Multiple effects of serum low-density lipoprotein on cultured human fibroblasts

1979 ◽  
Vol 57 (6) ◽  
pp. 684-691 ◽  
Author(s):  
M. J. Spain ◽  
L. O. Wosu ◽  
N. Kalant

The effects of serum low-density lipoproteins (LDL) were studied in cultures of human skin fibroblasts grown in medium supplemented with human serum deficient in lipoproteins and in platelet factor. The LDL led to a temporary increase in the rate of cell replication, to increases in the cell content of protein and cholesterol, to an increase in average cell size, and to an increased secretion of glycosaminoglycans. The increases in cholesterol and protein were proportional to the increase in cell size, suggesting that the additional protein and cholesterol were of a structural, rather than a storage, nature. The increase in cell protein during the first few days of exposure to LDL was due to a decrease in the rate of protein degradation. Ultrafiltration of the serum to remove substances of molecular weight < 30 000 did not reduce the basal rate of cell proliferation but did prevent the stimulation of proliferation by LDL; it did not alter the effect of LDL on cell protein and cholesterol, indicating that the latter responses are independent of the mitogenic action. The response of cells from diabetic donors did not differ from that of normal cells.

2021 ◽  
pp. 0021955X2098715
Author(s):  
Cosimo Brondi ◽  
Ernesto Di Maio ◽  
Luigi Bertucelli ◽  
Vanni Parenti ◽  
Thomas Mosciatti

This study investigates the effect of liquid-type organofluorine additives (OFAs) on the morphology, thermal conductivity and mechanical properties of rigid polyurethane (PU) and polyisocyanurate (PIR) foams. Foams were characterized in terms of their morphology (density, average cell size, anisotropy ratio, open cell content), thermal conductivity and compressive as well as flexural properties. Based on the results, we observed that OFAs efficiently reduced the average cell size of both PU and PIR foams, leading to improved thermal insulating and mechanical properties.


1985 ◽  
Vol 228 (1) ◽  
pp. 219-225 ◽  
Author(s):  
B B Lundberg ◽  
L A Suominen

The transfer of free cholesterol from [3H]cholesterol-labelled plasma lipoproteins to cultured human lung fibroblasts was studied in a serum-free medium. The uptake of [3H]cholesterol depended upon time of incubation, concentration of lipoprotein in the medium, and temperature. Modified (reduced and methylated) low-density lipoprotein (LDL), which did not enter the cells by the receptor pathway, gave a somewhat lower transfer rate than unmodified LDL, but if the transfer values for native LDL were corrected for the receptor-mediated uptake of cholesterol the difference was eliminated. The initial rates of transfer of [3H]cholesterol from LDL and high-density lipoprotein (HDL) were of the same order of magnitude (0.67 +/- 0.05 and 0.75 +/- 0.06 nmol of cholesterol/h per mg of cell protein, respectively) while that from very-low-density lipoprotein (VLDL) was much lower (0.23 +/- 0.02 nmol of cholesterol/h per mg) (means +/- S.D., n = 5). The activation energy for transfer of cholesterol from reduced, methylated LDL to fibroblasts was determined to be 57.5 kJ/mol. If albumin was added to the incubation medium the transfer of [3H]cholesterol was enhanced, while that of [14C]dipalmitoyl phosphatidylcholine was decreased compared with the protein-free system. The results demonstrate that, in spite of its low water solubility, free cholesterol can move from lipoproteins to cellular membranes, probably by aqueous diffusion. We propose that physicochemical transfer of free cholesterol may be a significant mechanism for net uptake of the sterol into the artery during atherogenesis.


Blood ◽  
2002 ◽  
Vol 99 (10) ◽  
pp. 3613-3622 ◽  
Author(s):  
Bruce S. Sachais ◽  
Alice Kuo ◽  
Taher Nassar ◽  
Jeanelle Morgan ◽  
Katalin Kariko ◽  
...  

The influence of platelets on the cellular metabolism of atherogenic lipoproteins has not been characterized in detail. Therefore, we investigated the effect of platelet factor 4 (PF4), a cationic protein released in high concentration by activated platelets, on the uptake and degradation of low-density lipoprotein (LDL) via the LDL receptor (LDL-R). LDL-R–dependent binding, internalization, and degradation of LDL by cultured cells were inhibited 50%, 80%, and 80%, respectively, on addition of PF4. PF4 bound specifically to the ligand-binding domain of recombinant soluble LDL-R (half-maximal binding 0.5 μg/mL PF4) and partially (approximately 50%) inhibited the binding of LDL. Inhibition of internalization and degradation by PF4 required the presence of cell-associated proteoglycans, primarily those rich in chondroitin sulfate. PF4 variants with impaired heparin binding lacked the capacity to inhibit LDL. PF4, soluble LDL-R, and LDL formed ternary complexes with cell-surface proteoglycans. PF4 induced the retention of LDL/LDL-R complexes on the surface of human fibroblasts in multimolecular clusters unassociated with coated pits, as assessed by immuno-electron microscopy. These studies demonstrate that PF4 inhibits the catabolism of LDL in vitro in part by competing for binding to LDL-R, by promoting interactions with cell-associated chondroitin sulfate proteoglycans, and by disrupting the normal endocytic trafficking of LDL/LDL-R complexes. Retention of LDL on cell surfaces may facilitate proatherogenic modifications and support an expanded role for platelets in the pathogenesis of atherosclerosis.


