Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pone.0034206
Title: Unique cell type-specific junctional complexes in vascular endothelium of human and rat liver sinusoids
Authors: Géraud C.
Evdokimov K. 
Straub B.K.
Peitsch W.K.
Demory A.
Dörflinger Y.
Schledzewski K.
Schmieder A.
Schemmer P.
Augustin H.G.
Schirmacher P.
Goerdt S.
Keywords: alpha catenin
beta catenin
cadherin
cell membrane protein
cell receptor
claudin 5
Fc receptor IIb
junctional adhesion molecule A
mannose receptor
occludin
plakoglobin
protein JAM B
protein JAM C
protein p120
protein ZO1
protein ZO2
stabilin 1 protein
stabilin 2 protein
unclassified drug
cadherin
cell adhesion molecule
claudin
CLDN5 protein, human
JAM3 protein, human
leukocyte antigen
membrane protein
occludin
vascular endothelial cadherin
adult
aged
animal cell
article
blood vessel permeability
cell function
cell junction
cell migration
cell specificity
cell type
clinical article
controlled study
endothelium cell
female
hepatitis
human
human tissue
immunoreactivity
liver metastasis
liver sinusoid
lymph vessel endothelium
male
nonhuman
protein expression
protein structure
rat
tight junction
vascular endothelium
animal
antibody specificity
blood vessel
cytology
endothelium cell
gene expression regulation
genetics
liver
liver disease
metabolism
middle aged
pathology
protein transport
Sprague Dawley rat
tumor cell line
vascularization
Rattus
Aged
Animals
Antigens, CD
Blood Vessels
Cadherins
Cell Adhesion Molecules
Cell Line, Tumor
Claudins
Endothelial Cells
Female
Gene Expression Regulation
Humans
Intercellular Junctions
Liver
Liver Diseases
Male
Membrane Proteins
Middle Aged
Organ Specificity
Protein Transport
Rats
Rats, Sprague-Dawley
Tight Junctions
Issue Date: 2012
Citation: Géraud C., Evdokimov K., Straub B.K., Peitsch W.K., Demory A., Dörflinger Y., Schledzewski K., Schmieder A., Schemmer P., Augustin H.G., Schirmacher P., Goerdt S. (2012). Unique cell type-specific junctional complexes in vascular endothelium of human and rat liver sinusoids. PLoS ONE 7 (4) : e34206. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0034206
Abstract: Liver sinusoidal endothelium is strategically positioned to control access of fluids, macromolecules and cells to the liver parenchyma and to serve clearance functions upstream of the hepatocytes. While clearance of macromolecular debris from the peripheral blood is performed by liver sinusoidal endothelial cells (LSECs) using a delicate endocytic receptor system featuring stabilin-1 and -2, the mannose receptor and CD32b, vascular permeability and cell trafficking are controlled by transcellular pores, i.e. the fenestrae, and by intercellular junctional complexes. In contrast to blood vascular and lymphatic endothelial cells in other organs, the junctional complexes of LSECs have not yet been consistently characterized in molecular terms. In a comprehensive analysis, we here show that LSECs express the typical proteins found in endothelial adherens junctions (AJ), i.e. VE-cadherin as well as ?-, ?-, p120-catenin and plakoglobin. Tight junction (TJ) transmembrane proteins typical of endothelial cells, i.e. claudin-5 and occludin, were not expressed by rat LSECs while heterogenous immunreactivity for claudin-5 was detected in human LSECs. In contrast, junctional molecules preferentially associating with TJ such as JAM-A, B and C and zonula occludens proteins ZO-1 and ZO-2 were readily detected in LSECs. Remarkably, among the JAMs JAM-C was considerably over-expressed in LSECs as compared to lung microvascular endothelial cells. In conclusion, we show here that LSECs form a special kind of mixed-type intercellular junctions characterized by co-occurrence of endothelial AJ proteins, and of ZO-1 and -2, and JAMs. The distinct molecular architecture of the intercellular junctional complexes of LSECs corroborates previous ultrastructural findings and provides the molecular basis for further analyses of the endothelial barrier function of liver sinusoids under pathologic conditions ranging from hepatic inflammation to formation of liver metastasis. © 2012 Géraud et al.
Source Title: PLoS ONE
URI: https://scholarbank.nus.edu.sg/handle/10635/161991
ISSN: 19326203
DOI: 10.1371/journal.pone.0034206
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