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Mannose receptor‐mediated endothelial cell activation contributes to B16 melanoma cell adhesion and metastasis in liver
Author(s) -
Mendoza Lorea,
Olaso Elvira,
Anasagasti Miren J.,
Fuentes Angela M.,
VidalVanaclocha Fernando
Publication year - 1998
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(199803)174:3<322::aid-jcp6>3.0.co;2-q
Subject(s) - mannose receptor , receptor , mannose , microbiology and biotechnology , in vitro , cell adhesion , paraformaldehyde , mannan , chemistry , cell culture , adhesion , biology , cell , biochemistry , polysaccharide , macrophage , genetics , organic chemistry
The role of mannose receptors from hepatic sinusoidal endothelium (HSE) in liver colonization by B16 melanoma (B16M) cells was studied. The expression of high mannose‐type oligosaccharides on the surface of B16M cells was enhanced by in vitro treatment with 1‐deoximannojirimycin (1‐DMM). There was a significant ( P < 0.01) enhancement of hepatic metastasis when B16M cells were 1‐DMM‐treated before being intrasplenically injected into C57BL/6J mice. Intraperitoneal administration of 5 mg/kg recombinant human interleukin‐1 receptor antagonist (rHuIL‐1Ra) inhibited the 1‐DMM‐induced enhancement of metastasis. Expression of high mannose‐type oligosaccharides on the surface of 1‐DMM‐treated B16M cells and their in vitro adhesion to the HSE was significantly correlated (R = 0.82). The addition of either 100 μg/ml mannan or paraformaldehyde (PFA)‐fixed 1‐DMM‐treated B16M cells to cultured HSE for a period of 12 h significantly ( P < 0.01) increased the release of IL‐1β from the HSE compared to that liberated by the HSE incubated with either basal medium or PFA‐fixed untreated B16M cells. The same HSE treatments also significantly ( P < 0.01) increased the degree of adhesion of other B16M cells to HSE, being abrogated by anti‐mouse vascular cell adhesion molecule‐1 (VCAM‐1) antibodies. The conditioned media from HSE cultures, activated by PFA‐fixed, 1‐DMM‐treated B16M cells significantly ( P < 0.01) increased B16M cell proliferation when compared to conditioned media from HSE cultures incubated with PFA‐fixed, untreated B16M cells. Thus, 1‐DMM treatment of B16M cells enhanced the development of hepatic metastasis by IL‐1‐dependent mechanisms. The mechanism is consistent with in vitro mannose receptor‐mediated melanoma cell attachment to the HSE, which subsequently upregulates IL‐1β release, VCAM‐1‐dependent adherence, and melanoma growth factor(s) release by HSE. J. Cell. Physiol. 174:322–330, 1998. © 1998 Wiley‐Liss, Inc.