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RNA sequencing of ICR and Gerbil wounded skin 3 days after wound

ABSTRACT: Mongolian gerbil / ICR mouse Raw sequence reads

PROVIDER: PRJNA362962 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5198908_1.fastq.gz	Fastqsanger.gz
	SRR5198908_2.fastq.gz	Fastqsanger.gz
	SRR5198909_1.fastq.gz	Fastqsanger.gz
	SRR5198909_2.fastq.gz	Fastqsanger.gz

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RNA sequencing of ICR and Gerbil wounded skin 3 days after wound

Project description:RNA sequencing was used to examine RNA expression changes in gerbil wounded skin.

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Transcriptome Profiling Provides Insights into Mongolian Gerbil as an Ideal NAFLD Model : Earlier Onset of Inflammation and Fibrosis as Well as High Expression of HCC-Associated Genes

Project description:Mongolian gerbil (Meriones unguiculatus) is an ideal animal model for non-alcoholic fatty liver disease/nonalcoholic steatohepatitis (NAFLD/NASH) which is under development. Currently, the research and application of Mongolian gerbils have been largely limited due to the lack of genomic and transcriptome information. In the present study, we sought to better understand the underlying mechanism of the rapid development of NASH in high-fat diet (HFD)-fed Mongolian gerbils by analyzing the transcriptome profilings of different modeling times. Eight hub genes CD44, APP, CDC42, CD68, CXCR4, CSF1R, ADGRE1 and FERMT3 were obtained, which are all involved in inflammation response and CDC42 and FERMT3 are associated with hepatocellular carcinoma (HCC). Most of the hub genes showed high expression levels in the first stage of modeling-building (HFD for 4 weeks). We observed that feeding HFD for 4 weeks is sufficient to induce high expression of pro-fibrotic factors such as PDGFB and CTGF and to form collagen deposits. Intriguingly, we found four significant independent prognostic factors for HCC: GPC1, ARPC1B, DAB2 and CFL exhibiting high expression levels during the modeling time. Our findings indicated that, Mongolian gerbil is an ideal NAFLD model with rapid progression in inflammation and fibrosis. Prolonging the modeling time may lead to the formation of NAFLD-related HCC and further research is needed to investigate this possibility.

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Project description:The responsive and abundant lncRNAs to pro-inflammatory factors in human ECs were screened and validated by RNA sequencing and qPCR. ICAM1-related non-coding RNA (ICR) was identified as the most potential candidate. In vivo data confirmed ICR was upregulated in atherosclerotic plaque. Knock down and overexpression experiments showed that ICR plays an essential role for EC adhesion and migration as well as for the expression of its adjacent ICAM1 gene. Mechanistically, we unexpectedly found in quiescent ECs, ICR regulates mRNA stabilization of ICAM1 through a RNA duplex formation mechanism while in activated ECs, ICR modulated ICAM1 transcription via a NF-κB-dependent manner. RNA-seq and PCR analysis demonstrated a vast number of pro-inflammatory genes downstream of NF-κB were regulated by ICR. Further, CHIP assay showed p65 directly binds to ICR promoter and facilitate the transcription. Interestingly, we found p65 phosphorylation and degradation was in turn regulated by ICR, forming a feedback activation of NF-κB signaling. Finally, we screened siRNA of mouse ICR and delivered the shRNA adenovirus by intravenous injection in a high fat diet induced ApoE-/- atherosclerosis model, it was found that both aortic root stenosis and plaque area could be markedly inhibited by suppressing ICR.

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Expression data from renal cortex of ICR-derived Glomerulonephritis (ICGN) mice and ICR mice

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