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在 3T3-L1 细胞的脂肪细胞分化过程中抑制脂肪生成转录因子。

Inhibits Adipogenic Transcription Factors during Adipocyte Differentiation in 3T3-L1 Cells.

机构信息

Research Institute of Medical Sciences, College of Medicine, Chungnam National University, 266 Munhwa-ro, Daejeon 35015, Jung-gu, Republic of Korea.

Department of Medical Science, College of Medicine, Chungnam National University, 266 Munhwa-ro, Daejeon 35015, Jung-gu, Republic of Korea.

出版信息

Int J Mol Sci. 2023 Feb 7;24(4):3251. doi: 10.3390/ijms24043251.

Abstract

Apurinic/apyrimidinic endonuclease 1/redox factor-1 () is a multifunctional protein involved in DNA repair and redox regulation. The redox activity of is involved in inflammatory responses and regulation of DNA binding of transcription factors related to cell survival pathways. However, the effect of on adipogenic transcription factor regulation remains unknown. In this study, we investigated the effect of on the regulation of adipocyte differentiation in 3T3-L1 cells. During adipocyte differentiation, expression significantly decreased with the increased expression of adipogenic transcription factors such as CCAAT/enhancer binding protein ()- and peroxisome proliferator-activated receptor ()-, and the adipocyte differentiation marker adipocyte protein 2 () in a time-dependent manner. However, overexpression inhibited , and expression, which was upregulated during adipocyte differentiation. In contrast, silencing or redox inhibition of using E3330 increased the mRNA and protein levels of , , and during adipocyte differentiation. These results suggest that inhibits adipocyte differentiation by regulating adipogenic transcription factors, suggesting that is a potential therapeutic target for regulating adipocyte differentiation.

摘要

脱嘌呤/脱嘧啶核酸内切酶 1/氧化还原因子-1 () 是一种多功能蛋白,参与 DNA 修复和氧化还原调节。 的氧化还原活性参与炎症反应和与细胞存活途径相关的转录因子的 DNA 结合调节。然而, 对脂肪生成转录因子调节的影响尚不清楚。在这项研究中,我们研究了 在 3T3-L1 细胞中脂肪细胞分化调节中的作用。在脂肪细胞分化过程中, 的表达随着脂肪生成转录因子如 CCAAT/增强子结合蛋白 ()- 和过氧化物酶体增殖物激活受体 ()- 的表达增加而显著降低,并且脂肪细胞分化标志物脂肪细胞蛋白 2 () 的表达呈时间依赖性。然而, 过表达抑制了 、 和 在脂肪细胞分化过程中上调的表达。相比之下,通过使用 E3330 沉默 或氧化还原抑制 可增加脂肪细胞分化过程中 、 、 和 的 mRNA 和蛋白水平。这些结果表明, 通过调节脂肪生成转录因子抑制脂肪细胞分化,表明 是调节脂肪细胞分化的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d884/9961804/b265c0a3f1e1/ijms-24-03251-g001.jpg

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