The mannose receptor on murine liver sinusoidal endothelial cells is the main denatured collagen clearance receptor

Malovic, Ivana; Sørensen, Karen Kristine; Elvevold, Kjetil; Nedredal, Geir I.; Paulsen, Steinar M.; Ерофеев, А. В.; Smedsrød, Bård; McCourt, Peter

doi:10.1002/hep.21639

Cited by 111 publications

(113 citation statements)

References 31 publications

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“…TRITC-labelled formaldehyde-treated BSA (FSA) and DTAFlabelled collagen I α-chains were produced according to standard protocols (5,6). FITClabelled AGE-modified BSA (AGE-BSA) was a kind gift from Dr. Berit Hansen, Heidelberg, Germany.…”

Section: Tail Vein Injections and Immunofluorescence Microscopymentioning

confidence: 99%

Stabilins are expressed in bone marrow sinusoidal endothelial cells and mediate scavenging and cell adhesive functions

Qian¹,

Johansson²,

McCourt³

et al. 2009

Biochemical and Biophysical Research Communications

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Bone marrow sinusoidal endothelial cells have a specific function as a site of transmigration of hematopoietic stem and progenitor cells and mature blood cells between bone marrow and blood stream. However, the specific characteristics of bone marrow sinusoidal endothelial cells are still largely unclear. We here report that these cells express stabilin-1 and stabilin-2, which in liver sinusoidal endothelial cells have been identified as endocytic scavenger receptors for several ligands, including SPARC and hyaluronan. We show here that intravenously injected formaldehyde-treated serum albumin, advanced glycation end-products, and collagen I α-chains were taken up by bone marrow sinusoidal endothelial cells, showing that these cells have a scavenging function and thereby may modulate bone marrow vascular stem cell niches. Importantly, we show that hyaluronan mediated adhesion of hematopoietic stem and progenitor cells to stabilin-2-transfected cells, suggesting that stabilin-2 has a role in adhering circulating stem and progenitor cells to bone marrow.

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Section: Tail Vein Injections and Immunofluorescence Microscopymentioning

confidence: 99%

Stabilins are expressed in bone marrow sinusoidal endothelial cells and mediate scavenging and cell adhesive functions

Qian¹,

Johansson²,

McCourt³

et al. 2009

Biochemical and Biophysical Research Communications

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“…To fulfill their clearance functions, LSECs express 3 major types of scavenger receptors: (a) the macrophage mannose receptor binding denatured collagen (3) and collagen peptides preventing gelatin formation in the circulation, tissue plasminogen activator regulating fibrinolytic activity, and lysosomal enzymes that are recruited for further use in LSEC (4); (b) the Fcγ receptors FcγRII in the human system (5) and FcγRIIB2 in the rat (6,7); and (c) the major LSEC hyaluronan (HA) scavenger receptor. Upon identification and cloning of the stabilin family of fasciclin-like HA receptor homologs by our group (8), the identity of the LSEC HA scavenger receptor was established as stabilin-2 on the basis of HA affinity purification and sequencing (9).…”

Section: Introductionmentioning

confidence: 99%

Deficiency of liver sinusoidal scavenger receptors stabilin-1 and -2 in mice causes glomerulofibrotic nephropathy via impaired hepatic clearance of noxious blood factors

Schledzewski¹,

Géraud²,

Arnold³

et al. 2011

J. Clin. Invest.

136

145

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Tissue homeostasis and remodeling are processes that involve high turnover of biological macromolecules. Many of the waste molecules that are by-products or degradation intermediates of biological macromolecule turnover enter the circulation and are subsequently cleared by liver sinusoidal endothelial cells (LSEC). Besides the mannose receptor, stabilin-1 and stabilin-2 are the major scavenger receptors expressed by LSEC. To more clearly elucidate the functions of stabilin-1 and -2, we have generated mice lacking stabilin-1, stabilin-2, or both stabilin-1 and -2 (Stab1 -/-Stab2 -/-mice). Mice lacking either stabilin-1 or stabilin-2 were phenotypically normal; however, Stab1 -/-Stab2 -/-mice exhibited premature mortality and developed severe glomerular fibrosis, while the liver showed only mild perisinusoidal fibrosis without dysfunction. Upon kidney transplantation into WT mice, progression of glomerular fibrosis was halted, indicating the presence of profibrotic factors in the circulation of Stab1 -/-Stab2 -/-mice. While plasma levels of known profibrotic cytokines were unaltered, clearance of the TGF-β family member growth differentiation factor 15 (GDF-15) was markedly impaired in Stab1 -/-Stab2 -/-mice but not in either Stab1 -/-or Stab2 -/-mice, indicating that it is a common ligand of both stabilin-1 and stabilin-2. These data lead us to conclude that stabilin-1 and -2 together guarantee proper hepatic clearance of potentially noxious agents in the blood and maintain tissue homeostasis not only in the liver but also distant organs.

