Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Hepatocyte-derived DPP4 regulates portal GLP-1 bioactivity, glucose production and its absence alters liver disease progression (LIVER)

ABSTRACT: Hepatocyte-derived DPP4 regulates portal GLP-1 bioactivity, glucose production and its absence alters liver disease progression (LIVER)

PROVIDER: PRJNA905423 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Hepatocyte-derived DPP4 regulates portal GLP-1 bioactivity, glucose production and its absence alters liver disease progression (LIVER)

Project description:Elevated circulating dipeptidyl-peptidase 4 (DPP4) is a biomarker for liver disease, but its involvement in gluconeogenesis and metabolic associated fatty liver disease (MAFLD) progression remains unclear. Here we identified that DPP4 in hepatocytes but not Tie2+ endothelial cells regulates the local bioactivity of incretin hormones and gluconeogenesis. However, the complete absence of DPP4 (Dpp4-/-) in aged mice with metabolic syndrome accelerates liver fibrosis without altering dyslipidemia and steatosis. Analysis of transcripts from the livers of Dpp4-/- mice displayed enrichment for inflammasome, p53, and senescence programs compared to littermate controls. High-fat high-cholesterol (HFHC)-feeding decreased Dpp4 expression in F4/80+ cells, with only minor changes in immune signaling.

2023-01-31 | GSE218765 | GEO

Hepatocyte-derived DPP4 regulates portal GLP-1 bioactivity, glucose production and its absence alters liver disease progression (F480+ CELLS)

2023-01-31 | GSE218766 | GEO

Hepatocyte-derived DPP4 regulates portal GLP-1 bioactivity, glucose production and its absence alters liver disease progression

Project description:Hepatocyte-derived DPP4 regulates portal GLP-1 bioactivity, glucose production and its absence alters liver disease progression

| PRJNA905419 | ENA

Hepatocyte-derived DPP4 regulates portal GLP-1 bioactivity, glucose production and its absence alters liver disease progression (F480+ CELLS)

Project description:Hepatocyte-derived DPP4 regulates portal GLP-1 bioactivity, glucose production and its absence alters liver disease progression (F480+ CELLS)

| PRJNA905422 | ENA

Hepatocyte-derived DPP4 regulates portal GLP-1 bioactivity, glucose production and its absence alters liver disease progression

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-01-31 | GSE218767 | GEO

Transcriptomic signatures of progressive and regressive liver fibrosis and portal hypertension

Project description:Persistent liver injury triggers a fibrogenic program that causes pathologic remodelling of the hepatic microenvironment (i.e., liver fibrosis) and portal hypertension. The dynamics of gene regulation during liver disease progression and regression remain understudied. Here, we generated hepatic transcriptome profiles in two well-established liver disease models at peak fibrosis and during spontaneous regression after the removal of the inducing agents. We linked the dynamics of key liver disease readouts, such as portal pressure, collagen proportionate area, and transaminase serum levels, to most differentially expressed genes, enabling the identification of transcriptomic signatures of progressive vs. regressive liver fibrosis and portal hypertension. These candidate biomarkers (e.g., Scube1, Tcf4, Src, Hmga1, Trem2, Mafk, Mmp7) were also validated in RNA-seq datasets of patients with cirrhosis and portal hypertension. Finally, deconvolution analysis identified major cell types and suggested an association of macrophage and portal hepatocyte signatures with portal hypertension and fibrosis area in both models.

2024-02-13 | E-MTAB-13804 | biostudies-arrayexpress

Identification of a portal vessel-associated fetal liver hematopoietic stem cell niche

Project description:Whereas the cellular basis of the hematopoietic stem cell (HSC) niche in the bone marrow has been characterized, the nature of the fetal liver (FL) niche is not yet elucidated. We show that Nestin+NG2+ pericytes associate with portal vessels, forming a niche promoting HSC expansion. Nestin+NG2+ cells and HSCs scale during development with the fractal branching patterns of portal vessels, tributaries of the umbilical vein. After closure of the umbilical inlet at birth, portal vessels undergo a transition from Neuropilin-1+Ephrin-B2+ artery to EphB4+ vein phenotype, associated with a loss of peri-portal Nestin+NG2+ cells and emigration of HSCs away from portal vessels. These data support a model in which HSCs are titrated against a peri-portal vascular niche with a fractal-like organization enabled by placental circulation. Characterization of the transcriptome of fetal liver and adult bone marrow niche using RNA-seq

2015-12-03 | E-GEOD-72341 | biostudies-arrayexpress

GIMAP5 maintains liver sinusoidal endothelial cell identity and prevents portal hypertension

Project description:Chronic liver disease is a major leading cause of portal hypertension that affects approximately 1.5 billion people globally. We show that GIMAP5, a small organellar GTPase, is selectively expressed in liver endothelial cells and human GIMAP5 deficiency causes portal hypertension with capillarization of liver sinusoidal endothelial cells (LSECs). LSEC capillarization is recapitulated in GIMAP5 loss-of-function (LOF) mice, and upon conditional Gimap5 deletion in endothelial cells. Single cell RNA-sequencing analyses reveals replacement of LSECs with capillarized endothelial cells and expansion of liver lymphatic endothelial cells in GIMAP5 LOF mice, and places GIMAP5 upstream of GATA4, a transcription factor required for LSEC-specification. Our studies reveal that GIMAP5 prevents portal hypertension by maintaining LSEC identity and suggest that LSEC is an induced endothelial cell state.

2021-03-01 | GSE158988 | GEO

Liver expression data from 1 week old mouse portal tracts

Project description:Intrahepatic biliary and arterial development proceed with complex orchestrations involving Notch, TgfB, Wnt and Vegf signaling within the portal tracts of the liver. These pathways coordinate morphogenesis and remodeling temporally and spatially from mid-gestation through early postnatal life. We used microarrays to examine changes in remodeling/differentiation programs in portal tracts at 1 week postanally, comparing Jag1+/-Rfng+/- and controls.

2014-11-05 | E-GEOD-62991 | biostudies-arrayexpress

Identification of a portal vessel-associated fetal liver hematopoietic stem cell niche

2015-12-03 | GSE72341 | GEO