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Role of contact inhibition in the regulation of receptor-mediated uptake of low density lipoprotein in cultured vascular endothelial cells.
Abstract
Bovine vascular endothelial cells during logarithmic growth bind, internalize, and degrade low density lipoprotein (LDL) via a receptor-mediated pathway. However, contact-inhibited (confluent) monolayers bind but do not internalize LDL. This is in contrast to aortic smooth muscle cells or endothelial cells that have lost the property of contact inhibition. These cells internalize and degrade LDL at both high and low cell densities. The LDL receptors of smooth muscle and sparse endothelial cells down-regulate in response to LDL. In contrast, normal endothelial cells at confluency show little response. When contact inhibition in endothelial monolayers was locally released by wounding, and LDL was present, only cells released from contact inhibition accumulated LDL cholesterol. In smooth muscle cells under the same conditions, the entire culture interiorized lipid. It thus appears that in endothelial cells, unlike smooth muscle cells, contact inhibition is the major factor regulating cellular uptake of LDL cholesteryl ester. Reversal of contact inhibition by wounding provides a mechanism by which the endothelium could be the primary initiator of the atherosclerotic plaque.
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Growing endothelial cells in culture bind LDL.
“A number of different studies have confirmed that growing ECs in culture also bind LDL (Vlodavsky et al., 1978).”
From Upregulation of the low density lipoprotein receptor at the blood-brain barrier: intercommunications between brain capillary endothelial cells and astrocytes. (1994) · cites this paper as Vlodavsky et al., 1978
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Research works printed but not linked: 8
- [6]Gospodarowicz, D., Greenburg, G., Bialecki, H. & Zetter, B., (1977) in Cellular Control of Proliferation, ed. Freed, C. In Vitro 13, in press.
- [5]Gospodarowicz, D., Moran, J., Braun, D. & Birdwell, C. (1976) Proc. Natl. Acad. Sci. USA 73, 4120–4124.
- [18]Greep, R. O. (1966) Histology (McGraw Hill, New York), pp. 285-289.
- [20]Vasiliev, J. M., Gelfand, I. M., Domnina, L. V., Zacharova, O. S. & Ljubimov, A. V. (1975) Proc. Natl. Acad. Sci. USA 72, 719– 722.
- [19]Schubert, D., Harris, A. J., Heinemann, S., Kidokoro, Y. & Patrick, J. (1973) in Tissue Culture of the Nervous System, ed. Sato, G. (Plenum Press, New York), p. 58.
- [21]Oliver, J. M., Ukena, T. E. & Berlin, R. D. (1974) Proc. Natl. Acad. Sci. USA 71, 394–398.
- [23]Gospodarowicz, D., Vlodavsky, I. & Fielding, P. E. (1977) in International Congress of Birth Defects 5th, ed. Peereboom, T. (Excerpta Medica, Amsterdam), in press.
- [22]Raff, M. C. & De Petris, S. (1973) Fed. Proc. Fed. Am. Soc. Exp. Biol. 32, 48–54.
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GWYNNE, J. T., & STRAUSS, J. F. (1982) · Endocrine Reviews · doi:10.1210/edrv-3-3-299 · Cited by 586
Dehouck, B., Dehouck, M. P., Fruchart, J. C., & Cecchelli, R. (1994) · The Journal of cell biology · doi:10.1083/jcb.126.2.465 · Cited by 240
Metadata
- Authors
- Vlodavsky, I., Fielding, P. E., Fielding, C. J., & Gospodarowicz, D.
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 1978-01
- Volume
- 75
- Issue
- 1
- Pages
- 356-360
- ISSN
- 0027-8424
- 1091-6490
- Cited by
- 116
- References
- 0
- Language
- en
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