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“…4,5 ManR mediates uptake of glycoconjugates carrying mannose in an end position. 6 Interestingly, this receptor uses a different binding domain to take up blood-borne collagen alpha chains, 7,8 and contributes to the adhesion of cancer cells to LSECs. [9][10][11] Furthermore, ManR is involved in antigen uptake, processing, and presentation to T cells by LSECs, 12 and it has been suggested that this process diminishes local immune response of the liver.…”

mentioning

confidence: 99%

Colon carcinoma cell interaction with liver sinusoidal endothelium inhibits organ-specific antitumor immunity through interleukin-1-induced mannose receptor in mice

et al. 2010

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Mannose receptor (ManR)-mediated liver sinusoidal endothelial cell (LSEC) endocytosis plays a role in antigen presentation and innate immunity, but its role in hepatic metastasis is unknown. We studied ManR-mediated endocytosis during C26 colorectal cancer cell interaction with LSECs and its implications in metastasis. Uptake of labeled ManR ligands (mannan and ovalbumin) and immunohistochemistry were used to study ManR endocytosis and expression. Several interleukin (IL)-1 inhibitors and the cyclooxygenase-2 (COX-2) inhibitor celecoxib were used to analyze the role of IL-1 and COX-2 in ManR regulation. Anti-mouse ManR antibodies and ManR knockout (ManR 2/2 ) mice were used to identify ManR-dependent mechanisms during antitumor immune response of liver sinusoidal lymphocytes (LSLs) interacting with tumor-activated LSECs. ManR expression and endocytosis increased in tumor-activated LSECs through a two-step mechanism:(1) Release of COX-2-dependent IL-1-stimulating factors by lymphocyte function-associated antigen-1-expressing C26 cells in response to intercellular adhesion molecule-1 (ICAM-1), which was expressed and secreted by tumor-activated LSECs; and (2) widespread up-regulation of ManR in LSECs through tumor-induced IL-1. In addition, LSLs that had interacted with tumoractivated LSECs in vivo decreased their antitumor cytotoxicity and interferon (IFN)-gamma secretion while they increased IL-10 release ex vivo. IFN-gamma/IL-10 ratio also decreased in the hepatic blood from tumor-injected mice. Immunosuppressant effects of tumor-activated LSECs on LSLs were abrogated in both LSECs from ManR 2/2 mice and tumor-activated LSECs given antimouse ManR antibodies. Conclusion: ICAM-1-induced tumor COX-2 decreased antitumor activity during hepatic metastasis through IL-1-induced ManR. ManR constituted a common mediator for prometastatic effects of IL-1, COX-2, and ICAM-1. A rise in hepatic IFN-gamma/IL-10 ratio and antitumor cytotoxicity by way of ManR blockade is consistent with the antimetastatic effects of IL-1, COX-2, and ICAM-1 inhibitors. These data support ManR and ManR-stimulating factors as targets for hepatic colorectal metastasis therapy. (HEPATOLOGY 2010;51:2172-2182 Abbreviations: ASMA, alpha-smooth muscle actin; CM, cell-conditioned medium; COX-2, cyclooxygenase-2; CSPG, chondroitin sulfate proteoglycan; ELISA, enzyme-linked immunosorbent assay; FITC-OVA, fluorescein isothiocyanate-labeled ovalbumin; FSA, formaldehyde treated serum albumin; ICAM-1, intercellular adhesion molecule-1; ICE, IL-1-converting enzyme; IgG2a, immunoglobulin G2a; IL, interleukin; IL-1RI, IL-1 receptor type I; IL-1Ra, IL-1 receptor antagonist; LFA-1, lymphocyte function-associated antigen 1; LSEC, liver sinusoidal endothelial cell; LSL, liver sinusoidal lymphocyte; ManR, mannose receptor; ManR À/À , ManR knockout; SD, standard deviation; sICAM-1, soluble ICAM-1.From the

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The mannose receptor on murine liver sinusoidal endothelial cells is the main denatured collagen clearance receptor

Cited by 111 publications

References 31 publications

Stabilins are expressed in bone marrow sinusoidal endothelial cells and mediate scavenging and cell adhesive functions

Stabilins are expressed in bone marrow sinusoidal endothelial cells and mediate scavenging and cell adhesive functions

Deficiency of liver sinusoidal scavenger receptors stabilin-1 and -2 in mice causes glomerulofibrotic nephropathy via impaired hepatic clearance of noxious blood factors

Colon carcinoma cell interaction with liver sinusoidal endothelium inhibits organ-specific antitumor immunity through interleukin-1-induced mannose receptor in mice

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