کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8262336 | 1534836 | 2018 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Repetitive TLR3 activation in the lung induces skeletal muscle adaptations and cachexia
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کلمات کلیدی
PBSMuscle RING finger-1MyHCIFN-βMuRF-1mTORC1RSVGastrocnemiusPGC-1αEDLNF-κBperoxisome proliferator-activated receptor gamma coactivator 1-alpha - 1-آلفا کوآتیواتور گاما گیرنده فعال پرولیسینز فعالTRIF - Trif بهextensor digitorum longus - اکستانسور بلند شست انگشتانinterferon-beta - اینترفرون بتاChronic obstructive pulmonary disease - بیماری مزمن انسدادی ریهCOPD - بیماری مزمن انسدادی ریهMyosin heavy chain - زنجیره سنگین میوزینSol - سلSoleus - سولوسnuclear factor kappa-light-chain-enhancer of activated B cells - فاکتور هسته ای kappa-light-chain-enhancer از سلول های B فعال شده استPhosphate buffered saline - فسفات بافر شورmechanistic target of rapamycin complex 1 - هدف مکانیکی مجتمع رپامایسین 1Respiratory syncytial virus - ویروس سنسیتیال تنفسیpolyinosinic-polycytidylic acid - پلیسی سمی-پلیسییدیدیل اسید
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Due to immunosenescence, older adults are particularly susceptible to lung-based viral infections, with increased severity of symptoms in those with underlying chronic lung disease. Repeated respiratory viral infections produce lung maladaptations, accelerating pulmonary dysfunction. Toll like 3 receptor (TLR3) is a membrane protein that senses exogenous double-stranded RNA to activate the innate immune response to a viral infection. Polyinosinic-polycytidylic acid [poly(I:C)] mimics double stranded RNA and has been shown to activate TLR3. Utilizing an established mouse viral exacerbation model produced by repetitive intranasal poly(I:C) administration, we sought to determine whether repetitive poly(I:C) treatment induced negative muscle adaptations (i.e. atrophy, weakness, and loss of function). We determined skeletal muscle morphological properties (e.g. fiber-type, fiber cross-sectional area, muscle wet mass, etc.) from a treated group ((poly(I:C), nâ¯=â¯9) and a sham-treated control group (PBS, nâ¯=â¯9); age approximately 5â¯months. In a subset (nâ¯=â¯4 for both groups), we determined in vivo physical function (using grip test for strength, rotarod for overall motor function, and treadmill for endurance) and muscle contractile properties with in vitro physiology (in the EDL, soleus and diaphragm). Our findings demonstrate that poly(I:C)-treated mice exhibit both muscle morphological and functional deficits. Changes of note when comparing poly(I:C)-treated mice to PBS-treated controls include reductions in fiber cross-sectional area (â27% gastrocnemius, â25% soleus, â16% diaphragm), contractile dysfunction (soleus peak tetanic force, â26%), muscle mass (gastrocnemius â19%, soleus â23%), physical function (grip test â34%), body mass (â20%), and altered oxidative capacity (140% increase in succinate dehydrogenase activity in the diaphragm, but 66% lower in the gastrocnemius). Our data is supportive of a new model of cachexia/sarcopenia that has potential for future research into the mechanisms underlying muscle wasting.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Gerontology - Volume 106, June 2018, Pages 88-100
Journal: Experimental Gerontology - Volume 106, June 2018, Pages 88-100
نویسندگان
Ted G. Graber, Brandy L. Rawls, Bing Tian, William J. Durham, Camille R. Brightwell, Allan R. Brasier, Blake B. Rasmussen, Christopher S. Fry,