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CXCR4 DRIVES HEPATOCYTE REPROGRAMMING IN ALCOHOL-RELATED LIVER DISEASE

ABSTRACT: CXCR4 DRIVES HEPATOCYTE REPROGRAMMING IN ALCOHOL-RELATED LIVER DISEASE

PROVIDER: PRJNA818680 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18432523.fastq.gz	Fastqsanger.gz
	SRR18432524.fastq.gz	Fastqsanger.gz
	SRR18432525.fastq.gz	Fastqsanger.gz
	SRR18432526.fastq.gz	Fastqsanger.gz
	SRR18432527.fastq.gz	Fastqsanger.gz

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CXCR4 DRIVES HEPATOCYTE REPROGRAMMING IN ALCOHOL-RELATED LIVER DISEASE

Project description:Backgruound and aims: Loss of hepatocyte identity is associated with impaired liver function in alcohol-related hepatitis (AH). However, the mechanisms and the impact of hepatocyte reprogramming in liver disease are poorly understood. Here we show that both hepatocytes expressing KRT7 (hepatobiliary (HB) cells) and ductular reaction cells were increased in decompensated cirrhotic patients and AH, but only HB cells correlated with poor liver function, reduced liver synthetic capacity and poor outcome. Transcriptomic analysis of microdissected HB cells revealed the expression of biliary-specific genes and a mild reduction of hepatocyte metabolism. Functional analysis identified pathways involved in hepatocyte reprogramming together with inflammatory, stemness and cancer gene programs. In this context, CXCR4 pathway was highly enriched in HB cells, and CXCR4 correlated with disease severity and reduced expression of hepatocyte transcription factors and albumin. Mechanistically, TGFβ induced the expression of CXCR4 in primary hepatocytes, and its ligand CXCL12 promoted hepatocyte reprogramming. Liver overexpression of CXCR4 in chronic liver injury decreased hepatocyte gene expression and promoted liver injury. Pharmacological inhibition of CXCR4 reverted hepatocyte loss of identity and reduced ductular reaction and fibrosis progression. Conclusions: This study shows the association of hepatocyte reprogramming with disease progression and poor outcome in AH. Moreover, we identify CXCR4 as a driver of hepatocyte reprogramming as well as a potential therapeutic target in chronic liver injury.

2023-04-06 | GSE199168 | GEO

NOTCH-YAP1/TEAD-DNMT1 axis drives hepatocyte reprogramming into intrahepatic cholangiocarcinoma

Project description:NOTCH-YAP1/TEAD-DNMT1 axis drives hepatocyte reprogramming into intrahepatic cholangiocarcinoma

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NOTCH-YAP1/TEAD-DNMT1 axis drives hepatocyte reprogramming into intrahepatic cholangiocarcinoma [ChIP-Seq]

Project description:NOTCH-YAP1/TEAD-DNMT1 axis drives hepatocyte reprogramming into intrahepatic cholangiocarcinoma [ChIP-Seq]

| PRJNA824732 | ENA

NOTCH-YAP1/TEAD-DNMT1 axis drives hepatocyte reprogramming into intrahepatic cholangiocarcinoma [RNA-Seq]

Project description:NOTCH-YAP1/TEAD-DNMT1 axis drives hepatocyte reprogramming into intrahepatic cholangiocarcinoma [RNA-Seq]

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Gene expression pattern in CXCR4+ and CXCR4- subpopulation of breast cancer cells

Project description:The goal of this study was to identify signalling molecules downstream of CXCR4 in breast cancer cells. For this purpose, we sorted CXCR4-positive and CXCR4-negative cells from MDA-MB-231 breast cancer cell line by flow cytometry and performed microarrays analysis. Three sets of samples, each in quadruplicate, were analyzed. These include CXCR4-positive subpopulation, CXCR4-positive subpopulation treated with SDF-1 (ligand for CXCR4, also called CXCL12) for one hour and CXCR4-negative subpopulation.

2010-04-28 | E-GEOD-15893 | biostudies-arrayexpress

NOTCH-YAP1/TEAD-DNMT1 axis drives hepatocyte reprogramming into intrahepatic cholangiocarcinoma [bulk RNA-Seq]

Project description:NOTCH-YAP1/TEAD-DNMT1 axis drives hepatocyte reprogramming into intrahepatic cholangiocarcinoma [bulk RNA-Seq]

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CXCR4 drives lympho-myeloid fate of hematopoietic progenitors via mTOR and mitochondrial metabolic pathways

Project description:Hematopoietic stem and progenitor cells (HSPCs), including the multipotent progenitors (MPPs), are responsible for replenishing immune cells. They reside in bone marrow (BM) endosteal and (peri)-vascular niches, which provide all cellular and molecular components required for their lifelong maintenance and fate. Among them, the CXCL12 chemokine and one of its receptor, CXCR4, exert a dominant role in promoting HSPC retention and quiescence. These processes are deregulated in the WHIM Syndrome (WS), a rare immunodeficiency caused by inherited heterozygous autosomal gain-of-function CXCR4 mutations that affect homologous desensitization of the receptor. Clinically, WS is notably characterized by severe, chronic circulating lymphopenia whose mechanisms remain to be elucidated. Using a mouse model carrying a naturally occurring WS-linked Cxcr4 mutation, we explored the possibility that the lymphopenia in WS originates from defects at the MPP level in BM. The global strategy consists in performing high-throughput RNA-seq analyses of the different MPP subsets bearing or not the WS-linked Cxcr4 mutation to investigate the impact of the gain-of-Cxcr4-function on the molecular identity of MPP subsets.

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Gene expression pattern in CXCR4+ and CXCR4- subpopulation of breast cancer cells

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Project description:Antibodies and derivative drugs targeting immune checkpoints have been approved for the treatment of several malignancies, but there are fewer responses in patients with pancreatic cancer. Here, we designed a nanobody molecule with bi-targeting on PD-L1 and CXCR4, as both targets are overexpressed in many cancer cells and play important roles in tumorigenesis. The nanobody sequences targeting PD-L1 and CXCR4 were linked by the (G4S)3 flexible peptide to construct the anti-PD-L1/CXCR4 bispecific nanobody. The bispecific nanobody was expressed in E. coli cells and purified by affinity chromatography. The purified nanobody was biochemically characterized by mass spectrometry, Western blotting and flow cytometry to confirm the molecule and its association with both PD-L1 and CXCR4. The biological function of the nanobody and its anti-tumour effects were examined.

2023-03-11 | PXD037102 | Pride

CXCR4 drives lympho-myeloid fate of hematopoietic progenitors via mTOR and mitochondrial metabolic pathways

Project description:CXCR4 drives lympho-myeloid fate of hematopoietic progenitors via mTOR and mitochondrial metabolic pathways

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