Osteoglycin (Ogn), a class III SLRP member with multiple glycosylation sites, has been proposed to be engaged in cardiac dysfunction and adverse remodeling in human heart failure following myocardial infarction. However, the underlying mechanism remains to be elucidated. Thus, we sought to define the role of Ogn in regulation of the Wnt pathway on myocardial fibrosis and epithelial/endothelial‐mesenchymal transformation (EMT/EndMT) in mice with myocarditis. The pathological changes are observed, while hematoxylin–eosin staining and picric acid Sirius red staining were conducted in successfully constructed myocarditis mouse models. Immunohistochemistry and enzyme‐linked immunosorbent assay were adopted to determine Ogn and β‐catenin levels and serum procollagen propeptide concentrations in the mouse myocardial tissues, respectively. Expression of Ogn and Wnt signaling pathway‐related factors were measured by reverse transcription quantitative polymerase chain reaction and western blot assay, cell viability by 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay, and cell cycle distribution and apoptosis by flow cytometry. We saw indicative pathological changes accompanied by many Ogn and β‐catenin positive cells and increased serum procollagen propeptide, in the mouse myocardial tissues. Loss function assays showed reduced levels of Ogn, β‐catenin, LRP6, TGF‐β1, Twist, FSP‐1, α‐SMA and higher levels of E‐cadherin and VE‐cadherin, together with decreased proliferation rate, as well as increased apoptosis rate, indicating that the Wnt signaling pathway, proliferation were inhibited while apoptosis was enhanced with upon gene silencing. Coherently, depletion of Ogn inhibits myocardial fibroblasts proliferation and EMT/EndMT while facilitating myocardial fibroblasts apoptosis in myocarditis through the Wnt signaling pathway, thus serving as an intervention target for the molecular treatment of myocarditis.

中文翻译：

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骨甘氨酸沉默对心肌炎小鼠模型中的心肌纤维化和上皮/内皮-间充质转化产生抑制作用

骨甘氨酸 (Ogn) 是具有多个糖基化位点的 III 类 SLRP 成员，已被提议参与心肌梗塞后人类心力衰竭的心脏功能障碍和不良重塑。然而，潜在的机制仍有待阐明。因此，我们试图确定 Ogn 在调节 Wnt 通路对心肌炎小鼠心肌纤维化和上皮/内皮-间充质转化 (EMT/EndMT) 的作用。观察病理变化，同时在成功构建的心肌炎小鼠模型中进行苏木精-伊红染色和苦味酸天狼星红染色。采用免疫组织化学和酶联免疫吸附试验分别测定小鼠心肌组织中的 Ogn 和 β-catenin 水平和血清原胶原前肽浓度。Ogn 和 Wnt 信号通路相关因子的表达通过逆转录定量聚合酶链反应和蛋白质印迹测定，细胞活力通过 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物测定，以及通过流式细胞术检测细胞周期分布和细胞凋亡。我们在小鼠心肌组织中观察到伴随许多 Ogn 和 β-catenin 阳性细胞和血清原胶原前肽增加的指示性病理变化。损失函数分析显示 Ogn、β-catenin、LRP6、TGF-β1、Twist、FSP-1、α-SMA 水平降低，E-cadherin 和 VE-cadherin 水平升高，增殖率降低，以及增加细胞凋亡率，表明 Wnt 信号通路，增殖受到抑制，而基因沉默后细胞凋亡增强。连贯地，