کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10537649 | 962804 | 2005 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A novel scheme of dystrophin disruption for the progression of advanced heart failure
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کلمات کلیدی
DCMDAPδ-SarcoglycanrAAVHCMLVPDystrophin - دیستروفینleft ventricular pressure - فشار بطن چپheart failure - نارسایی قلبیrecombinant adeno-associated virus - ویروس مرتبط با آدنوئید نوترکیبProteolysis - پروتئولیزDystrophin-associated proteins - پروتئین های مرتبط با دیستروفینGene therapy - ژن درمانیCardiomyopathy - کاردیومیوپاتیDilated cardiomyopathy - کاردیومیوپاتی دیلاته، کاردیومیوپاتی کاملHypertrophic cardiomyopathy - کاردیومیوپاتی هایپرتروفیک Calpain - کالپین
موضوعات مرتبط
مهندسی و علوم پایه
شیمی
شیمی آنالیزی یا شیمی تجزیه
پیش نمایش صفحه اول مقاله
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چکیده انگلیسی
The precise mechanism of the progression of advanced heart failure is unknown. We assessed a new scheme in two heart failure models: (I) congenital dilated cardiomyopathy (DCM) in TO-2 strain hamsters lacking δ-sarcoglycan (SG) gene and (II) administration of a high-dose of isoproterenol, as an acute heart failure in normal rats. In TO-2 hamsters, we followed the time course of the histological, physiological and metabolic the progressions of heart failure to the end stage. Dystrophin localization detected by immunostaining age-dependently to the myoplasm and the in situ sarcolemma fragility evaluated by Evans blue entry was increased in the same cardiomyocytes. Western blotting revealed a limited cleavage of the dystrophin protein at the rod domain, strongly suggesting a contribution of endogenous protease(s). We found a remarkable up-regulation of the amount of calpain-1 and -2, and no change of their counterpart, calpastatin. After supplementing TO-2 hearts with the normal δ-SG gene in vivo, these pathological alterations and the animals' survival improved. Furthermore, dystrophin but not δ-SG was disrupted by a high dose of isoproterenol, translocated from the sarcolemma to the myoplasm and fragmented. These results of heart failure, irrespective of the hereditary or acquired origin, indicate a vicious cycle formed by the increased sarcolemma permeability, preferential activation of calpain over calpastatin, and translocation and cleavage of dystrophin would commonly lead to advanced heart failure.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics - Volume 1751, Issue 1, 1 August 2005, Pages 73-81
Journal: Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics - Volume 1751, Issue 1, 1 August 2005, Pages 73-81
نویسندگان
Tomie Kawada, Fujiko Masui, Asaki Tezuka, Takashi Ebisawa, Hiroyuki Kumagai, Mikio Nakazawa, Teruhiko Toyo-oka,