| First Author | Ren J | Year | 2007 |
| Journal | Mech Ageing Dev | Volume | 128 |
| Issue | 3 | Pages | 276-85 |
| PubMed ID | 17250874 | Mgi Jnum | J:118617 |
| Mgi Id | MGI:3699980 | Doi | 10.1016/j.mad.2006.12.007 |
| Citation | Ren J, et al. (2007) Cardiac overexpression of antioxidant catalase attenuates aging-induced cardiomyocyte relaxation dysfunction. Mech Ageing Dev 128(3):276-85 |
| abstractText | Catalase, an enzyme which detoxifies H(2)O(2), may interfere with cardiac aging. To test this hypothesis, contractile and intracellular Ca(2+) 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 (TPS(90)), time-to-90% relengthening (TR(90)), half-width duration (HWD), maximal velocity of shortening/relengthening (+/-dL/dt) and intracellular Ca(2+) levels or decay rate. Levels of advanced glycation endproduct (AGE), Na(+)/Ca(2+) exchanger (NCX), sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA2a), phospholamban (PLB), myosin heavy chain (MHC), membrane Ca(2+) 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, TR(90) and intracellular Ca(2+) 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 Ca(2+) 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 Kv(1.2) K(+) channel was significantly reduced although levels of PLB, L-type Ca(2+) channel dihydropyridine receptor and beta-MHC isozyme remained unchanged in aged FVB hearts. Catalase restored NCX and Kv(1.2) 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 Ca(2+) handling. |
