Lipocalin-2/Neutrophil Gelatinase-B Associated Lipocalin Is Strongly Induced in Hearts of Rats With Autoimmune Myocarditis and in Human Myocarditis
Lipocalin-2/Neutrophil Gelatinase-B Associated Lipocalin Is Strongly Induced in Hearts of Rats With Autoimmune Myocarditis and in Human Myocarditis
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DOI：
10.1253/circj.cj-09-0485
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发表时间：
2010-03-01
影响因子：
3.3
通讯作者：
Aizawa, Yoshifusa
中科院分区：
文献类型：
--
作者：
Ding, Limin;Hanawa, Haruo;Aizawa, Yoshifusa
背景：Lipocalin-2/中性粒细胞明胶酶-B 相关脂质运载蛋白 (Lcn2/NGAL) 参与铁的转运，似乎在炎症中发挥重要作用。最近的一项研究报告称，它也在衰竭的心脏中表达，并且可能不仅是肾衰竭的生物标志物，而且可能是心力衰竭的生物标志物。由于Lcn2/NGAL被认为是由白细胞介素-1诱导的，因此在心肌炎存在时它可能被强烈诱导。方法和结果：本研究调查了Lcn2/NGAL在大鼠实验性自身免疫性心肌炎(EAM)和人类心肌炎中的表达。在 EAM 心脏中，Lcn2/NGAL 的表达显着增加（早期>100 倍），并且在人类心肌炎中，与非炎症性衰竭心脏相比，Lcn2/NGAL 的表达也很高。患有 EAM 和人心肌炎的心脏中表达 Lcn2/NGAL 的细胞被鉴定为心肌细胞、血管壁细胞、成纤维细胞和中性粒细胞。 EAM 大鼠中的 Lcn2/NGAL 也在肝脏中表达。血浆Lcn2/NGAL水平在EAM早期突然升高，并且在炎症阶段最初维持高水平，然后随着恢复而降低。相反，随着疾病的进展，B型利尿钠肽的水平仅缓慢增加。结论：心肌炎中的心肌细胞、血管壁细胞和成纤维细胞通过促炎细胞因子强烈表达Lcn2/NGAL。 （Circ J 2010；74：523-530）
Background: Lipocalin-2/neutrophil gelatinase-B associated lipocalin (Lcn2/NGAL) is involved in the transport of iron and seems to play an important role in inflammation. A recent study has reported that it is also expressed in the failing heart and may be a biomarker not only for renal failure but also for heart failure. Because Lcn2/NGAL is thought to be induced by interleukin-1, it might be strongly induced in the presence of myocarditis.Methods and Results: This study investigated the expression of Lcn2/NGAL in rat experimental autoimmune myocarditis (EAM) and in human myocarditis. In EAM hearts, the expression of Lcn2/NGAL was markedly increased (>100-fold at an early stage), and in human myocarditis it was also highly expressed compared with non-inflammatory failing hearts. Lcn2/NGAL expressing cells in hearts with EAM and human myocarditis were identified as cardiomyocytes, vascular wall cells, fibroblasts and neutrophils. Lcn2/NGAL in EAM rats was also expressed in the liver. Plasma Lcn2/NGAL levels abruptly increased at an early stage of EAM, and high levels were initially sustained during the inflammatory stage, then decreased with recovery. In contrast, levels of B-type natriuretic peptide increased only slowly as the disease progressed.Conclusions: Cardiomyocytes, vascular wall cells and fibroblasts in myocarditis strongly express Lcn2/NGAL via proinflammatory cytokines. (Circ J 2010; 74: 523-530)