2021 ◽  
pp. 026248932110068
Author(s):  
Youming Chen ◽  
Raj Das ◽  
Hui Wang ◽  
Mark Battley

In this study, the microstructure of a SAN foam was imaged using a micro-CT scanner. Through image processing and analysis, variations in density, cell wall thickness and cell size in the foam were quantitatively explored. It is found that cells in the foam are not elongated in the thickness (or rise) direction of foam sheets, but rather equiaxed. Cell walls in the foam are significantly straight. Density, cell size and cell wall thickness all vary along the thickness direction of foam sheets. The low density in the vicinity of one face of foam sheets leads to low compressive stiffness and strength, resulting in the strain localization observed in our previous compressive tests. For M80, large open cells on the top face of foam sheets are likely to buckle in compressive tests, therefore being another potential contributor to the strain localization as well. The average cell wall thickness measured from 2D slice images is around 1.4 times that measured from 3D images, and the average cell size measured from 2D slice images is about 13.8% smaller than that measured from 3D images. The dispersions of cell wall thickness measured from 2D slice images are 1.16–1.20 times those measured from 3D images. The dispersions of cell size measured from 2D slice images are 1.12–1.36 times those measured from 3D images.


1979 ◽  
Vol 83 (3) ◽  
pp. 588-594 ◽  
Author(s):  
H S Kruth ◽  
J Avigan ◽  
W Gamble ◽  
M Vaughan

The effect of cell density on low density lipoprotein (LDL) binding by cultured human skin fibroblasts was investigated. Bound LDL was visualized by indirect immunofluorescence. Cellular lipid and cholesterol were monitored by fluorescence in cells stained with phosphine 3R and filipin, respectively. LDL binding and lipid accumulation were compared in cells in stationary and exponentially growing cultures, in sparsely and densely plated cultures, in wounded and non-wounded areas of stationary cultures, and in stationary cultures with and without the addition of lipoprotein-deficient serum. We conclude that LDL binding and cholesterol accumulation induced by LDL are influenced by cell density. It appears that, compared to rapidly growing cells, quiescent (noncycling) human fibroblasts exhibit fewer functional LDL receptors.


1973 ◽  
Vol 30 (2) ◽  
pp. 143-155 ◽  
Author(s):  
A. Prakash ◽  
Liv Skoglund ◽  
Britt Rystad ◽  
Arne Jensen

An extended exponential growth phase and a higher maximum population characterized growth of planktonic algae in a dialysis system compared with that in a batch system. Algal cells grown in a dialysis culture had higher chlorophyll content and a larger average cell size than those grown in a batch culture. In both types of culture, changes in cell-size distribution were related to the phases of the growth cycle with maximum cell-size during the stationary phase. Various interactions of the component reactions of photosynthesis leading to changes in growth pattern and cell-size distribution are discussed.


1996 ◽  
Vol 314 (1) ◽  
pp. 103-108 ◽  
Author(s):  
Catherine S. BOURGEOIS ◽  
David WIGGINS ◽  
Geoffrey F. GIBBONS

Male Wistar rats were fitted with subcutaneous osmotic minipumps that delivered insulin at a constant rate of 0.20 i.u./h for 7 days. This treatment raised the plasma insulin concentration from 31±4 to 201±64 μ-i.u./ml. Hepatocytes prepared from the hyperinsulinaemic animals secreted very-low-density lipoprotein (VLDL) triacylglycerol (TAG) at a higher rate (172±21 μg per 24 h per mg cell protein) than did those from sham-operated controls (109±12 μg per 24 h per mg) (P < 0.05). However, chronic exogenous hyperinsulinaemia had no stimulatory effect on the secretion of VLDL apolipoprotein B (apoB) in derived hepatocytes compared with those from the sham-operated controls (2.32±0.38 compared with 3.09±0.40 μg per 24 h per mg). Hepatocytes from the hyperinsulinaemic rats thus secreted larger VLDL particles as evidenced by the increased TAG:apoB ratio (78.4±13.1 compared with 38.4±7.6; P < 0.05). In hepatocytes from the hyperinsulinaemic rats a larger proportion of the newly synthesized TAG was secreted as VLDL. Hepatocytes from the hyperinsulinaemic and the sham-operated control animals were equally sensitive to the inhibitory effect of insulin added in vitro on the secretion of VLDL TAG. Insulin added in vitro to the culture medium of hepatocytes from hyperinsulinaemic animals significantly decreased the TAG:apoB ratio of the secreted VLDL. This change did not occur in hepatocytes from sham-operated rats. These results suggest that, in vivo, chronic hyperinsulinaemia is not in itself sufficient to desensitize the liver to the acute inhibitory effect of insulin on the secretion of VLDL.


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