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Aging‐induced proinflammatory shift in cytokine expression profile in rat coronary arteries
Author(s) -
Csiszar Anna,
Ungvari Zoltan,
Koller Akos,
Edwards John G.,
Kaley Gabor
Publication year - 2003
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.02-1049fje
Subject(s) - proinflammatory cytokine , coronary arteries , cytokine , tumor necrosis factor alpha , blot , medicine , receptor , chemokine , interleukin 6 , vascular smooth muscle , phenotype , endocrinology , biology , pathology , inflammation , artery , gene , smooth muscle , biochemistry
The phenotypic and functional changes of coronary arteries with aging promote ischemic heart disease. We hypothesized that these alterations reflect an aging‐induced proinflammatory shift in vascular regulatory mechanisms. Thus, in isolated coronary arteries of young (3‐month‐old) and aged (25‐month‐old) male Fischer 344 rats the expression of 96 cytokines, chemokines, and their receptors were screened by a cDNA‐based microarray technique. In aged vessels expressions of tumor necrosis factor (TNF)‐α (3.3x), interleukin (IL)‐1β (3.0x), IL‐6 (2.9x), IL‐6Rα (2.8x) and IL‐17 (6.1x) genes were significantly increased over young vessels. Quantitative reverse transcriptase‐polymerase chain reaction confirmed these results. Western blotting demonstrated that protein expressions of TNF‐α, IL‐1β, IL‐6, and IL‐17 were also significantly increased in vessels of aged rats compared with those of young rats. Immunofluorescent double labeling showed that in aged vessels IL‐1β and IL‐6 are predominantly localized in the endothelium, whereas TNF‐α and IL‐17 are localized in smooth muscle. Thus, a proinflammatory shift in the profile of vascular cytokine expression may contribute to the aging‐induced phenotypic changes in coronary arteries, promoting the development of ischemic heart disease in the elderly.