scholarly journals Functional Proteomic Analysis of Experimental Autoimmune Myocarditis-Induced Chronic Heart Failure in the Rat

2010 ◽  
Vol 33 (3) ◽  
pp. 477-486 ◽  
Author(s):  
Yoshiki Sanzen ◽  
Minami Ito ◽  
Yoshimi Ohta ◽  
Yutaka Yoshida ◽  
Tomie Kawada ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Proteomic Analysis ◽  
Autoimmune Myocarditis ◽  
Experimental Autoimmune Myocarditis ◽  
Experimental Autoimmune

Carvedilol Inhibits Matrix Metalloproteinase-2 Activation in Experimental Autoimmune Myocarditis: Possibilities of Cardioprotective Application

2017 ◽  
Vol 23 (1) ◽  
pp. 89-97 ◽  
Author(s):  
Monika Skrzypiec-Spring ◽  
Katarzyna Haczkiewicz ◽  
Agnieszka Sapa ◽  
Tomasz Piasecki ◽  
Joanna Kwiatkowska ◽  
...  
Keyword(s):  
Heart Failure ◽  
Troponin I ◽  
Heart Function ◽  
Heart Diseases ◽  
Acute Myocarditis ◽  
Study Groups ◽  
Matrix Metalloproteinase 2 ◽  
Autoimmune Myocarditis ◽  
Experimental Autoimmune Myocarditis ◽  
Experimental Autoimmune

Aims: Acute myocarditis is a potentially lethal inflammatory heart disease that frequently precedes the development of dilated cardiomyopathy and subsequent heart failure. At present, there is no effective standardized therapy for acute myocarditis, besides the optimal care of heart failure and arrhythmias in accordance with evidence-based guidelines and specific etiology-driven therapy for infectious myocarditis. Carvedilol has been shown to be cardioprotective by reducing cardiac pro-inflammatory cytokines present in oxidative stress in certain heart diseases. However, effects of carvedilol administration in acute myocarditis with its impact on matrix metalloproteinases’ (MMPs) activation have not been elucidated. Methods and Results: Carvedilol in 3 doses (2, 10, and 30 mg/kg) was given daily to 3 study groups of rats (n = 8) with experimental autoimmune myocarditis by gastric gavage for 3 weeks. In comparison to untreated rats (n = 8) with induced myocarditis, carvedilol significantly prevented the left ventricle enlargement and/or systolic dysfunction depending on the dose in study groups. Performed zymography showed enhanced MMP-2 activity in untreated rats, while carvedilol administration reduced alterations. This was accompanied by prevention of troponin I release and myofilaments degradation in cardiac muscle tissue. Additionally, severe inflammatory cell infiltration was detected in the nontreated group. Carvedilol in all doses tested, had no impact on severity of inflammation. The severity of inflammation did not differ between study groups and in relation to the untreated group. Conclusions: The protective effects of carvedilol on heart function observed in the acute phase of experimental autoimmune myocarditis seem to be associated with its ability to decrease MMP-2 activity and subsequently prevent degradation of myofilaments and release of troponin I while not related to suppression of inflammation.

Olmesartan attenuates the development of heart failure after experimental autoimmune myocarditis in rats through the modulation of ANG 1–7 mas receptor

2012 ◽  
Vol 351 (2) ◽  
pp. 208-219 ◽  
Author(s):  
Vijayakumar Sukumaran ◽  
Punniyakoti T. Veeraveedu ◽  
Narasimman Gurusamy ◽  
Arun Prasath Lakshmanan ◽  
Ken’ichi Yamaguchi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Autoimmune Myocarditis ◽  
Mas Receptor ◽  
Experimental Autoimmune Myocarditis ◽  
Experimental Autoimmune

scholarly journals Programmed Death-Ligand 2 Deficiency Exacerbates Experimental Autoimmune Myocarditis in Mice

2021 ◽  
Vol 22 (3) ◽  
pp. 1426
Author(s):  
Siqi Li ◽  
Kazuko Tajiri ◽  
Nobuyuki Murakoshi ◽  
DongZhu Xu ◽  
Saori Yonebayashi ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Receptor ◽  
Cd4 T Cell ◽  
Myocardial Inflammation ◽  
Autoimmune Myocarditis ◽  
Inflammatory Infiltration ◽  
Programmed Death ◽  
Experimental Autoimmune Myocarditis ◽  
Deficient Mice ◽  
Experimental Autoimmune

Programmed death ligand 2 (PD-L2) is the second ligand of programmed death 1 (PD-1) protein. In autoimmune myocarditis, the protective roles of PD-1 and its first ligand programmed death ligand 1 (PD-L1) have been well documented; however, the role of PD-L2 remains unknown. In this study, we report that PD-L2 deficiency exacerbates myocardial inflammation in mice with experimental autoimmune myocarditis (EAM). EAM was established in wild-type (WT) and PD-L2-deficient mice by immunization with murine cardiac myosin peptide. We found that PD-L2-deficient mice had more serious inflammatory infiltration in the heart and a significantly higher myocarditis severity score than WT mice. PD-L2-deficient dendritic cells (DCs) enhanced CD4+ T cell proliferation in the presence of T cell receptor and CD28 signaling. These data suggest that PD-L2 on DCs protects against autoreactive CD4+ T cell expansion and severe inflammation in mice with EAM.

Immunomodulatory Effects of Erythropoietin on the Experimental Autoimmune Myocarditis of Rats

2005 ◽  
Vol 11 (9) ◽  
pp. S284
Author(s):  
Hisahito Shinagawa ◽  
Takayuki Inomata ◽  
Hironari Nakano ◽  
Toshimi Koitabashi ◽  
Tsutomu Ohsaka ◽  
...  
Keyword(s):  
Immunomodulatory Effects ◽  
Autoimmune Myocarditis ◽  
Experimental Autoimmune Myocarditis ◽  
Experimental Autoimmune
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