This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ketis, N. V. Articles by Karnovsky, M. J. Search for Related Content PubMed PubMed Citation Articles by Ketis, N. V. Articles by Karnovsky, M. J.

Effects of Hyperthermia on Cell Survival and Patterns of Protein Synthesis in Endothelial Cells from Different Origins¹

Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115

Thermotolerance, transient resistance to heat induced by heat itself, is generally thought to be linked to the accumulation of heat-shock proteins in eukaryotic cells. The induction of thermotolerance and the synthesis of heat-shock proteins in primary and passage cultures of bovine aortic endothelium, passage cultures of bovine brain capillaries, and passage cultures of rat epididymal capillaries were examined. Primary and passage cultures of bovine aortic endothelial cells readily acquired thermotolerance; however, passage cultures of rat epididymal capillary cells and bovine brain capillary cells were very heat sensitive. In all endothelial cell types examined except rat epididymal capillary cells, the levels of HSP71, the most inducible of the HSP70 family, correlated well with thermotolerance. With prolonged passage, rat epididymal capillary cells and bovine brain capillary cells lost their ability to acquire heat resistance. Endothelial cells from different origins (aortic endothelium versus capillary endothelium) but from the same species and about the same passage number had a notably different response in terms of thermotolerance and synthesis of proteins after exposure to hyperthermia. The results of this study suggest that, while the expression of HSP71 may be a good indicator of heat resistance, the reverse is not necessarily true. Furthermore, the data show that endothelial cells from different origins are dissimilar in their response to hyperthermia.

¹ This work was supported by Grants HL-17747 and HL-26191 from the NIH. Part of this work was presented at the Heat Shock Meeting at Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, on August 29, 1985, and at the American Society for Cell Biology Annual Meetings, St. Louis, MO, on November 20, 1987, and appeared in abstract forms (20, 21).

² Recipient of a fellowship from the Medical Research Council of Canada.

Received 6/26/86. Revised 10/22/86. Revised 8/10/87. Revised 12/18/87. Accepted 1/20/88.

This article has been cited by other articles:

				I. A. Mawji, G. B. Robb, S. C. Tai, and P. A. Marsden Role of the 3'-Untranslated Region of Human Endothelin-1 in Vascular Endothelial Cells: CONTRIBUTION TO TRANSCRIPT LABILITY AND THE CELLULAR HEAT SHOCK RESPONSE J. Biol. Chem., March 5, 2004; 279(10): 8655 - 8667. [Abstract] [Full Text] [PDF]

				M. B. Harris, M. A. Blackstone, H. Ju, V. J. Venema, and R. C. Venema Heat-induced increases in endothelial NO synthase expression and activity and endothelial NO release Am J Physiol Heart Circ Physiol, June 5, 2003; 285(1): H333 - H340. [Abstract] [Full Text] [PDF]

				J. P. Leger, F. M. Smith, and R. W. Currie Confocal Microscopic Localization of Constitutive and Heat Shock-Induced Proteins HSP70 and HSP27 in the Rat Heart Circulation, October 3, 2000; 102(14): 1703 - 1709. [Abstract] [Full Text] [PDF]