scholarly journals Chinese hamster ovary cell adhesion to human platelet thrombospondin is dependent on cell surface heparan sulfate proteoglycan.

1989 ◽  
Vol 83 (3) ◽  
pp. 994-1001 ◽  
Author(s):  
P R Kaesberg ◽  
W B Ershler ◽  
J D Esko ◽  
D F Mosher
Keyword(s):  
Cell Adhesion ◽  
Cell Surface ◽  
Heparan Sulfate ◽  
Chinese Hamster Ovary Cell ◽  
Chinese Hamster Ovary ◽  
Human Platelet ◽  
Chinese Hamster ◽  
Heparan Sulfate Proteoglycan ◽  
Ovary Cell ◽  
Sulfate Proteoglycan

Heparan sulfate proteoglycan deficiency up-regulates the intracellular production of nitric oxide in Chinese hamster ovary cell lines

2017 ◽  
Vol 233 (4) ◽  
pp. 3176-3194 ◽  
Author(s):  
Sheyla V. Lucena ◽  
Gioconda E. D. D. Moura ◽  
Tiago Rodrigues ◽  
Carolina M. Watashi ◽  
Fabiana H. Melo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heparan Sulfate ◽  
Cell Lines ◽  
Chinese Hamster Ovary Cell ◽  
Chinese Hamster Ovary ◽  
Chinese Hamster ◽  
Heparan Sulfate Proteoglycan ◽  
Ovary Cell ◽  
Sulfate Proteoglycan

scholarly journals Cell Surface Heparan Sulfate Promotes Replication of Toxoplasma gondii

2005 ◽  
Vol 73 (9) ◽  
pp. 5395-5401 ◽  
Author(s):  
Joseph R. Bishop ◽  
Brett E. Crawford ◽  
Jeffrey D. Esko
Keyword(s):  
Toxoplasma Gondii ◽  
Cell Surface ◽  
Heparan Sulfate ◽  
Chinese Hamster Ovary Cell ◽  
Chinese Hamster Ovary ◽  
Chinese Hamster ◽  
Cell Types ◽  
Ovary Cell ◽  
Toxoplasma Infection ◽  
Mammary Tumor Cells

ABSTRACT Previous work suggests that cell surface heparan sulfate acts as a receptor for the Apicomplexan parasite Toxoplasma gondii. Using Chinese hamster ovary cell mutants defective in heparan sulfate biosynthesis, we show that heparan sulfate is necessary and sufficient for infectivity. Further, we demonstrate that the parasite requires N sulfation of heparan sulfate initiated by N-deacetylase/N-sulfotransferase-1, but 2-O sulfation and 6-O sulfation appear to be dispensable. In order to study the role of heparan sulfate in other cell types, we created a conditional allele for N-deacetylase/N-sulfotransferase-1 by using Cre-loxP technology. Mammary tumor cells lacking N-deacetylase/N-sulfotransferase-1 exhibited reduced toxoplasma infectivity like Chinese hamster ovary cell mutants. Surprisingly, heparin, chemically modified heparinoids, and monoclonal antibodies to heparan sulfate had no effect on toxoplasma infection. T. gondii attachment and invasion were unchanged in N-deacetylase/N-sulfotransferase-1-inactivated cells as well, but replication was reduced. Thus, heparan sulfate does not appear to function as a receptor for T. gondii but instead facilitates parasite replication postinvasion.

Surface polypeptides of the Chinese hamster ovary cell; an immunochemical study

1976 ◽  
Vol 54 (2) ◽  
pp. 185-191 ◽  
Author(s):  
M. Behar-Bannelier ◽  
R. L. Juliano
Keyword(s):  
Cell Surface ◽  
Chinese Hamster Ovary Cell ◽  
Chinese Hamster Ovary ◽  
Chinese Hamster Ovary Cells ◽  
Chinese Hamster ◽  
Ovary Cell ◽  
Immunochemical Study ◽  
Ovary Cells ◽  
Molecular Weights ◽  
Label Technique

Antibodies elicited by the injection of live Chinese hamster ovary cells (CHO) into rabbits precipitated four major components from detergent extracts of CHO membranes. The four components, of molecular weights 200 000, 125 000, 95 000 and 41 000 daltons, corresponded to cell surface components identified by the lactoperoxidase surface label technique.

scholarly journals Infectivity of Chlamydia trachomatisSerovar LGV but Not E Is Dependent on Host Cell Heparan Sulfate

2001 ◽  
Vol 69 (2) ◽  
pp. 968-976 ◽  
Author(s):  
Maria Taraktchoglou ◽  
Allan A. Pacey ◽  
Jeremy E. Turnbull ◽  
Adrian Eley
Keyword(s):  
Heparan Sulfate ◽  
Host Cell ◽  
Cell Lines ◽  
Chinese Hamster Ovary Cell ◽  
Chinese Hamster Ovary ◽  
Competitive Inhibition ◽  
Chinese Hamster ◽  
Female Reproductive Tract ◽  
Ovary Cell ◽  
Deficient Cell

ABSTRACT The ability of heparan sulfate, heparin, and other glycosaminoglycans to inhibit the infectivity of Chlamydia trachomatis serovars E and LGV was examined using a simple competitive inhibition assay with three cell types from the human female reproductive tract, including primary human endosalpingeal cells. With the majority of the glycosaminoglycans tested, LGV was more significantly inhibited than serovar E. We have compared chlamydial infectivity between a wild-type Chinese hamster ovary cell line and two glycosaminoglycan-deficient cell lines. LGV was shown to be unable to infect heparan sulfate-deficient and GAG-deficient Chinese hamster ovary cell lines, whereas the E serovar infected these cells as efficiently as the control (nondeficient) cells. These two sets of experiments confirmed that serovar LGV is more dependent on a heparan sulfate-related mechanism of infectivity than is serovar E. This is further supported by the fact that attempts to purify a heparan sulfate-like molecule from either serovar cultured in glycosaminoglycan-deficient cell lines were nonproductive. Previous reports have suggested that chlamydia are able to produce a heparan sulfate-like molecule that is important for attachment and infectivity. We have attempted to detect possible binding of a specific heparan sulfate antibody to C. trachomatis by flow cytometry. Results showed no binding of the heparan sulfate antibody to C. trachomatis serovar LGV or E. Our results strongly indicate that chlamydiae do not produce a heparan sulfate-like molecule but rather use host cell heparan sulfate in order to infect cells.

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