|  Help  |  About  |  Contact Us

Publication : Age-related changes in the metabolism of acetylated low-density lipoproteins by peritoneal macrophages from C57BL/6CrScl mice.

First Author  Araki A Year  1994
Journal  J Gerontol Volume  49
Issue  3 Pages  B104-9
PubMed ID  8169327 Mgi Jnum  J:17969
Mgi Id  MGI:65992 Doi  10.1093/geronj/49.3.b104
Citation  Araki A, et al. (1994) Age-related changes in the metabolism of acetylated low-density lipoproteins by peritoneal macrophages from C57BL/6CrScl mice. J Gerontol 49(3):B104-9
abstractText  Macrophages are major precursors of foam cells in atherosclerotic lesions. Acetylated low-density lipoproteins (acetyl LDL) taken up by macrophages through scavenger receptors are degraded by lysosomes and the released cholesterol is re-esterified, leading to foam cell formation. The ability of resident peritoneal macrophages from C57BL/6CrScl mice to form foam cells in relation to the donor age was assessed by the cholesterol esterification and the metabolism of acetyl LDL. The incorporation of 14C-oleate (complexed to albumin) into cellular cholesteryl esters in the presence of acetyl LDL (100 micrograms/ml) was significantly greater in macrophages from senescent mice (24-25 months) than in cells from young (3-4 months) mice (p < .001). The degradation and cellular association of acetyl LDL by macrophages from senescent mice were significantly greater than macrophages from mature mice, (p < .001 and p < .01, respectively), whereas the binding of acetyl LDL was similar in peritoneal macrophages from mature and senescent mice. These results suggest that the uptake and degradation of acetyl LDL, and the re-esterification by macrophages increase with advancing age and that the ability of macrophages to form foam cells increases with aging. The enhanced ability of senescent macrophages to form foam cells might contribute to the development and progression of atherosclerosis related to the aging process.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

0 Bio Entities

0 Expression