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Seminal plasma promotes decidualization of endometrial stromal fibroblasts from women with and without inflammatory disorders in a manner dependent on IL11 signaling

ABSTRACT: Seminal plasma promotes decidualization of endometrial stromal fibroblasts from women with and without inflammatory disorders in a manner dependent on IL11 signaling

PROVIDER: PRJNA559534 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9940500_1.fastq.gz	Fastqsanger.gz
	SRR9940500_2.fastq.gz	Fastqsanger.gz
	SRR9940510_1.fastq.gz	Fastqsanger.gz
	SRR9940510_2.fastq.gz	Fastqsanger.gz
	SRR9940520_1.fastq.gz	Fastqsanger.gz

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Seminal plasma promotes decidualization of endometrial stromal fibroblasts from women with and without inflammatory disorders in a manner dependent on IL11 signaling

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Seminal plasma promotes decidualization of endometrial stromal fibroblasts from women with and without inflammatory disorders in a manner dependent on IL11 signaling

Project description:Seminal plasma promotes decidualization of endometrial stromal fibroblasts from women with and without inflammatory disorders in a manner dependent on IL11 signaling

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Endometrial extracellular vesicle decidualization

Project description:Proper decidualization is vital in preparation for a potential embryo receptivity, placentation, menstrual health and subsequent endometrial regeneration. Given the importance of extracellular vesicles (EVs) in intercellular communication, and recently in embryo implantation and indicators of menstrual cycle and fertility, we investigated their role during decidualization. Overall, this study provides an insight into distinct variation in sEV composition depending upon the level of decidualization of endometrial stromal cells, with the signaling potential to coordinate endometrial health ranging from embryo implantation, facilitating placentation and subsequent endometrial regeneration.

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Seminal plasma promotes decidualization of endometrial stromal fibroblasts in vitro from women with and without inflammatory disorders in a manner dependent on interleukin-11 signaling.

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Endometrial gland impacts on stromal cell decidualization

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The role of Prokineticin 2 in endometrial decidualization

Project description:Recurrent implantation failure(RIF) is an urgent problem to be solved in reproduction.Currently, endometrium decidualization damage is considered as one of the important causes, but the mechanism is still unclear. Prokineticin 2(PK2) is a newly discovered secreted protein with multiple biological functions, and its role in the endometrium is unknown.Our previous study showed that PK2 was significantly increased in RIF patients, but endometrial decidualization markers PRL and IGFBP1 were lower compared with the control group. We performed transcriptome sequencing, we found there were significant differences between the PK2 overexpression group and the control group. Differential genes mainly involved in decidualization process including adhesion, immunity, chemotaxis, ect.

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Project description:We hypothesized that seminal plasma, the acellular seminal fluid component, influences the endometrium stimulating the immune system and facilitating the implantation. We designed a randomized, double-blinded, placebo-controlled trial, and we used microarray analysis to evaluate differences in the endometrial transcriptomic profile after vaginal seminal plasma application. Differential gene pathways analysis showed an upregulation of pathways associated with the immune response, cell viability, proliferation and cellular movement, implantation, embryo development, oocyte maturation and angiogenesis. We compared our results with similar studies in pigs, mice and in vitro human endometrial cells and found similar and found comparable results. Our data show that seminal plasma has a positive effect on the endometrium during the implantation window.

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Expression data from porcine endometrial epithelial cells induced by seminal exosomes

Project description:Purpose: Seminal fluid (SF) is considered as a regulator on environment establishing in female reproductive tract of various mammal species without mechanism elucidated completely. This study aimed to identified the function of exosome isolated from SF on porcine endometrium. Methods: Total RNA profiles of porcine endometrial epithelial cells with seminal exosomes treatment (EXO.) or not (CTRL.) were generated by deep sequencing, in triplicate, using HiSeq 2500. Trimmed sequences were analyzed on the basis of the TopHat/Cufflinks pipeline based on the porcine genome and reference annotations obtained from Ensembl genome browser (https://www.ensembl.org). Results: 10916 transcripts, from which 70 genes were up-regulated and 114 genes were down-regulated with q-values less than 0.05 in EECs with seminal exosome treatment compared to those without exosome treatment. Conclusions: Through the gene ontology (GO) biological process and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis which revealed significantly enriched or decreased molecular functions, Our work demonstrated that exosomes derived from porcine seminal fluid induced endometrial immune and inflammatory response via CCL20 and AMCFII regulation specifically, which may facilitate sperm cells survival and activation, and resulting in appropriate environment required for fertilization and even implantation.

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IL11 is elevated in systemic sclerosis and IL11-dependent ERK signaling is needed for the profibrotic activity of TGFβ in dermal fibroblasts

Project description:Objectives: Interleukin 11 (IL11) is highly upregulated in skin and lung fibroblasts from patients with systemic sclerosis (SSc). Here we tested whether IL11 is mechanistically linked with human dermal fibroblast (HDF) activation. Methods: We measured serum IL11 levels in healthy volunteers and patients with early diffuse SSc and manipulated IL11 signalling in HDFs using gain- and loss-of-function approaches. Results: In patients with SSc, serum IL11 levels are elevated as compared to healthy controls. Transforming growth factor beta (TGFβ) isoforms 1, 2 or 3 induced IL11 secretion from HDFs, which highly express IL11RA and the gp130 co-receptor, suggestive of an autocrine loop of IL11 activity in HDFs. IL11 consistently and robustly stimulated ERK activation in HDFs and resulted in HDF-to-myofibroblast transformation. IL11 induced STAT phosphorylation to a lesser extent than ERK and only at high IL11 concentrations. IL11-stimulated ERK activation and fibrosis phenotypes were absent in skin fibroblasts from patients with homozygous loss-of-function mutation in IL11RA. Inhibition of IL11 signaling using either a neutralizing antibody against IL11 or siRNA against IL11RA reduced TGFβ-induced HDF proliferation, matrix production and cell migration, which was phenocopied by pharmacologic inhibition of ERK activity. Conclusions: These data reveal an important contribution of IL11-related ERK activity for TGFβ-stimulated fibrosis phenotypes in HDFs and suggest IL11 as a potential therapeutic target in SSc.

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