Testosterone and interleukin - 1 β increase cardiac remodeling 1 during coxsackievirus B 3 myocarditis via serpin A
نویسندگان
چکیده
Testosterone and interleukin-1β increase cardiac remodeling 1 during coxsackievirus B3 myocarditis via serpin A 3n 2 3 Michael J. Coronado, Jessica E. Brandt, Eunyong Kim, Adriana Bucek, Djahida 4 Bedja, Eric D. Abston, Jaewook Shin, Kathleen L. Gabrielson, Wayne Mitzner, 5 and DeLisa Fairweather* 6 7 Department of Environmental Health Sciences, Bloomberg School of Public Health and 8 Department of Pathology, School of Medicine, Johns Hopkins University, Baltimore MD, USA 9 10 11 12 *Corresponding author: DeLisa Fairweather, PhD, Department of Environmental Health 13 Sciences, Johns Hopkins University Bloomberg School of Public Health, 615 N. Wolfe St., Rm. 14 E7628, Baltimore, MD 21205. Ph: +1 410 955 4712; Fax: +1 410 955 0116; Email: 15 [email protected] 16 17 18 Running head: Serpin A 3n promotes cardiac remodeling 19 20 Articles in PresS. Am J Physiol Heart Circ Physiol (February 10, 2012). doi:10.1152/ajpheart.00783.2011
منابع مشابه
Testosterone and interleukin-1β increase cardiac remodeling during coxsackievirus B3 myocarditis via serpin A 3n.
Myocarditis and dilated cardiomyopathy (DCM) are often caused by viral infections and occur more frequently in men than in women, but the reasons for the sex difference remain unclear. The aim of this study was to assess whether gene changes in the heart during coxsackievirus B3 (CVB3) myocarditis in male and female BALB/c mice predicted worse DCM in males. Although myocarditis (P = 4.2 × 10(-5...
متن کاملCardiac Fibroblasts Aggravate Viral Myocarditis: Cell Specific Coxsackievirus B3 Replication
Myocarditis is an inflammatory disease caused by viral infection. Different subpopulations of leukocytes enter the cardiac tissue and lead to severe cardiac inflammation associated with myocyte loss and remodeling. Here, we study possible cell sources for viral replication using three compartments of the heart: fibroblasts, cardiomyocytes, and macrophages. We infected C57BL/6j mice with Coxsack...
متن کاملIn Vivo Delivery of Adenoviral Vector Containing Interleukin-17 Receptor A Reduces Cardiac Remodeling and Improves Myocardial Function in Viral Myocarditis Leading to Dilated Cardiomyopathy
Th17 cells have been implicated in the pathogenesis of myocarditis. Interleukin (IL)-17A produced by Th17 cells is dispensable for viral myocarditis but essential for the progression to dilated cardiomyopathy (DCM). This study investigated whether the adenoviral transfer of the IL-17 receptor A reduces myocardial remodeling and dysfunction in viral myocarditis leading to DCM. In a mouse model o...
متن کاملHormonal regulation of CD4(+) T-cell responses in coxsackievirus B3-induced myocarditis in mice.
Coxsackievirus B3 infection causes significant cardiac inflammation in male, but not female, B1.Tg.Ealpha mice. This gender difference in disease susceptibility correlates with selective induction of CD4(+) Th1 (gamma interferon-positive) cell responses in animals with testosterone, whereas estradiol promotes preferential CD4(+) Th2 (interleukin-4 positive [IL-4(+)]) cell responses. Differences...
متن کاملAdoptive Transfer of Regulatory T Cells Protects against Coxsackievirus B3-Induced Cardiac Fibrosis
BACKGROUND Cardiac fibrogenesis in the late stage of viral myocarditis causing contractile dysfunction and ventricular dilatation, is a major pathogenic factor for the progression of myocarditis to serious cardiovascular diseases including dilated cardiomyopathy (DCM) and congestive heart failure (HF). Recent studies indicate that regulatory T cells (Tregs) are involved in the fibrotic process ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره شماره
صفحات -
تاریخ انتشار 2012