Cardiac overexpression of antioxidant catalase attenuates aging-induced cardiomyocyte relaxation dysfunction.

Cardiac overexpression of antioxidant catalase attenuates aging-induced cardiomyocyte relaxation dysfunction. Research Abstract Details 

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Cardiac overexpression of antioxidant catalase attenuates aging-induced cardiomyocyte relaxation dysfunction. Abstract Text:

Jun Ren,Qun Li,Shan Wu,Shi-Yan Li,Sara A Babcock,

Catalase, an enzyme which detoxifies H2O2, may interfere with cardiac aging. To test this hypothesis, contractile and intracellular Ca2+ properties were evaluated in cardiomyocytes from young (3-4 months) and old (26-28 months) FVB and transgenic mice with cardiac overexpression of catalase. Contractile indices analyzed included peak shortening (PS), time-to-90% PS (TPS90), time-to-90% relengthening (TR90), half-width duration (HWD), maximal velocity of shortening/relengthening (+/-dL/dt) and intracellular Ca2+ levels or decay rate. Levels of advanced glycation endproduct (AGE), Na+/Ca2+ exchanger (NCX), sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA2a), phospholamban (PLB), myosin heavy chain (MHC), membrane Ca2+ and K+ channels were measured by western blot. Catalase transgene prolonged survival while did not alter myocyte function by itself. Aging depressed+/-dL/dt, prolonged HWD, TR90 and intracellular Ca2+ decay without affecting other indices in FVB myocytes. Aged FVB myocytes exhibited a stepper decline in PS in response to elevated stimulus or a dampened rise in PS in response to elevated extracellular Ca2+ levels. Interestingly, aging-induced defects were nullified or significantly attenuated by catalase. AGE level was elevated by 5-fold in aged FVB compared with young FVB mice, which was reduced by catalase. Expression of SERCA2a, NCX and Kv1.2 K+ channel was significantly reduced although levels of PLB, L-type Ca2+ channel dihydropyridine receptor and beta-MHC isozyme remained unchanged in aged FVB hearts. Catalase restored NCX and Kv1.2 K+ channel but not SERCA2a level in aged mice. In summary, our data suggested that catalase protects cardiomyocytes from aging-induced contractile defect possibly via improved intracellular Ca2+ handling.

Cardiac overexpression of antioxidant catalase attenuates aging-induced cardiomyocyte relaxation dysfunction. Publishing Authors By Initials

J Ren,Q Li,S Wu,SY Li,SA Babcock,

For similar human activities: survival research abstracts see: human activities: survival research

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Cardiac overexpression of antioxidant catalase attenuates aging-induced cardiomyocyte relaxation dysfunction. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Mechanisms of ageing and development

VOLUME: 128

Page Numbers: 276-85

Journal Abbreviation: Mech. Ageing Dev.

ISSN: 0047-6374

DAY: 27

MONTH: 12

YEAR: 2006

Cardiac overexpression of antioxidant catalase attenuates aging-induced cardiomyocyte relaxation dysfunction. Information

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LANGUAGE: eng

NlmUniqueID: 347227

Cardiac overexpression of antioxidant catalase attenuates aging-induced cardiomyocyte relaxation dysfunction. Keywords Mesh Terms:

KEYWORDS: Survival

MESH TERMS: metabolism

Chemical & Substance for Abstract: Cardiac overexpression of antioxidant catalase attenuates aging-induced cardiomyocyte relaxation dysfunction. Information

Substance Name: Sarcoplasmic Reticulum Calcium-Transport

Registry Number: EC 3.6.3.8

Grant and Affiliation Information for Cardiac overexpression of antioxidant catalase attenuates aging-induced cardiomyocyte relaxation dysfunction.

AFFILIATION: Division of Pharmaceutical Sciences & Center for Cardiovascular Research and Alternative Medicine, University of Wyoming, Laramie, WY 82071-2000, United States. jren@uwyo.edu

Country: Ireland

AGENCY: United States NIA

GRANT: R03 AG021324-02

ACRONYM: AG

MEDLINETA: Mech Ageing Dev

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