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The effects of Mkp-1 knockout and systemic E. coli infection on the transcriptome of the liver

ABSTRACT: The effects of Mkp-1 knockout and systemic E. coli infection on the transcriptome of the liver

PROVIDER: PRJNA506211 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8209800.fastq.gz	Fastqsanger.gz
	SRR8209810.fastq.gz	Fastqsanger.gz
	SRR8209820.fastq.gz	Fastqsanger.gz
	SRR8209791.fastq.gz	Fastqsanger.gz
	SRR8209801.fastq.gz	Fastqsanger.gz

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The effects of Mkp-1 knockout and systemic E. coli infection on the transcriptome of the liver

Project description:Previously, I have found that Mkp-1 knockout exacerbates inflammation, perturbs lipid metabolism, increases organ damage, mortality, and bacterial burdens. To understand the role of Mkp-1 in the regulation of host defense, we performed RNA-seq analysis using total RNA isolated from livers of uninfected and E. coli-infected wildtype and Mkp-1 knockout mice. Specifically, Mkp-1 wildtype and knockout (both on the C57/129 background) mice were infected with E. coli (O55:B5, ATCC 12014) at a dose of 2.5×107 CFU/g of body weight i.v., or given same volume of PBS. Mice were sacrificed 24 h post-infection to harvest organs. Livers were frozen clamping in liquid nitrogen, and stored at -80°C . Total RNA was isolated with Trizol and used for RNA-seq. RNA-seq results indicate that both E. coli infection and Mkp-1 knockout caused profound changes in the transcriptomes in the mouse livers.

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Transcriptome analysis of potential candidate genes and molecular pathways in colitis-associated colorectal cancer of Mkp-1-deficient mice

Project description:The nuclear phosphatase mitogen-activate protein kinase phosphatase-1 (MKP-1) is a key negative regulator of the innate immune response through the regulation of the biosynthesis of proinflammatory cytokines. In colorectal cancer (CRC), which is induced mainly by chronic inflammation, Mkp-1 overexpression was found in addition to disturbances in Mkp-1 functions, which may play a role in cancer development in different types of tumors. However, the potential molecular mechanisms by which Mkp-1 influences CRC development is not clear. Here, we performed global gene expression profiling of Mkp-1 KO mice using RNA sequencing (RNA-seq) to explore the role of Mkp-1 in CRC progression using transcriptome analysis.

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Project description:Prenatal dexamethasone exposure (PDE) has long-term consequences in bone development. we investigated how PDE exerts persistent effect on bone metabolism in mouse offspring. Our results showed that PDE offspring exhibited reduced bone mass, fewer osteoblasts and diminished osteoprogenitors proliferation.And PDE increased MKP-1 expression, while decreasing H3 lysine 9 dimethylation (H3K9me2) at Mkp-1 gene locus. Mechanistically, dexamethasone suppressed osteoprogenitors proliferation by upregulating MKP-1 expression, notably through the inhibition of H3K9me2 modifications, which promoted demethylation and transcriptional activation of the Mkp-1 gene. Importantly, restoring histone methylation balance with PFI-90 treatment blocked the inhibitory effects of PDE on MAPK signaling in osteoprogenitors, and mitigated the detrimental impact of PDE on osteoprogenitor proliferation and bone development in the offspring. Therefore,we performed ChIP-seq for H3K9me2 to identify its role in related epigenetic changes.

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Project description::Systemic duress, like that elicited by sepsis, burns or trauma, predispose patients to nosocomial pneumonia, demanding better understanding of host pathways influencing this deleterious connection. These pre-existing circumstances are capable of triggering the hepatic acute phase response (APR), which we previously demonstrated is essential for limiting susceptibility to secondary lung infections. To identify potential mechanisms underlying protection afforded by the lung-liver axis, our studies aimed to evaluate liver-dependent lung reprogramming when a systemic inflammatory challenge precedes pneumonia. WT mice and APR-deficient littermates lacking hepatocyte STAT3 (hepSTAT3-/-), a transcription factor necessary for full APR initiation, were challenged intraperitoneally with LPS to induce endotoxemia. After 18h, pneumonia was induced by intratracheal E. coli instillation. Endotoxemia elicited significant transcriptional alterations in the lungs of WT and hepSTAT3-/- mice, with nearly 2,000 differentially expressed genes between genotypes. The gene signatures revealed exaggerated immune activity in the lungs of hepSTAT3-/- mice, which were compromised in their capacity to launch additional cytokine responses to secondary infection. Proteomics revealed substantial liver-dependent modifications in the airspaces of pneumonic mice, implicating a network of dispatched liver-derived mediators influencing lung homeostasis. These results indicate that following systemic inflammation, liver acute phase changes dramatically remodel the lungs, resulting in a modified landscape for any stimuli encountered thereafter. Based on the established vulnerability of hepSTAT3-/- mice to secondary lung infections, we believe that intact liver function is critical for maintaining the immunological responsiveness of the lungs. Further studies are needed to confirm whether and how such lung changes directly influence pneumonia susceptibility.

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Project description:We studied the response to infection and associated perturbations to the bovine liver’s normal function by examining gene transcription data from liver biopsies collected following an E. coli infection in the udder of primiparous dairy cows. This is the first study to examine gene transcription responses to systemic infection by the E. coli bacterium in dairy cows. First, we verified that the inoculation protocol resulted in systemic infection in the cows. This was done based on records on three clinical symptoms: body temperature and amount of E. coli bacteria and leukocytes in milk samples. Second, we examined gene transcription patterns underlying the clinical traits. Gene transcription levels at times of peak values for the clinical traits were estimated in the liver to study indications of an acute phase response to systemic E. coli infection in the cows. Finally, we compared gene transcription responses to E. coli infection and lipopolysaccaride (LPS) inoculation. Sixteen healthy, primiparous Danish Holstein-Friesian cows were challenged intramammarily with E. coli 4 to 6 weeks following parturition. Gene transcription levels for fifteen of the cows were used to study infection responses. We compared gene transcription levels before and after E. coli infection for all fourteen cows.

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