Cardiac-specific overexpression of catalase prolongs lifespan and attenuates ageing-induced cardiomyocyte contractile dysfunction and protein damage.

Cardiac-specific overexpression of catalase prolongs lifespan and attenuates ageing-induced cardiomyocyte contractile dysfunction and protein damage. Research Abstract Details 

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Cardiac-specific overexpression of catalase prolongs lifespan and attenuates ageing-induced cardiomyocyte contractile dysfunction and protein damage. Abstract Text:

Shan Wu,Qun Li,Min Du,Shi-Yan Li,Jun Ren,

1. Oxidative stress plays a role in senescence-associated organ deterioration. This is supported by the beneficial effects of anti-oxidants against ageing-related organ damage, although their role in cardiac ageing has not been elucidated. 2. The aim of the present study was to examine the impact of cardiac-specific overexpression of catalase, an enzyme for H(2)O(2) detoxification, on cardiac contractile function and protein damage in young (3-4 months) and old (26-28 months) male mice. Lifespan was analysed using the Kaplan-Meier survival curve. Cardiomyocyte contractile indices at various stimulus frequencies (0.1-5.0 Hz) were analysed, including peak shortening (PS), time to 90% PS, time to 90% relengthening (TR(90)) and maximal velocity of shortening/relengthening (+/-dL/dt). Protein damage was assessed using protein carbonyl formation. Catalase transgenic mice showed longer lifespan than wild-type FVB mice. The catalase transgene itself did not alter bodyweight or organ weight, or myocyte function. Ageing depressed +/-dL/dt and prolonged TR(90), but had no effect on other indices in FVB mice. Increased frequency triggered decreases in PS amplitude were exaggerated in aged FVB myocytes. Interestingly, ageing-induced mechanical defects were significantly attenuated in myocytes from catalase mice. Protein carbonyl formation was elevated in aged FVB compared with young FVB mice, which was significantly diminished in catalase mice. The proteomes of the myocardium of young or old FVB and catalase mice were compared using two-dimensional gel electrophoresis and mass spectrometry. Six proteins with differential expression between young and old FVB groups were tentatively identified, some of which were reversed by catalase. 3. In summary, the present data suggest that catalase protects cardiomyocytes from ageing-induced contractile defects and protein damage.

Cardiac-specific overexpression of catalase prolongs lifespan and attenuates ageing-induced cardiomyocyte contractile dysfunction and protein damage. Publishing Authors By Initials

S Wu,Q Li,M Du,SY Li,J Ren,

For similar proteins research abstracts see: proteins research

PUBMED ID PMID:

MEDLINE DATE: 2007 Jan-Feb

Cardiac-specific overexpression of catalase prolongs lifespan and attenuates ageing-induced cardiomyocyte contractile dysfunction and protein damage. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Clinical and experimental pharmacology & physiolog

VOLUME: 34

Page Numbers: 81-7

Journal Abbreviation: Clin. Exp. Pharmacol. Physiol.

ISSN: 0305-1870

DAY: 3

MONTH: 12

YEAR: 2007

Cardiac-specific overexpression of catalase prolongs lifespan and attenuates ageing-induced cardiomyocyte contractile dysfunction and protein damage. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 425076

Cardiac-specific overexpression of catalase prolongs lifespan and attenuates ageing-induced cardiomyocyte contractile dysfunction and protein damage. Keywords Mesh Terms:

KEYWORDS: Proteins

MESH TERMS: analysis

Chemical & Substance for Abstract: Cardiac-specific overexpression of catalase prolongs lifespan and attenuates ageing-induced cardiomyocyte contractile dysfunction and protein damage. Information

Substance Name: Catalase

Registry Number: EC 1.11.1.6

Grant and Affiliation Information for Cardiac-specific overexpression of catalase prolongs lifespan and attenuates ageing-induced cardiomyocyte contractile dysfunction and protein damage.

AFFILIATION: Division of Pharmaceutical Sciences & Center for Cardiovascular Research and Alternative Medicine, University of Wyoming, Laramie, Wyoming 82071-3375, USA.

Country: Australia

AGENCY: United States NIAAA

GRANT: 1R15 AA13575-01

ACRONYM: AA

MEDLINETA: Clin Exp Pharmacol Physiol

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