SUBSET OF VASCULAR DENDRITIC CELLS TRANSFORMING INTO FOAM CELLS IN HUMAN ATHEROSCLEROTIC LESIONS

Citation
Yv. Bobryshev et T. Watanabe, SUBSET OF VASCULAR DENDRITIC CELLS TRANSFORMING INTO FOAM CELLS IN HUMAN ATHEROSCLEROTIC LESIONS, Cardiovascular pathology, 6(6), 1997, pp. 321-331
Citations number
81
Categorie Soggetti
Pathology,"Cardiac & Cardiovascular System
Journal title
ISSN journal
10548807
Volume
6
Issue
6
Year of publication
1997
Pages
321 - 331
Database
ISI
SICI code
1054-8807(1997)6:6<321:SOVDCT>2.0.ZU;2-P
Abstract
It has been previously demonstrated that S-100 positive vascular dendr itic cells are involved in human atherosclerosis and they usually show a low level of accumulation of lipids in their cytoplasm, even though they located among foam cells and cellular debris in atherosclerotic lesions. During ongoing immunohistochemical investigations, however, w e have found that a few S-100 positive cells exhibited a foam cell app earance. Therefore, we undertook an electronmicroscopic examination to see if any foam cells exhibit the distinctive features of vascular de ndritic cells such as the presence of dense granules and a tubulovesic ular system uniquely found in well differentiated dendritic cells. Foa m cells exhibiting the typical characteristics of vascular dendritic c ells were indeed found. Their cytoplasm contained a large number of li pid vacuoles and cisterns of the tubulovesicular system as well as den se granules which, in contrast to lysosomes present in macrophages, di d not transform into phagolysosomes. The formation of a central lamina inside cisterns of the tubulovesicular system was also detected. Thes e pentalaminal structures, comprised of two parallel limiting membrane s and a central lamina, are similar to the Birbeck granules present in human epidermal Langerhans cells. From our present observations we sp eculate that the defense mechanisms against extensive lipid accumulati on may be broken in some vascular dendritic cells, causing them to tra nsform into foam cells. (C) 1997 by Elsevier Science Inc.