Time-course analysis of cardiac and serum galectin-3 in viral myocarditis after an encephalomyocarditis virus inoculation

Time-course analysis of cardiac and serum galectin-3 in viral myocarditis after an encephalomyocarditis virus inoculation
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DOI:
10.1371/journal.pone.0210971
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发表时间:
2019-01-23
期刊:
影响因子:
3.7
通讯作者:
Hara, Akira
Hara, Akira
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Noguchi, Kei;Tomita, Hiroyuki;Hara, Akira

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Galectin-3是一种β-半乳糖苷结合凝集素,在细胞增殖和凋亡调控中起重要作用。最近,血清半乳糖凝集素-3已被证明具有作为心力衰竭的生物标志物的预后价值。脑心肌炎病毒(Encephalomyocarditis virus,EMCV)可引起包括小鼠在内的多种动物严重的心肌炎、充血性心力衰竭、扩张性心肌病和脑炎。半乳凝素-3在病毒感染后急性心肌炎中的病理生理作用尚未完全清楚。本研究的目的是确定心脏定位和半乳糖凝集素-3表达的时间过程中的心力衰竭病毒接种EMCV后。在腹腔内接种EMCV后12、24、48、96小时、7和10天,对动物进行组织学检查并分析半乳糖凝集素-3和lba 1的表达。Galectin-3在病毒接种后96小时的心脏组织变性纤维化病变中上调,随后是心肌纤维化。同时,在炎症部位观察到lba 1阳性巨噬细胞。半乳糖凝集素-3阳性细胞的数量和退化的纤维化病变的心脏面积之间的时间过程相关性被检测到,血清半乳糖凝集素-3在96小时增加,并且与心脏半乳糖凝集素-3阳性细胞的数量相关性良好。我们的研究结果表明,半乳糖凝集素-3的表达可能是一个有用的生物标志物的心脏纤维变性在急性心肌炎病毒感染。此外,测定血清半乳糖凝集素-3水平可能是检测急性心肌炎心脏变性的早期诊断方法。
Galectin-3 is a P-galactoside-binding lectin which is important in cell proliferation and apoptotic regulation. Recently, serum galectin-3 has been shown to have prognostic value as a biomarker in heart failure. Encephalomyocarditis virus (EMCV) can cause severe myocarditis, congestive heart failure and dilated cardiomyopathy as well as encephalitis in various animals including mice. The pathophysiological role of galectin-3 in acute myocarditis following viral infection is not fully understood. The goal of this study is to determine the cardiac localization and the time-course of galectin-3 expression in heart failure after viral inoculation with EMCV. At 12, 24, 48, 96 hours, 7 and 10 days after intraperitoneal EMCV inoculation, animals were examined histologically and analyzed for the expression of galectin-3 and lba1. Galectin-3 was up-regulated in degenerated fibrotic lesions of cardiac tissues 96 hours after viral inoculation and were followed by myocardial fibrosis. At the same time, lba1 positive macrophages were observed within the inflammatory sites. A time-course correlation between the number of galectin-3 positive cells and the cardiac area of degenerated fibrotic lesions was detected serum galectin-3 increased at 96 hours and correlated well with the number of cardiac galectin-3 positive cells. Our results indicate that galectin-3 expression may be a useful biomarker of cardiac fibrotic degeneration in acute myocarditis following viral infection. In addition, measuring serum galectin-3 levels might be an early diagnostic method for detecting cardiac degeneration in acute myocarditis.