RGD Reference Report - Expression and functional analysis of endoglin in isolated liver cells and its involvement in fibrogenic Smad signalling. - Rat Genome Database

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Expression and functional analysis of endoglin in isolated liver cells and its involvement in fibrogenic Smad signalling.

Authors: Meurer, SK  Tihaa, L  Borkham-Kamphorst, E  Weiskirchen, R 
Citation: Meurer SK, etal., Cell Signal. 2011 Apr;23(4):683-99. doi: 10.1016/j.cellsig.2010.12.002. Epub 2010 Dec 10.
RGD ID: 7257529
Pubmed: PMID:21146604   (View Abstract at PubMed)
DOI: DOI:10.1016/j.cellsig.2010.12.002   (Journal Full-text)

Endoglin is an accessory component of the TGF-beta-binding receptor complex that differentially modulates TGF-beta and BMP responses. The existence of two splice variants L- and S-endoglin which differ in their cytoplasmic domain has already been shown in human and mice. Endoglin is located on the cell surfaces of cultured hepatic stellate cells and transdifferentiated myofibroblasts suggesting that this receptor might be associated with the profibrogenic attributes of these liver cell subpopulations. We now show that endoglin expression is increased in transdifferentiating hepatic stellate cells and in two models of liver fibrosis (i.e. bile duct ligation and carbon tetrachloride model) and further detectable in cultured portal fibroblasts representing another important fibrogenic cell type but not in hepatocytes. In respect to TGF-beta1-signalling, we demonstrate that endoglin interacts with and is phosphorylated by TbetaRII. In hepatic stellate cells, TGF-beta1 upregulates endoglin expression most likely via the ALK5 pathway and requires the SP1 transcription factor. We further identified a novel rat splice variant that is structurally and functionally different from that identified in human and mouse. Transient overexpression of endoglin resulted in a strong increase of TGF-beta1-driven Smad1/5 phosphorylation and alpha-smooth muscle actin expression in a hepatic stellate cell line. In supernatants of respective cultures, we could detect the ectodomain of endoglin suggesting that shedding is a further key process involved in the regulation of this surface receptor.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Chemical and Drug Induced Liver Injury  ISOEng (Rattus norvegicus)7257529; 7257529protein:increased expression:liver (rat)RGD 
Chemical and Drug Induced Liver Injury  IEP 7257529protein:increased expression:liver (rat)RGD 
cholestasis  ISOEng (Rattus norvegicus)7257529; 7257529protein:increased expression:liver (rat)RGD 
cholestasis  IEP 7257529protein:increased expression:liver (rat)RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
positive regulation of gene expression  IMP 7257529Acta2RGD 
positive regulation of protein phosphorylation  IMP 7257529Smad1 and Smad5RGD 

Molecular Function

Objects Annotated

Genes (Rattus norvegicus)
Eng  (endoglin)
Tgfbr2  (transforming growth factor, beta receptor 2)

Genes (Mus musculus)
Eng  (endoglin)

Genes (Homo sapiens)
ENG  (endoglin)


Additional Information