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Bone morphogenetic protein-2 (BMP2) and estradiol-17β (E2)-induced changes in ovarian transcriptome during primordial follicle formation in the mouse ovary

ABSTRACT: Bone morphogenetic protein-2 (BMP2) and estradiol-17β (E2)-induced changes in ovarian transcriptome during primordial follicle formation in the mouse ovary

PROVIDER: PRJNA809013 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18090671.fastq.gz	Fastqsanger.gz
	SRR18090672.fastq.gz	Fastqsanger.gz
	SRR18090673.fastq.gz	Fastqsanger.gz
	SRR18090674.fastq.gz	Fastqsanger.gz
	SRR18090675.fastq.gz	Fastqsanger.gz

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Bone morphogenetic protein-2 (BMP2) and estradiol-17β (E2)-induced changes in ovarian transcriptome during primordial follicle formation in the mouse ovary

Project description:Estradiol-17β (E2) has been shown to promote primordial follicle (PF) formation and to involve BMP2 as a downstream effector to promote PF in the hamsters. However, the molecular mechanism whereby these factors regulate ovarian somatic cells to pre-granulosa cells (preGC) transition leading to PF formation remains unclear. The objective of this study was to determine whether BMP2 and/or E2 would regulate the expression of specific ovarian transcriptome during preGC transition and PF formation in the mouse ovary. BMP2 mRNA level increased during the period of PF formation with concurrent presence of BMP2 protein in ovarian somatic cells. E2 but not BMP2 exposure led to increased expression of ovarian BMP2 mRNA, and the effect of E2 could not be suppressed by LDN 193189 (LDN). Either BMP2 or E2 stimulated PF formation without inducing apoptosis. RNAseq analysis of ovaries exposed to exogenous BMP2 or E2 revealed differential expression of several thousand genes. Most of the differentially expressed genes (DEG), which were common between BMP2 or E2 treatment demonstrated concordant changes, reinforcing the idea of cooperativity between E2 and BMP2 during PF formation. Further, we have Identified E2, in cooperation with BMP2, could affect the expression of three major transcription factors GATA2, GATA4 and EGR2 and one serine protease, hepsin in preGC during PF formation. Taken together, results of this study suggest that E2 and BMP2 may regulate ovarian gene expression that promote somatic cells to preGC transition and PF formation in the mouse ovary.

2022-05-31 | GSE197122 | GEO

Time course experiment of 17β-estradiol (E2) treatment in the zebrafish

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Stimulation of primordial follicle assembly by estradiol-17? requires the action of bone morphogenetic protein-2 (BMP2).

Project description:Primordial follicle (PF) pool determines the availability of follicles for ovulation in all mammals. Premature depletion of the PF reserve leads to subfertility or infertility. Bone morphogenetic protein 2 (BMP2) promotes PF formation by facilitating oocyte and granulosa cell development. Estradiol-17? (E2) upregulates PF formation in developing hamster ovaries. However, if BMP2 mediates E2 effect is not known. We hypothesize that E2 facilitates the effect of BMP2 on somatic to granulosa cell transition. BMP2 and E2 together significantly upregulated the percentage of PFs in hamster fetal ovaries in vitro compared with either of the treatments alone. E2 also promoted BMP2 expression in vivo. Inhibition of BMP2 receptors suppressed E2-stimulation of PF formation while knockdown of BMP2 in vitro significantly suppressed the E2 effect. In contrast, estrogen receptor blocker did not affect BMP2 action. Inhibition of the activity of E2 or BMP2 receptors, either alone or combined during the last two days of the culture (C6-C8) resulted in a significant decrease in PF formation by C8, suggesting that both BMP2 and E2 action is essential for somatic cell differentiation for PF formation. Together, the results suggest that E2 activates BMP2-BMPR system leading to the formation of primordial follicles.

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Bmp2 Is Critical for the Murine Decidual Response

Project description:The role of bone morphogenetic protein 2 (Bmp2)in regulating the transformation of the uterine stroma during embryo implantation in the mouse was investigated by the conditional ablation of Bmp2 in the uterus using the (PR-cre) mouse. Keywords: Genetic modification

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Expression data from the study of the oestrognic activity of glabridin in Ishikawa cells in comparison to 17β-oestradiol (17β-E2)

Project description:The general objective of this study was to investigate the effects of glabridin in Ishikawa cells in comparison to 17β-oestradiol by studying its mechanism of action via Affymetrix GeneChip® PrimeViewTM array The treatments were the unctreated control, 10µM glabridin, 100nM glabridin, 1nM 17β-E2 and the combination treatment of 1nM 17β-E2 with 100nM glabridin. The cells were treated for 72 hours and the RNA were extracted for microarray and RT-qPCR study.

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Mouse primary osteoblasts treated with/without BMP2

2012-03-29 | E-GEOD-36925 | biostudies-arrayexpress

The Conformations of 17β-Estradiol (E2) and 17α-Estradiol as Determined by Solution NMR.

Project description:The conformational structures of the hormone 17β-estradiol (E2) and the epimeric 17α-estradiol determined by solution NMR spectroscopy and restrained molecular dynamics calculations found a single low energy conformation.

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Gene expression profiling of human endometrial stromal cells transduced with BMP2- and WNT4-adenovirus.

Project description:Our previous studies have shown that bone morphogenetic protein 2 (BMP2), a morphogen belonging to the TGFβ superfamily, is markedly induced in human primary endometrial stromal cells (HESC) as they undergo differentiation in response to steroid hormones and cAMP. WNT4 is a downstream target of BMP2 regulation in these cells. To identify the common downstream targets of BMP2 and WNT4 in human endometrial stromal cells, we performed gene expression profling of human ensometrial stromal cell transduced with BMP2 or WNT4 adenovirus. Gene expression profiling revealed that FOXO1, a forkhead family transcription factor and a known regulator of HESC differentiation, is a common downstream mediator of both BMP2 and WNT4 signaling. These studies uncovered a linear pathway involving BMP2, WNT4, and FOXO1 that operates in human endometrium to critically control decidualization.

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