衰老和热应激对肝脏血红素加氧酶-1蛋白的差异调节
Differential regulation of hepatic heme oxygenase-1 protein with aging and heat stress.
作者信息
Bloomer Steven A, Zhang Hannah J, Brown Kyle E, Kregel Kevin C
机构信息
Department of Integrative Physiology, 532 FH, University of Iowa, Iowa City, IA 52242, USA.
出版信息
J Gerontol A Biol Sci Med Sci. 2009 Apr;64(4):419-25. doi: 10.1093/gerona/gln056. Epub 2009 Feb 4.
Abstract
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.
摘要
血红素加氧酶-1（HO-1）在生理应激反应下表达增加被认为是一种保护性反应，而这种反应可能会随着衰老而改变。在本研究中，通过对年轻（6个月）和年老（24个月）的Fischer 344大鼠的肝脏匀浆和分离的肝细胞进行免疫印迹以及免疫组织化学方法，评估热应激后HO-1的表达情况。年老大鼠的肝脏显示出较高的HO-1基线水平，其主要定位于库普弗细胞。热应激后，年轻动物肝脏中HO-1的相对增加幅度更大，部分原因是对HO-1免疫反应阳性的非实质细胞数量增加。与这些数据一致，仅在年轻大鼠的肝细胞中，高温体外处理后HO-1显著上调。因此，衰老以细胞特异性方式改变应激诱导的HO-1表达，这可能导致在老年生物体中观察到的应激耐受性降低。
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