Department of Cardiac Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
The Institute of Medical Science Research, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
BMC Cardiovasc Disord. 2020 May 6;20(1):214. doi: 10.1186/s12872-020-01478-1.
Epicardial adipose tissue (EAT) remodeling and adipocytokines are associated with structural remodeling in atrial fibrillation (AF). However, the role of omentin-1, a novel adipocytokine, in structural remodeling remains unknown.
Hematoxylin and eosin (H&E) and Masson's trichrome stains were used to investigate the histology of EAT and right atrial appendages. The expression levels of adipocytokines in these human samples were determined by immunohistochemical assay and western blotting. Models of transforming growth factor (TGF)-β1-induced activation of cardiac fibroblasts (CFs) and TGF-β1-induced endothelial-mesenchymal transition (EndMT) of human umbilical vein endothelial cell (HUVEC) were established to explore roles of omentin-1 in these processes. To determine changes in adipocytokines secretion under hypoxia conditions, adipocytes were treated with 5% O and 95% N, and then CFs and HUVECs were co-cultured with the conditioned medium of adipocytes to determine the effects of hypoxia-treated adipocytes on these cells.
Expression of omentin-1 was downregulated in the EAT and right atrial appendages from patients with AF compared to samples from patients without AF, while the TGF-β1 level was upregulated in EAT from patients with AF. EAT from patients with AF exhibited adipocyte hypertrophy and severe interstitial fibrosis. Omentin-1 inhibited TGF-β1-induced CF activation and reversed TGF-β1-induced HUVEC EndMT. Adipocytes treated with hypoxia exhibited downregulation of omentin-1 and partly activated CFs.
This study demonstrated that omentin-1 was an antifibrotic adipocytokine and was downregulated in patients with AF, which was partly mediated by hypoxia.
心外膜脂肪组织（EAT）重塑和脂肪细胞因子与心房颤动（AF）的结构重塑有关。然而，一种新的脂肪细胞因子网膜素-1在结构重塑中的作用尚不清楚。
使用苏木精和伊红（H&E）和马松三色染色法研究 EAT 和右心耳的组织学。通过免疫组织化学检测和 Western blot 法测定这些人组织样本中脂肪细胞因子的表达水平。建立了转化生长因子（TGF）-β1 诱导的心肌成纤维细胞（CF）激活和 TGF-β1 诱导人脐静脉内皮细胞（HUVEC）内皮-间质转化（EndMT）的模型，以探讨网膜素-1在这些过程中的作用。为了确定缺氧条件下脂肪细胞因子分泌的变化，用 5%O 和 95%N 处理脂肪细胞，然后用脂肪细胞的条件培养基共培养 CF 和 HUVEC，以确定缺氧处理的脂肪细胞对这些细胞的影响。
与非 AF 患者相比，AF 患者的 EAT 和右心耳中的网膜素-1表达下调，而 EAT 中的 TGF-β1 水平上调。AF 患者的 EAT 表现出脂肪细胞肥大和严重的间质纤维化。用缺氧处理的脂肪细胞表现出网膜素-1下调和部分激活 CF。
本研究表明，网膜素-1是一种抗纤维化的脂肪细胞因子，在 AF 患者中下调，部分是由缺氧介导的。
