Altered Expression of Troponin T Isoforms in Mild Left Ventricular Hypertrophy in the Rabbit

Autor: Chen, Zengyi, Higashiyama, Akihiro, Yaku, Hitoshi, Bell, Stephen, Fabian, Judit, Watkins, Matthew W., Schneider, David J., Maughan, David W., LeWinter, Martin M.
Zdroj: Journal of Molecular and Cellular Cardiology; September 1997, Vol. 29 Issue: 9 p2345-2354, 10p
Abstrakt: Alterations in troponin T (TnT) isoforms have been reported in severe human and experimental heart failure (HF), and may play a role in the depressed myofibrillar ATPase activity observed in this condition. It is unclear whether these alterations reflect very severe hemodynamic derangement or are a component of mild hypertrophic stress. Therefore, we studied the expression of TnT isoforms (SDS-PAGE, Western blots), myosin isoforms, myofibrillar ATPase activity, and left ventricular (LV) mechanoenergetics (rbc perfused, isovolumically contracting isolated heart) in a rabbit model of mild hypertrophy (LVH) due to gradual hypertension caused by 12 weeks of cellophane wrap of the kidneys (n=12). LV/body weight ratio increased by 28% in LVH compared to shams (P<0.001); no animals had evidence of HF. In LVH, the percentage of TnT2was modestly but significantly increased compared to shams [6.2±1.9 (±S.D.)v3.7±1.0%,P<0.05], mainly as a consequence of a parallel decrease in TnT4(P=0.07). Sham hearts ranged from 75–100% V3isomyosin, whereas all LVH hearts had 100% of the V3form. There were no significant differences in myofibrillar ATPase activity or mechanical variables, including contraction and relaxation rates. The slope of the VO2-pressure–volume–area relation (a measure of the energy conversion efficiency of the contractile machinery) was also unchanged. We conclude that in the rabbit, shifts in TnT isoforms toward a more “fetal” pattern occur during mild LVH and, therefore, are likely to be a general feature of the response to hemodynamic stress, rather than a phenomenon confined to end-stage disease. These modest shifts are not associated with major alterations in LV myofibrillar ATPase activity or mechanoenergetics.
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