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Stress-regulated miR-708-5p affects recognition memory and manic-like behavior through Neuronatin downregulation.

ABSTRACT: Stress-regulated miR-708-5p affects recognition memory and manic-like behavior through Neuronatin downregulation.

PROVIDER: PRJNA1086400 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28288492.fastq.gz	Fastqsanger.gz
	SRR28288493.fastq.gz	Fastqsanger.gz
	SRR28288494.fastq.gz	Fastqsanger.gz
	SRR28288495.fastq.gz	Fastqsanger.gz
	SRR28288496.fastq.gz	Fastqsanger.gz

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Stress-regulated miR-708-5p affects recognition memory and manic-like behavior through Neuronatin downregulation.

Project description:microRNAs are posttranscriptional regulators that bind to target mRNAs. We tested the regulatory effect of miR-708-5p, a miRNA associated with Bipolar Disorder, in the mouse hippocampus. To unveil molecular mechanisms downstream of miR-708-5p, we stereotactically injected a virus overexpressing miR-708-5p for target discovery.

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Project description:Aging is a major risk factors for osteoarthritis (OA), and cartilage of the elder are more sensitive to mechanical loading stress. Recently, cartilage progenitor cells (CPCs) arose much interests due to its important role in maintaining cartilage homeostasis. However, the potential mechanism of increased sensitivity to mechanical stress in CPCs has not been elucidated. The aim of this study was to investigate the potential links between aging and age-related OA through establish CPCs replicative senescence model and fluid flow shear stress (FFSS) stimulated degeneration model. Small RNA and mRNA sequence were conducted to investigate miRNA-related mechanisms in this process. By gain-and-lost strategy we investigated the age-related miRNAs and their impacts on exacerbating the progression of biomechanical stimulated TMJ-OA. miR-708-5p was identified as age-related miRNA in CPCs, and TLR4 was identified as its direct target through luciferase report assay. Age-related miR-708-5p deficiency increased sensitivity of CPCs for exposure to FFSS by liberating TLR4 expression. Intra-articular delivery agomiR-708-5p alleviated TMJ osteoarthritic cartilage lesions in mice. In conclusion, age-related miR-708-5p deficiency increases the sensitivity to mechanical loading stress and promotes CPCs senescence like degeneration via TLR4.

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Project description:Ageing related deficiency of miR-708-5p in osteoarthritic cartilage lesions

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Project description:Ageing related deficiency of miR-708-5p in osteoarthritic cartilage lesions [RNA]

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Project description:Ageing related deficiency of miR-708-5p in osteoarthritic cartilage lesions [miRNA]

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Downregulation of miR-192-5p and miR-204-5p in nonclassic apparent mineralocorticoid excess

Project description:Downregulation of miR-192-5p and miR-204-5p in nonclassic apparent mineralocorticoid excess

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Suppression of miRNA-708 by polycomb group promotes metastases by calcium-induced cell migration

Project description:The progression of cancer to metastatic disease is a major cause of death. We identified miR-708 being transcriptionally repressed by polycomb repressor complex (PRC2)-induced H3-K27 trimethylation in metastatic breast cancer. miR-708 targets the endoplasmic reticulum protein neuronatin (Nnat) to decrease intracellular calcium (Ca2+) level, resulting in reduction of activation of ERK and FAK, decreased cell migration, and impaired metastases. Functional complementation experiments with Nnat-3’UTR mutant, which is refractory to suppression by miR-708, rescued cell migration and metastasis defects. In breast cancer patients, miR-708 expression was decreased in lymph node and distal metastases, suggesting a metastasis-suppressive role. Our findings uncover a mechanistic role for miR-708 in metastasis and provide a rationale for developing miR-708 as a therapeutic agent against metastatic breast cancer.

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Suppression of miRNA-708 by polycomb group promotes metastases by calcium-induced cell migration

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Increased miR-708 expression in NSCLC and its association with poor survival in lung adenocarcinoma from Never Smokers

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2012-08-03 | GSE36681 | GEO

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