Effect of oxidized-LDL on NF-kappaB nuclear translocation in aortic smooth muscle cells originated from rats of different ages.
- Author:
Jun-hua ZHANG
1
;
Li ZHOU
;
Hong-chao YIN
;
Pei-mao LIU
;
Hua ZHANG
;
Ming-peng SHE
Author Information
- Publication Type:Journal Article
- MeSH: Age Factors; Animals; Aorta; cytology; Cell Nucleus; metabolism; Cells, Cultured; Culture Media; Lipoproteins, HDL; pharmacology; Lipoproteins, LDL; pharmacology; Male; Myocytes, Smooth Muscle; metabolism; NF-kappa B; metabolism; Proto-Oncogene Proteins c-sis; metabolism; Rats; Rats, Wistar
- From: Chinese Medical Sciences Journal 2005;20(2):112-115
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the molecular mechanism of atherosclerosis that related to age.
METHODSImmunohistochemistry staining and Western blot were adopted to determine the nuclear translocation of nuclear factor-kappa B (NF-kappaB) and expression of platelet-derived growth factor B (PDGF-B) in smooth muscle cells (SMCs) co-cultured with low density lipoprotein (LDL), oxidized LDL (ox-LDL), and ox-LDL+high density lipoprotein (HDL) originated from rats of 2 and 10 months old respectively. Fat stain was used to identify the lipid intake in SMCs.
RESULTSThe optimal stimulation time of ox-LDL to SMCs was 12 hours. NF-kappaB intensity increased in most nuclei of SMCs that originated from rats of either 2 or 10 months old co-cultured with ox-LDL. The intensity of NF-KB and the amount of intracellular lipid taken in SMCs were more obvious in cells from 10-month-old rats than from the younger ones. Change of PDGF-B expression in SMCs was not remarkable in each group of rats.
CONCLUSIONSThe 10-month-old rats are more susceptive to ox-LDL than 2-month-old rats in activating nuclear translocation of NF-kappaB. Maybe this is one of the important reasons contributing to the difference between the older and younger rats on the initiation and development of atherosclerosis lesion. Expression of PDGF-B is not associated with the activity of nuclear translocation of NF-kappaB.