Postmortem proteolysis is reduced in transgenic mice overexpressing calpastatin.

摘要: Using both in vitro and vivo approaches, numerous studies have provided evidence that mu-calpain is responsible for postmortem proteolysis. This paper reports the effect of overexpression calpastatin on proteolysis transgenic mice. Transgenic mice (n = 8) with a human gene, whose expression was driven by skeletal muscle actin promoter, were killed along control nontransgenic littermates 5). Hind limbs removed stored at 4 degrees C, samples dissected 0, 1, 3, 7 d analyzed individually. At time active expressed murine level 370-fold greater (P 0.05) transgene as assessed immunoreactivity 0. Over d, 33% at-death 80-kDa isoform lost transgenics compared to an 87% loss controls, indicating autolysis slowed Desmin degradation also inhibited < when controls. Control 6, 78, 91% native desmin postmortem, respectively; conversely, only 17% same times. A similar trend observed examining troponin-T. Interestingly, m-calpain seemed undergo mice, which tissue indicative Further investigation revealed mu- are normal muscle. In conclusion, high achieved, which, virtue its inhibitory specificity, determined be directly decrease