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高迁移率族蛋白 B1(HMGB1)通过 JNK 信号通路由 3T3-L1 脂肪细胞分泌,脂联素部分抑制其分泌。

HMGB1 is secreted by 3T3-L1 adipocytes through JNK signaling and the secretion is partially inhibited by adiponectin.

机构信息

Department of Laboratory and Vascular Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan.

Department of Biochemistry and Molecular Biology, University of Rajshahi, Rajshahi, Bangladesh.

出版信息

Obesity (Silver Spring). 2016 Sep;24(9):1913-21. doi: 10.1002/oby.21549. Epub 2016 Jul 19.

Abstract

OBJECTIVE

Obesity is a chronic inflammatory disease, and adipocytes contribute to obesity-associated inflammation by releasing inflammatory mediators. High mobility group box 1 (HMGB1), a highly conserved DNA-binding protein, mainly localized to cell nuclei, has been recently recognized as an innate pro-inflammatory mediator when released extracellularly. It was hypothesized that HMGB1 is an adipocytokine that acts as an innate pro-inflammatory mediator in white adipose tissue (WAT) of patients with obesity and is associated with insulin resistance. Additionally, it was hypothesized that HMGB1 secretion is regulated by adiponectin.

METHODS

3T3-L1 cells were differentiated into mature adipocytes. After tumor necrosis factor-α (TNF-α) stimulation, HMGB1 in culture media was measured. Localizations of HMGB1 in 3T3-L1 adipocytes and human WAT were examined by immunostaining.

RESULTS

HMGB1 was secreted from TNF-α-induced 3T3-L1 adipocytes through JNK signaling. HMGB1-activated MAP kinases (ERK1/2, JNK) and suppressed insulin-stimulated Akt phosphorylation in 3T3-L1 adipocytes. The cytoplasm in 3T3-L1 adipocytes and adipocytes of WAT from a patient with obesity was intensely stained with HMGB1. Adiponectin partially inhibited TNF-α-induced HMGB1 secretion from 3T3-L1 adipocytes.

CONCLUSIONS

These findings suggest that HMGB1 is a pro-inflammatory adipocytokine involved in WAT inflammation and insulin resistance in patients with obesity, which may contribute to the progression of metabolic syndrome, and that adiponectin protects against HMGB1-induced adipose tissue inflammation.

摘要

目的

肥胖是一种慢性炎症性疾病,脂肪细胞通过释放炎症介质促进肥胖相关炎症。高迁移率族蛋白 B1(HMGB1)是一种高度保守的 DNA 结合蛋白,主要位于细胞核内,最近被认为是一种细胞外释放的固有促炎介质。研究假设 HMGB1 是一种脂肪细胞因子,作为肥胖患者白色脂肪组织(WAT)中的固有促炎介质,与胰岛素抵抗相关。此外,还假设 HMGB1 的分泌受脂联素调节。

方法

将 3T3-L1 细胞分化为成熟脂肪细胞。用肿瘤坏死因子-α(TNF-α)刺激后,测量培养基中 HMGB1 的含量。通过免疫染色法检测 HMGB1 在 3T3-L1 脂肪细胞和人 WAT 中的定位。

结果

HMGB1 通过 JNK 信号通路从 TNF-α 诱导的 3T3-L1 脂肪细胞中分泌。HMGB1 激活了 MAP 激酶(ERK1/2、JNK),并抑制了 3T3-L1 脂肪细胞中胰岛素刺激的 Akt 磷酸化。肥胖患者的 WAT 中 3T3-L1 脂肪细胞和脂肪细胞的细胞质中 HMGB1 染色强烈。脂联素部分抑制了 3T3-L1 脂肪细胞中 TNF-α诱导的 HMGB1 分泌。

结论

这些发现表明,HMGB1 是一种促炎脂肪细胞因子,参与肥胖患者的 WAT 炎症和胰岛素抵抗,可能导致代谢综合征的进展,而脂联素可防止 HMGB1 诱导的脂肪组织炎症。

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