Differential Regulation of Hepatic Heme Oxygenase-1 Protein With Aging and Heat Stress

被引:28
作者
Bloomer, Steven A. [1 ]
Zhang, Hannah J. [1 ]
Brown, Kyle E. [2 ,3 ,4 ]
Kregel, Kevin C. [1 ,4 ]
机构
[1] Univ Iowa, Dept Integrat Physiol, Iowa City, IA 52242 USA
[2] Iowa City Vet Adm Med Ctr, Iowa City, IA USA
[3] Univ Iowa, Dept Internal Med, Div Gastroenterol Hepatol, Iowa City, IA 52242 USA
[4] Univ Iowa, Roy J & Lucille A Carver Coll Med, Dept Radiat Oncol, Program Free Radical & Radiat Biol, Iowa City, IA 52242 USA
来源
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES | 2009年 / 64卷 / 04期
基金
美国国家卫生研究院;
关键词
Oxidative stress; Kupffer cells; Inflammation; Hyperthermia; OXIDATIVE STRESS; RAT-LIVER; ANTIOXIDANT ENZYME; KUPFFER CELLS; MONONUCLEAR PHAGOCYTES; GENE-EXPRESSION; CARBON-MONOXIDE; AGE; HEPATOCYTES; INJURY;
D O I
10.1093/gerona/gln056
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
030301 [社会学]; 100201 [内科学];
摘要
Increased expression of heme oxygenase-1 (HO-1) in response to physiological stress is considered to be a protective response, which may be altered with aging. In this study, HO-1 expression was assessed following heat stress by immunoblotting of liver homogenates and isolated hepatocytes from young (6 months) and old (24 months) Fischer 344 rats and by immunohistochemistry. Livers of old rats showed higher baseline levels of HO-1, which was predominately localized to Kupffer cells. After heat stress, young animals showed a greater relative increase in hepatic HO-1, part of which was caused by increased numbers of nonparenchymal cells that were immunoreactive to HO-1. Consistent with these data, HO-1 was significantly upregulated after hyperthermia in vitro only in hepatocytes from young rats. Hence, aging alters stress-induced expression of HO-1 in a cell-specific manner, which may contribute to the diminished stress tolerance observed in older organisms.
引用
收藏
页码:419 / 425
页数:7
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