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缺氧会增加眼眶成纤维细胞的脂肪生成并影响脂肪细胞因子的产生——这可能是吸烟与Graves眼病之间联系的一种解释。

Hypoxia increases adipogenesis and affects adipocytokine production in orbital fibroblasts-a possible explanation of the link between smoking and Graves' ophthalmopathy.

作者信息

Chng Chiaw Ling, Lai Oi Fah, Chew Charmaine Sze-Min, Peh Yu Pei, Fook-Chong Stephanie Man-Chung, Seah Lay Leng, Khoo Daphne Hsu-Chin

机构信息

Department of Endocrinology, Singapore General Hospital, Level 3, the Academia, 20 College Road 169856, Singapore.

Department of Clinical Research, Academia Discovery Tower Level 9 Research Office 2, 20 College Road 169856, Singapore.

出版信息

Int J Ophthalmol. 2014 Jun 18;7(3):403-7. doi: 10.3980/j.issn.2222-3959.2014.03.03. eCollection 2014.

DOI:10.3980/j.issn.2222-3959.2014.03.03
PMID:24967181
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4067649/
Abstract

AIM

To assess the effects of hypoxia on human orbital fibroblasts (OF) on adipogenesis and adipocytokine production.

METHODS

Human OF were derived from tissues obtained from patients with Graves' ophthalmopathy (GO) and from patients without known thyroid diseases undergoing blepharoplasty. The OF were cultured separately under normoxic and hypoxic conditions. Comparisons of adipocytokine concentrations using multiplex ELISA and lipid accumulation in the cells using Oil Red O staining were subsequently performed.

RESULTS

There was increased adipogenesis in OF from GO subject when exposed to hypoxic culture conditions. This was not observed in OF from normal controls. Hypoxia led to an increase in leptin and a decrease in MCP-1 secretion in OF cultures.

CONCLUSION

Hypoxia induces adipogenesis in OF and may represent a mechanism by which smoking contributes to deterioration of GO. We also found novel changes to leptin and MCP-1 production in OF cultures exposed to hypoxia suggesting important roles of these cytokines in the disease process.

摘要

目的

评估缺氧对人眼眶成纤维细胞(OF)脂肪生成和脂肪细胞因子产生的影响。

方法

人OF取自格雷夫斯眼病(GO)患者以及接受眼睑成形术的无已知甲状腺疾病患者的组织。OF分别在常氧和缺氧条件下培养。随后使用多重酶联免疫吸附测定法比较脂肪细胞因子浓度,并使用油红O染色法检测细胞中的脂质积累。

结果

暴露于缺氧培养条件下时,GO患者来源的OF脂肪生成增加。正常对照来源的OF未观察到这种情况。缺氧导致OF培养物中瘦素增加,单核细胞趋化蛋白-1(MCP-1)分泌减少。

结论

缺氧诱导OF脂肪生成,可能是吸烟导致GO恶化的一种机制。我们还发现缺氧条件下OF培养物中瘦素和MCP-1产生有新变化,表明这些细胞因子在疾病过程中起重要作用。

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Divergent expression of IL-1 receptor antagonists in CD34⁺ fibrocytes and orbital fibroblasts in thyroid-associated ophthalmopathy: contribution of fibrocytes to orbital inflammation.白细胞介素-1 受体拮抗剂在甲状腺相关眼病 CD34⁺纤维细胞和成纤维细胞中的差异表达:纤维细胞对眼眶炎症的贡献。
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