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ABSTRACT: GT1 cuttag-seq

PROVIDER: PRJNA1196702 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31675907_1.fastq.gz	Fastqsanger.gz
	SRR31675907_2.fastq.gz	Fastqsanger.gz
	SRR31675908_1.fastq.gz	Fastqsanger.gz
	SRR31675908_2.fastq.gz	Fastqsanger.gz
	SRR31675909_1.fastq.gz	Fastqsanger.gz

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Project description:Stress is defined as a systemic nonspecific adaptive response to the stimulations from internal and external environment or psychological factors through coordinating series of complex systems, like nervous system, immune system and respiratory system. While it is well known that stress have profound negative effects on reproductive function, the mechanism of reproductive dysfunction is still far from perfect. Kisspeptin, which are known for regulating GnRH synthesis and secretion, affect the initiation of puberty and reproduction, have been shown to express glucocorticoid receptors(GR),and both acute and chronic stress significantly inhibit Kisspeptin expression. So, this study speculated that Kisspeptin might participate in the process of reproductive regulation during stress. However, when constructed stress models of GT1-7 cells(Derived from mouse hypothalamic neurons, could not only transcribe endogenous GnRH mRNA and release GnRH when depolarization, but also express Kisspeptin, G protein-coupled receptors) with DEX and tried to analyze the specific mechanism of stress inhibited Kisspeptin expression, opposite results(Dex improved Kisspeptin expression of GT1-7 cells) were obtained. Based on the neuroimmune system hypothesis of stress, this study speculated that the direct reason of stress inhibited Kisspeptin expression might be stress-induced inflammatory response rather than stress-elevated GC. Even so, the transcription of Il-1β decreased in BV-2 cells(Derived from mouse Microglia) after treated with DEX. Due to the proximity of Kisspeptin neurons and Microgila in arcuate nucleus(ARC) of hypothalamus, it is speculated that there maight be interaction between them. So, this study co-cultured GT1-7 cells and BV-2 cells, and found transcription of Kiss1 decreased and Il-1β increased. Decreased Kisspeptin expression due to inflammation of BV-2 cells and inflammation of BV-2 cells must due to changes of certain substances or molecules in GT1-7 cells after treated with DEX. To further explore the possible mechanism, this study used the highly sensitive miRNAs array to screen miRNAs which not only changed significantly in GT1-7 cells after treated with DEX but also associated with inflammation. Finally, 10 miRNAs obtained and further confirmed mmu-miR-146a-5P could inhibited the LPS-induced BV-2 cells inflammation, M1 polarization and apoptosis.

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