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Bypassing the Brain Barriers: Upregulation of Serum miR-495 and miR-543-3p Reflects Thyroid-Mediated Developmental Neurotoxicity in the Rat

ABSTRACT: Bypassing the Brain Barriers: Upregulation of Serum miR-495 and miR-543-3p Reflects Thyroid-Mediated Developmental Neurotoxicity in the Rat

PROVIDER: PRJNA1002231 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25516519.fastq.gz	Fastqsanger.gz
	SRR25516520.fastq.gz	Fastqsanger.gz
	SRR25516521.fastq.gz	Fastqsanger.gz
	SRR25516522.fastq.gz	Fastqsanger.gz
	SRR25516523.fastq.gz	Fastqsanger.gz

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Bypassing the brain barriers: upregulation of serum miR-495 and miR-543-3p reflects thyroid-mediated developmental neurotoxicity in the rat.

Project description:Evaluating the neurodevelopmental effects of thyroid-disrupting chemicals is challenging. Although some standardized developmental and reproductive toxicity studies recommend serum thyroxine (T4) measures in developing rats, extrapolating between a serum T4 reduction and neurodevelopmental outcomes is not straightforward. Previously, we showed that the blood-brain and blood-cerebrospinal fluid barriers may be affected by developmental hypothyroidism in newborn rats. Here, we hypothesized that if the brain barriers were functionally disturbed by abnormal thyroid action, then small molecules may escape from the brain tissue and into general circulation. These small molecules could then be identified in blood samples, serving as a direct readout of thyroid-mediated developmental neurotoxicity. To address these hypotheses, pregnant rats were exposed to propylthiouracil (PTU, 0 or 3 ppm) to induce thyroid hormone insufficiency, and dams were permitted to give birth. PTU significantly reduced serum T4 in postnatal offspring. Consistent with our hypothesis, we show that tight junctions of the brain barriers were abnormal in PTU-exposed pups, and the blood-brain barrier exhibited increased permeability. Next, we performed serum microRNA Sequencing (miRNA-Seq) to identify noncoding RNAs that may reflect these neurodevelopmental disturbances. Of the differentially expressed miRNAs identified, 7 were upregulated in PTU-exposed pups. Validation by qRT-PCR shows that miR-495 and miR-543-3p were similarly upregulated in males and females. Interestingly, these miRNAs have been linked to cell junction dysfunction in other models, paralleling the identified abnormalities in the rat brain. Taken together, these data show that miR-495 and miR-543-3p may be novel in vivo biomarkers of thyroid-mediated developmental neurotoxicity.

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Bypassing the Brain Barriers: Upregulation of Serum miR-495 and miR-543-3p Reflects Thyroid-Mediated Developmental Neurotoxicity in the Rat

Project description:We investigated if a serum microRNA signatured correlated with the presence of thyroid-mediated developmental neurotoxicity in the rat. We isolated serum from control (euthyroid) and exposed (hypothyroid) rat pups on PN8. The maternal exposure utilized to induce developmental hypothyroidism was propylthiouracil (PTU). PTU was administered in the drinking water during pregnancy and lactation.

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Project description:Revealing Dominant Regulatory MicroRNA-495-3p that Governs Multiple Epigenetic Modifiers in Gastric Carcinogenesis In this study, we identified miR-495-3p targeting multiple epigenetic modifiers through comprehensive miRNA and mRNA profiling analysis with in silico target prediction in GC. Western blotting assay or quantitative real time PCR was performed to confirm the expression of miR-495-3p and targets of it. We applied miRNA mimics to ectopic overexpression in gastric cancer cells and observed tumor suppressive effects of miR-495-3p in the growth and metastasis of cancer. Also, we confirmed the status of CpG islands of miR-495-3p promoter using methylation specific PCR analysis.

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Project description:The goal of the study was to determine the effect of lentiviral- mediated overexpression of miR-495 (LV-miR-495) on the levels of gene expression in the nuclues accumbens of rats relative to control rats injected with the empty vector (LV-GFP). We used Rat Gene 2.0 ST Affymetrix expression arrays ( to identify genes whose expression levels were downregulated by overexpression of miR-495.

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