白细胞介素-17 通过抑制金属硫蛋白-2 的自噬降解,防止氧化应激破坏成骨细胞的形成

IF 1.3 4区 医学 Q4 ENDOCRINOLOGY & METABOLISM Endocrine journal Pub Date : 2024-04-20 DOI:10.1507/endocrj.ej24-0050
Xueyan Ling, Cuixia Wang, Qin Feng, Tao Zhang
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引用次数: 0

摘要

白细胞介素 17A(IL-17A)是一种促进成骨细胞形成的关键细胞因子,有助于成骨。IL-17A 在成骨细胞内发挥抑制自噬的功能。金属硫蛋白-2(MT-2)是一种重要的活性氧(ROS)清除分子,可防止氧化应激破坏成骨细胞的形成。IL-17A调节的自噬与氧化应激下MT-2的产生之间的关系值得进一步探讨。在本研究中,我们首先研究了 IL-17A 在过氧化氢(H2O2)存在下对成骨细胞分化和成骨细胞前体中 ROS 生成的作用。接着,我们探讨了在 H2O2 存在的情况下,IL-17A 对成骨细胞前体自噬活性和 MT-2 蛋白表达的影响。最后,我们利用自噬药理激动剂(雷帕霉素)和慢病毒转导技术,进一步阐明了自噬、IL-17A 调节的 MT-2 蛋白表达和 IL-17A 调节的 ROS 产生之间的关系。结果表明,在 H2O2 存在的情况下,IL-17A 可促进成骨细胞分化并抑制 ROS 的产生。此外,在 H2O2 存在的情况下,IL-17A 可抑制自噬活性并促进成骨细胞前体中 MT-2 蛋白的表达。重要的是,雷帕霉素可逆转 IL-17A 促进的 MT-2 蛋白水平和抑制的 ROS 生成。此外,MT-2沉默也能阻止IL-17A抑制ROS的产生。总之,IL-17A 通过抑制 MT-2 的自噬降解来促进 ROS 的清除,从而保护成骨细胞的形成免受氧化应激。
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Interleukin-17 prevents oxidative stress from damaging osteoblast formation by inhibiting autophagic degradation of metallothionein-2

Interleukin 17A (IL-17A) is a key cytokine promoting osteoblast formation, which contributes to osteogenesis. IL-17A functions in autophagy inhibition within osteoblasts. Metallothionein-2 (MT-2), as an important reactive oxygen species (ROS)-scavenging molecule, prevents oxidative stress from damaging osteoblast formation. The relationship between IL-17A-regulated autophagy and MT-2 production under oxidative stress deserves further exploration. In this study, we first investigated the roles of IL-17A in osteoblastic differentiation and ROS production in osteoblast precursors in the presence of hydrogen peroxide (H2O2). Next, we explored the effects of IL-17A on autophagic activity and MT-2 protein expression in osteoblast precursors in the presence of H2O2. Ultimately, by using autophagic pharmacological agonist (rapamycin) and lentiviral transduction technology, the relationship between autophagy, IL-17A-regulated MT-2 protein expression and IL-17A-regulated ROS production was further elucidated. Our results showed that in the presence of H2O2, IL-17A promoted osteoblastic differentiation and inhibited ROS production. Moreover, in the presence of H2O2, IL-17A inhibited autophagic activity and promoted MT-2 protein expression in osteoblast precursors. Importantly, IL-17A-promoted MT-2 protein levels and -inhibited ROS production were reversed by autophagy activation with rapamycin. Furthermore, IL-17A-inhibited ROS production were blocked by MT-2 silencing. In conclusion, IL-17A promotes ROS clearance by inhibiting autophagic degradation of MT-2, thereby protecting osteoblast formation from oxidative stress.

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来源期刊
Endocrine journal
Endocrine journal 医学-内分泌学与代谢
CiteScore
4.30
自引率
5.00%
发文量
224
审稿时长
1.5 months
期刊介绍: Endocrine Journal is an open access, peer-reviewed online journal with a long history. This journal publishes peer-reviewed research articles in multifaceted fields of basic, translational and clinical endocrinology. Endocrine Journal provides a chance to exchange your ideas, concepts and scientific observations in any area of recent endocrinology. Manuscripts may be submitted as Original Articles, Notes, Rapid Communications or Review Articles. We have a rapid reviewing and editorial decision system and pay a special attention to our quick, truly scientific and frequently-citable publication. Please go through the link for author guideline.
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