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ABSTRACT: Hepatocyte-specific EGFR deletion in mice

PROVIDER: PRJNA1093138 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28491060_1.fastq.gz	Fastqsanger.gz
	SRR28491060_2.fastq.gz	Fastqsanger.gz
	SRR28491061_1.fastq.gz	Fastqsanger.gz
	SRR28491061_2.fastq.gz	Fastqsanger.gz
	SRR28491062_1.fastq.gz	Fastqsanger.gz

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Hepatocyte-specific epidermal growth factor receptor (EGFR) deletion attenuates acetaminophen-induced liver injury in mice [RNA-seq Illumina]

Project description:Epidermal growth factor receptor (EGFR) is mostly known for its proliferative role in liver. Our earlier investigations indicated a paradoxical cell-death promoting facet of EGFR in acetaminophen (APAP)-induced liver injury (AILI) model. The current study investigates this unexpected role of EGFR in promoting AILI using a hepatocyte-specific EGFR deletion mouse model. Hepatocyte-specific EGFR-deficient mice were generated by administering AAV8-TBG-CRE in EGFRfl/fl mice and were subsequently treated with a severely toxic dose (500 mg/kg) of APAP. Liver injury, regeneration and associated signaling pathways were assessed at different time intervals. EGFR deletion significantly attenuated the progression of liver injury (beyond 12hr post-APAP) without altering early liver injury (up to 6 hr) following APAP overdose. Consistently, the key injury initiating events such as APAP-protein adducts formation and early JNK activation remained intact in EGFR-deficient mice. However, EGFR deletion restricted prolonged JNK activation and its mitochondrial translocation, resulting in reduced propagation of mitochondrial damage and release of cell death drivers. Further, the replenishment of antioxidant glutathione (GSH), which is known to limit the progression of liver injury, was strikingly faster in EGFR-deficient mice. RNA-seq analysis and consequent validation revealed marked upregulation of autophagy and its transcriptional regulator TFEB, a key response to remove damaged mitochondria, in EGFR-deficient mice. Paradoxically, EGFR deletion also promoted compensatory liver proliferative response secondary to decreased progression of liver injury. Overall, hepatocyte-specific EGFR deletion halted the progression of AILI. Our study established an unexpected death promoting function of EGFR in AILI progression, which has wide implications in liver biology.

2025-11-13 | GSE309117 | GEO

Hepatocyte-specific epidermal growth factor receptor (EGFR) deletion attenuates acetaminophen-induced liver injury in mice [RNA-seq AVITI]

2025-11-13 | GSE309115 | GEO

Hepatocyte-specific epidermal growth factor receptor (EGFR) deletion attenuates acetaminophen-induced liver injury in mice

Project description:Hepatocyte-specific epidermal growth factor receptor (EGFR) deletion attenuates acetaminophen-induced liver injury in mice

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Mus musculus

Project description:RNA-sequencing of hepatocyte specific ABCA1 deletion mice

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Hepatocyte-specific epidermal growth factor receptor (EGFR) deletion attenuates acetaminophen-induced liver injury in mice [RNA-seq AVITI]

Project description:Hepatocyte-specific epidermal growth factor receptor (EGFR) deletion attenuates acetaminophen-induced liver injury in mice [RNA-seq AVITI]

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Hepatocyte-specific epidermal growth factor receptor (EGFR) deletion attenuates acetaminophen-induced liver injury in mice [RNA-seq Illumina]

Project description:Hepatocyte-specific epidermal growth factor receptor (EGFR) deletion attenuates acetaminophen-induced liver injury in mice [RNA-seq Illumina]

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Hepatocyte-specific MET deletion exacerbates acetaminophen-induced hepatotoxicity in mice

Project description:Hepatocyte-specific MET deletion exacerbates acetaminophen-induced hepatotoxicity in mice

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The Skin Barrier Defects Caused by Keratinocyte-Specific Deletion of ADAM17 or EGFR are Based on Highly Similar Proteome and Degradome Alterations

Project description:ADAM17 and EGFR are essential key players for epidermal integrity. Keratinocyte-specific deletion of ADAM17 in mice results in pronounced alterations in terminal differentiation of keratinocytes leading to severe epidermal barrier defects with enhanced transepidermal water loss. Thereby, mice deficient for ADAM17 in keratinocytes phenocopy mice with a keratinocyte-specific deletion of EGFR, highlighting the role of ADAM17 as a “ligand sheddase”, as it sheds membrane bound EGFR ligands from the cell surface and finally modulates EGFR signaling. In this study we aim for the first proteomic / degradomic approach to characterize the disruption of the ADAM17-EGFR signaling axis and its consequences for epidermal barrier formation. Proteomic profiling of the epidermal proteome of mice deficient for either ADAM17 or EGFR in keratinocytes at postnatal days 3 and 10 revealed highly similar protein alterations for ADAM17 and EGFR deficiency. These include massive proteome alterations of structural and regulatory components important for barrier formation, like transglutaminases, involucrin, S100 protein family members and S100 fused-type proteins, such as filaggrin, filaggrin-2 and hornerin. Cleavage site analysis using TAILS reveals, among other ADAM17 dependent cleavage sites, increased proteolytic processing of S100 fused-type proteins, including filaggrin-2. Alterations in proteolytic processing are supported by altered protein abundance of numerous proteases upon keratinocyte-specific Adam17 or Egfr deletion, among them kallikreins, cathepsins and their inhibitors. In addition, N-terminal proteomics indicated usage of alternative translation start sites. This study highlights the essential role of proteolytic processing for maintenance of a functional epidermal barrier. Furthermore it suggests that most defects in formation of the postnatal epidermal barrier upon keratinocyte-specific ADAM17 deletion are mediated via EGFR.

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Project description:Hepatocyte-specific deletion of DNA methyltransferases Dnmt3a and Dnmt3b in mice

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RNA-sequencing of hepatocyte specific ABCA1 deletion mice

Project description:ATP binding cassette transporter A1 (ABCA1) regulates cellular cholesterol efflux. We characterized the gene expression changes following hepatocyte specific ABCA1 deletion in mice. We report that genes and pathways related to lipogenesis were downregulated in mice with hepatocyte specific ABCA1 deletion compared to floxed controls.

2017-06-06 | GSE96093 | GEO

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