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Biomedical subjects

T Henriksen

Publications and source records attributed to T Henriksen.

At least 91 records · Page 5Linked to original sources
PubMed1982

Injury to human cells in culture induced by low density lipoprotein: an effect independent of receptor binding and endocytotic uptake of low density lipoprotein.

Cultured human endothelial cells isolated from umbilical cord veins and erythrocytes obtained from healthy donors were injured when exposed to low density lipoprotein (LDL). A close relationship between the amount of 125I-LDL associated with the cell surface and the degree of cell injury was demonstrated. This association occurred before any morphological signs of cell injury were observed and before any substantial release of 51Cr into the medium could be measured. Subsequent endocytotic uptake and lysosomal degradation of LDL did not seem to be a prerequisite for the LDL-induced cell injury to occur. Human serum albumin had an inhibitory effect on the association of 125I-LDL with the cell surface and in parallel a lowering effect on the 51Cr release.

Arteriosclerosis↗
PubMed1981

Enhanced macrophage degradation of low density lipoprotein previously incubated with cultured endothelial cells: recognition by receptors for acetylated low density lipoproteins.

Human low density lipoprotein (LDL) was incubated with an established line of rabbit aortic endothelial cells. Density gradient fractionation showed a time-, concentration-, and temperature-dependent increase in the average density of the LDL (from about 1.036 to as high as 1.070 g/ml). Incubation without cells or with other types of cultured cells (fibroblasts, hepatocytes, 3T3-L1 cells) caused no significant change in density. 125I-Labeled LDL (125I-LDL) recovered after incubation with endothelial cells (EC-modified LDL) was taken up and degraded 3 to 4 times more rapidly than control LDL by resident mouse peritoneal macrophages and by an established tumor line of mouse macrophages (J774 cells). Macrophage degradation of EC-modified 125I-LDL exhibited saturation kinetics (greater than 85% inhibited by excess unlabeled EC-modified LDL). Degradation was also inhibited by unlabeled acetylated LDL and, conversely, unlabeled EC-modified LDL inhibited degradation of acetylated 125I-LDL. Incubation of LDL with conditioned medium-removed from endothelial cell cultures modified neither its density nor its rate of degradation by macrophages. These studies show that endothelial cells have the potential to metabolically modify the LDL molecule, generating a form that is more rapidly degraded by macrophages and that is recognized by the macrophage receptor for acetylated LDL. This process may play a significant role in the pathogenesis of atherosclerosis.

Animals↗
PubMed1979

The effect of serum lipoproteins on cholesterol content and sterol exchange in cultured human endothelial cells.

Cultured human endothelial cells preincubated with the infranatant of human serum increased their content of cholesterol when subsequently exposed to low density lipoproteins (LDL) as compared to control cultures further incubated in the presence of infranatant only. Replacing LDL with high density lipoproteins (HDL) resulted in no change in the cellular cholesterol content compared to the control. The addition of HDL did not influence the increase in cellular cholesterol content mediated by LDL. HDL stimulated the efflux of endogenously synthesized 14C-labelled sterols compared to the infranatant fraction, whereas LDL had only a slight effect. Cells preincubated with whole serum did not change their cholesterol content when subsequently exposed to LDL, compared to cultures further incubated in presence of whole serum. Replacing whole serum (during the final incubation) with infranatant, resulted in a decrease of the cellular cholesterol content, which was not influenced by further addition of HDL.

Cells, Cultured↗
PubMed1979

Injury to human endothelial cells in culture induced by low density lipoproteins.

Low density lipoproteins (LDL) have been shown to injure culture endothelial cells derived from the human umbilical cord. During a 48 h incubation period LDL significantly increased 51Cr release from prelabelled cells and induced marked cellular injury if the ratio between the LDL cholesterol and the infranatant proteins was kept above 0.1-0.12 mmol/g protein. Actually, an injurious effect of a fixed concentration of LDL could be completely prevented by increasing the concentration of infranatant proteins. High density lipoproteins within physiological concentration ranges had no effect when tested in the presence of infranatant proteins. The effects of LDL were not cell specific because normal as well as LDL receptor negative human skin fibroblasts were injured by LDL.

Arteriosclerosis↗
PubMed1979

Injury to cultured endothelial cells induced by low density lipoproteins: protection by high density lipoproteins.

Cultured human endothelial cells derived from umbilical cord veins were injured when exposed to low density lipoproteins (LDL). Addition of high density lipoproteins (HDL), together with LDL, inhibited the cellular injury induced by LDL as demonstrated by lowered 51Cr release and prevention of morphological changes. Serum albumin had a similar, but far weaker effect. Preincubation of the cells with HDL did not reduce injury inflicted during a subsequent incubation with LDL, while preincubation with LDL aggravated later damage. The protective effect of HDL could be overcome by increasing the DLD concentration.

Arteriosclerosis↗
PubMed1976

Free radicals in pyrimidines: 5-thymyl radical nitrogen splitting in irradiated thymidine.

Single crystals of thymidine irradiated with 4.0 MeV electrons exhibit the well-known eight-line e.s.r. spectrum due to the 5-thymyl radical. A careful analysis of these lines revealed an extra hyperfine splitting, which by a combination of INDO-MO calculations and experiments, was attributed to an interaction between the unpaired electron and the N3-H group.

Electron Spin Resonance Spectroscopy↗
PubMed1975

Ultrastructural identification of umbilical cord vein endothelium in situ and in culture.

The ultrastructure of human umbilical cord vein endothelium in situ, after isolation by collagenase treatment, and in primary culture is described. The cultured cells formed a monolayer with typical "butt" and interdigitated junctions with specialized areas, and contained Weibel-Palade bodies, rod-shaped tubular organelles considered specific of endothelial cells. These morphological features were not present in cultures of human skin fibroblasts and fibroblast-like cells derived from umbilical cords. It is thus concluded that endothelial cells retain their characteristic fine structure in primary culture. Simple ultrastructural studies can thus be used to identify endothelial cells in culture.

Cells, Cultured↗
PubMed1975

The human mixed lymphocyte-endothelium culture interaction.

Cells separated from the wall of the umbilical cord vein by collagenase digestion could be identified as endothelial by their characteristic ultrastructure, their growth pattern in culture, and their microscopical morphology. These cells, both freshly explanted and after long-term culturing, were capable of stimulating allogeneic lymphocytes in vitro. Control experiments indicated that this stimulation was not attributable to contamination of the endothelial cell suspensions by foetal fibroblasts or passenger lymphocytes. The dose response characteristics and kinetics of the lymphoproliferative response using endothelial stimulating cells was similar to mixed lymphocyte cultures. Sera which were capable of inhibiting the mixed lymphocyte culture response were relatively ineffective in inhibiting the stimulation caused by endothelial cells.

Carbon Radioisotopes↗
PubMed1975

Human fetal endothelial cells in cluture.

Human endothelial cells were isolated from the umbilical cord vein by collagenase treatment and cultured for periods up to 6 weeks. The cultured cells were identified as endothelium by cell morphology and growth pattern, the presence of Weibel-Palade bodies, and their ability to stimulate allogeneic lymphocytes (Hirschberg et al 1974). Cultured fibroblast-like cells derived from the umbilical cord were clearly different in all three respects. Approximately one third of the primary endothelial cultures showed clear evidence of proliferation during the first 3-4 days in culture as judged by cell counting. Replicating ability in a culture was correlated with cell density at the time of seeding. Autoradiography of endothelial cells after exposure to 3-H-thymidine showed a 30-fold increase in nuclear labelling from day 1 to day 3 in culture. The endothelial cells have so far been subcultured three times.

Cell Division↗