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Mechanisms of ageing and development (1)
Ikeno, Yuji (2)
Chaudhuri, Asish R (1)
Cortez, Lisa A. (1)
Goins, Beth A (1)
Grubbs, Barry (1)
Herman, Brian (1)
Hubbard, Gene B. (1)
Lee, Shuko (1)
Lew, Christie M. (1)
Mundy, Gregory R (1)
Padalecki, Susan S (1)
Richardson, Arlan (1)
Waal, Eric De (1)
Webb, Celeste R. (1)
Zhang, Yingpei (1)
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Caspase-2 Deficiency Enhances Aging-Related Traits in Mice
Padalecki, Susan S
Chaudhuri, Asish R
Waal, Eric De
Goins, Beth A
Mundy, Gregory R
Mechanisms of ageing and development
Alteration of apoptotic activity has been observed in a number of tissues in aging mammals, but it remains unclear whether and/or how apoptosis may affect aging. Caspase-2 is a member of the cysteine protease family that plays a critical role in apoptosis. To understand the impact of compromised apoptosis function on mammalian aging, we conducted a comparative study on caspase-2 deficient mice and their wild-type littermates with a specific focus on the aging-related traits at advanced ages. We found that caspase-2 deficiency enhanced a number of traits commonly seen in premature aging animals. Loss of caspase-2 was associated with shortened maximum lifespan, impaired hair growth, increased bone loss, and reduced body fat content. In addition, we found that the livers of caspase-2 deficient mice had higher levels of oxidized proteins than those of age-matched wild-type mice, suggesting that caspase-2 deficiency compromised the animal's ability to clear oxidatively damaged cells. Collectively, these results suggest that caspase-2 deficiency affects aging in the mice. This study thus demonstrates for the first time that disruption of a key apoptotic gene has a significant impact on aging.
caspase-2; maximum lifespan; bone; hair growth; fat
Do long-lived mutant and calorie-restricted mice share common anti-aging mechanisms?—a pathological point of view
Lew, Christie M.
Cortez, Lisa A.
Webb, Celeste R.
Hubbard, Gene B.
Rodent models are an invaluable resource for studying the mechanism of mammalian aging. In recent years, the availability of transgenic and knockout mouse models has facilitated the study of potential mechanisms of aging. Since 1996, aging studies with several long-lived mutant mice have been conducted. Studies with the long-lived mutant mice, Ames and Snell dwarf, and growth hormone receptor/binding protein knockout mice, are currently providing important clues regarding the role of the growth hormone/insulin like growth factor-1 axis in the aging process. Interestingly, these studies demonstrate that these long-lived mutant mice have physiological characteristics that are similar to the effects of calorie restriction, which has been the most effective experimental manipulation capable of extending lifespan in various species. However, a question remains to be answered: do these long-lived mutant and calorie-restricted mice extend their lifespan through a common underlying mechanism?
aging; growth hormone receptor/binding protein; knockout mouse; neoplastic disease
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