLT on oocyte growth and quality in mice and goat, used RNA-seq to explore the mechanism underlying MLT’s effects on oocyte growth and quality, and generated SNAT-knockout mice to assess the effects of endogenous MLT on oocyte growth and quality. Lastly, we investigated the feasibility of short-term MLT intake to improve the fertility of older mice. Result: we revealed that the follicle-stimulating hormone induces the expression of intra-ovarian SNAT, resulting in increased levels of intra-ovarian MLT in mice. Administering MLT during the gonadotropin-dependent phase improved the oocyte size and quality in both mice and goat by enhancing nutrient accumulation and mitochondrial function. Deficiency of MLT in mice reduced oocyte size and weakened mitochondrial function. Furthermore, our findings demonstrate that short-term MLT intake during the gonadotropin phase improves the litter size of older mice. Conclusion: This study reveals that endogenous MLT is involved in determining oocyte quality as a target molecule of follicle-stimulating hormone, shedding light on its potential utilization in improving oocyte quality or rejuvenating aged mammalian oocytes.

2023-08-12 | GSE240209 | GEO

Testicular development in mice lacking receptors for follicle stimulating hormone and androgen.

Project description: Not available

| S-EPMC3325994 | biostudies-literature

Transcription profiling of mouse testicular response to recombinant follicle stimulating hormone (rFSH) in hypogonadal males

Project description:In the normal mouse the pituitary gonadotrophins determine development, maturation and physiological regulation of the testis with follicle-stimulating hormone (FSH) activating the Sertoli cell and luteinising hormone (LH) the Leydig cell. To look at the potential interaction of cell types within the testis following hormone stimulation we have investigated the effect of rFSH on testicular gene expression in the hypogonadal (hpg) male mouse. Due to a deletion in the gene encoding gonadotrophin-releasing hormone (GnRH), FSH and LH levels are at the lower limit of detection in the circulation and mice remain in a pre-pubertal state throughout life unless given exogenous hormone. Here we have addressed important question of changes in the global gene expression profile of testicular tissue following hormone stimulation (rFSH) for 12, 24 and 72h following injections compared to control untreated hpg males of the same age. Experiment Overall Design: Adult 10 week old hpg males were injected sc with 8 I.U. of rFSH (Gonal F, Serono Pharmaceuticals) in 0.2ml of PBS (Sigma,UK) every 12 h for 12, 24 and 72 h. Mice were killed one hour after the last injection by cervical dislocation, testes dissected out, weighed and snap frozen in liquid nitrogen. Tissue was stored at -70oC until use. RNA was extracted using Qiagen RNeasy Lipid Tissue Mini kit (Qiagen, Valencia, CA) according to the manufacturerâs instructions and quantified on a NanoDrop ND-1000 (NanoDrop Wilmington, DE). RNA quality was checked using the Agilent bioanalyzer 2100 (Agilent, Santa Clara, CA). Testicular gene expression was examined in four individual mice at 12 and 72 h and 3 mice at 24h using high-density oligonucleotide mouse MOE430A arrays (Affymetrix, Santa Clara, CA), comparison was made with a group of 7 untreated hpg males of the same age.

2009-08-22 | E-GEOD-8924 | biostudies-arrayexpress

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