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New life sciences data have been reported by scientists at University of Minnesota
2009 AUG 3 - (NewsRx.com) -- According to recent research published in the journal Plos Medicine, "The loss of dystrophin compromises muscle cell membrane stability and causes Duchenne muscular dystrophy and/or various forms of cardiomyopathy. Increased expression of the dystrophin homolog utrophin by gene delivery or pharmacologic up-regulation has been demonstrated to restore membrane integrity and improve the phenotype in the dystrophin-deficient mdx mouse." "However, the lack of a viable therapy in humans predicates the need to explore alternative methods to combat dystrophin deficiency. We investigated whether systemic administration of recombinant full-length utrophin (Utr) or Delta R4-21 ''micro'' utrophin (mu Utr) protein modified with the cell-penetrating TAT protein transduction domain could attenuate the phenotype of mdx mice. and Findings: Recombinant TAT-Utr and TAT-mu Utr proteins were expressed using the baculovirus system and purified using FLAG-affinity chromatography. Age-matched mdx mice received six twice-weekly intraperitoneal injections of either recombinant protein or PBS. Three days after the final injection, mice were analyzed for several phenotypic parameters of dystrophin deficiency. Injected TAT-mu Utr transduced all tissues examined, integrated with members of the dystrophin complex, reduced serum levels of creatine kinase (11,290 +/- 920 U versus 5,950 +/- 61,120 U; PBS versus TAT), the prevalence of muscle degeneration/regeneration (54% +/- 65% versus 37% +/- 64% of centrally nucleated fibers; PBS versus TAT), the susceptibility to eccentric contraction-induced force drop (72% +/- 65% versus 40% +/- 68% drop; PBS versus TAT), and increased specific force production (9.7 +/- 1.1 N/cm(2) versus 12.8 +/- 60.9 N/cm(2); PBS versus TAT)," wrote K.J. Sonnemann and colleagues, University of Minnesota. The researchers concluded: "These results are, to our knowledge, the first to establish the efficacy and feasibility of TAT-utrophin-based constructs as a novel direct protein-replacement therapy for the treatment of skeletal and cardiac muscle diseases caused by loss of dystrophin." Sonnemann and colleagues published their study in Plos Medicine (Functional Substitution by TAT-Utrophin in Dystrophin-Deficient Mice. Plos Medicine, 2009;6(5):83). For additional information, contact K.J. Sonnemann, University of Minnesota, Dept. of Biochemistry Molecular Biology & Biophysics, Minneapolis, MN 55455, USA. The publisher's contact information for the journal Plos Medicine is: Public Library Science, 185 Berry St., Ste. 1300, San Francisco, CA 94107, USA. Keywords: United States, Minneapolis, Life Sciences, Cardiomyopathy, Biotechnology, Gene Therapy, Genetics, Genomics, Neurology, Duchenne Muscular Dystrophy, Muscular Dystrophies, Cardiomyopathies, Virology, Baculovirus, Treatment, Chromatography, Pharmaceuticals, University of Minnesota. This article was prepared by Biotech Business Week editors from staff and other reports. Copyright 2009, Biotech Business Week via NewsRx.com.
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