کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8474178 | 1550420 | 2015 | 32 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Macrophages and galectin 3 play critical roles in CVB3-induced murine acute myocarditis and chronic fibrosis
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کلمات کلیدی
DCMDPIqRT-PCRSCIDRT-PCRBNPCoxsackievirus B3αSMAANPCCL-2cTnIPVDFCVB3PBSProcollagen type IMOI - MEquantitative RT-PCR - RT-PCR کمیα-smooth muscle actin - اکتین عضله آلفا صافIHC - ایمونوهیستوشیمیImmunohistochemistry - ایمونوهیستوشیمیIntraperitoneally - داخل صفاقیdays post-infection - روز بعد از عفونتreverse transcription PCR - رونویسی معکوس PCRPhosphate buffered saline - فسفات بافر شورFibrosis - فیبروز یا فساد الیافcardiac troponin I - قلب تروپونین IMacrophages - ماکروفاژها،درشت خوارهاMyocarditis - میوکاردیتViral myocarditis - میوکاردیت ویروسیheart failure - نارسایی قلبیwild type - نوع وحشیplaque forming units - واحدهای تشکیل پلاکpfu - پفوPolyvinylidene fluoride - پلی وینیلیدین فلورایدmultiplicity of infection - چندین عفونتDilated cardiomyopathy - کاردیومیوپاتی دیلاته، کاردیومیوپاتی کاملsevere combined immunodeficiency - کمبود شدید مصدومchemokine (C–C motif) ligand 2 - کیموکین (C-C motif) لیگاند 2Gal-3 - گال سومgalectin 3 - گالکتین 3
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Macrophage influx and galectin 3 production have been suggested as major players driving acute inflammation and chronic fibrosis in many diseases. However, their involvement in the pathogenesis of viral myocarditis and subsequent cardiomyopathy are unknown. Our aim was to characterise the role of macrophages and galectin 3 on survival, clinical course, viral burden, acute pathology, and chronic fibrosis in coxsackievirus B3 (CVB3)-induced myocarditis. Our results showed that C3H/HeJ mice infected with CVB3 and depleted of macrophages by liposome-encapsulated clodronate treatment compared with infected untreated mice presented higher viral titres but reduced acute myocarditis and chronic fibrosis, compared with untreated infected mice. Increased galectin 3 transcriptional and translational expression levels correlated with CVB3 infection in macrophages and in non-depleted mice. Disruption of the galectin 3 gene did not affect viral titres but reduced acute myocarditis and chronic fibrosis compared with C57BL/6J wild-type mice. Similar results were observed after pharmacological inhibition of galectin 3 with N-acetyl-d-lactosamine in C3H/HeJ mice. Our results showed a critical role of macrophages and their galectin 3 in controlling acute viral-induced cardiac injury and the subsequent fibrosis. Moreover, the fact that pharmacological inhibition of galectin 3 induced similar results to macrophage depletion regarding the degree of acute cardiac inflammation and chronic fibrosis opens up the possibility of new pharmacological strategies for viral myocarditis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 85, August 2015, Pages 58-70
Journal: Journal of Molecular and Cellular Cardiology - Volume 85, August 2015, Pages 58-70
نویسندگان
Carolina Jaquenod De Giusti, AgustÃn E. Ure, Leonardo Rivadeneyra, Mirta Schattner, Ricardo M. Gomez,