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Biomedical subjects

B Westermark

Publications and source records attributed to B Westermark.

At least 235 records · Page 13Linked to original sources
PubMed1978

Composition and distribution of glycosaminoglycans in cultures of human normal and malignant glial cells.

The glycosaminoglycans of human cultured normal glial and malignant glioma cells were studied. [35S]Sulphate or [3H]glucosamine added to the culture medium was incorporated into glycosaminoglycans; labelled glycosaminoglycans were isolated by DEAE-cellulose chromatography or gel chromatography. A simple procedure was developed for measurement of individual sulphated glycosaminoglycans in cell-culture fluids. In normal cultures the glycosaminoglycans of the pericellular pool (trypsin-susceptible material), the membrane fraction (trypsin-susceptible material of EDTA-detached cells) and the substrate-attached material consisted mainly of heparan sulphate. The intra- and extra-cellular pools showed a predominance of dermatan sulphate. The net production of hyaluronic acid was low. The accumulation of 35S-labelled glycosaminoglycans in the extracellular pool was essentially linear with time up to 72h. The malignant glioma cells differed in most aspects tested. The total production of glycosaminoglycans was much greater owing to a high production of hyaluronic acid and hyaluronic acid was the major cell-surface-associated glycosaminoglycan in these cultures. Among the sulphated glycosaminoglycans chondroitin sulphate, rather than heparan sulphate, was the predominant species of the pericellular pool. This was also true for the membrane fraction and substrate-attached material. Furthermore, the accumulation of extracellular 35S-labelled glycosaminoglycans was initially delayed for several hours and did not become linear with time until after 24 h of incubation. The glioma cells produced little dermatan sulphate and the dermatan sulphate chains differed from those of normal cultures with respect to the distribution of iduronic acid residues. The observed differences between normal glial and malignant glioma cells were not dependent on cell density; rather they were due to the malignant transformation itself.

Cells, Cultured↗
PubMed1978

Properties of human malignant glioma cells in vitro.

The properties of human glia and glioma cells in culture are reviewed. Glia-like cells from non-neoplastic brain show all accepted hallmarks of normalcy: limited life span, low terminal cell density, strong density dependent inhibition of proliferation, diploidy and contact inhibition of membrane mobility. Twenty five glioma lines have been studied. They all showed infinite life span, increased terminal cell density, relaxed density dependent inhibition of proliferation, aneuploidy and deficient contact inhibition of membrane mobility. So far all attempts to explain these departures from normal on the basis of a single metabolic defect have failed. Instead, all tested lines have shown an individual mosaic of structural and/or metabolic abnormalities characteristic for each line. This was particulary well demonstrated in studies of the glycosaminoglykans. The possibility is discussed that a malignant phenotype can a rise and exist in an almost infinite number of ways. The essential feature may be the acquisition of infinite growth potential which will set the stage for multiplication of genetic variants with an ever increasing fitness for proliferation and spread.

Adult↗
PubMed1977

Local starvation for epidermal growth factor cannot explain density-dependent inhibition of normal human glial cells.

Mouse epidermal growth factor (mEGF) is a potent growth promoter of human glial cells in sparse cultures, whereas very little stimulation of growth in dense cultures is induced by the factor. In the present communication, the possibility that the density-dependent inhibition is caused by a reduced binding/uptake of the factor was scrutinized. It was found that the number of mEGF binding sites was 20,000 and 35,000 per cell in sparse and dense cultures, respectively. The dissociation constant of the binding reaction was not influenced by the cell density. It was concluded that crowded cells are not starved for the factor and that a decrease in number or affinity of the EGF receptors can be excluded as a cause of the inhibition.

Animals↗