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通过刺猬信号通路调节3T3-L1前脂肪细胞的增殖和分化。

Regulates Proliferation and Differentiation of 3T3-L1 Preadipocytes Through the Hedgehog Signaling Pathway.

作者信息

Jin Xinlin, Zhang Yu, Wang Yunzhou, Cao Hongzhen, Song Qi, Huang Jingsen, Chen Wei, Tang Hui, Zeng Yongqing

机构信息

Shandong Provincial Key Laboratory for Livestock Germplasm Innovation & Utilization, College of Animal Science and Technology, Shandong Agricultural University, Tai'an 271018, China.

Department of Veterinary Medicine, Shandong Vocational Animal Science and Veterinary College, Weifang 261061, China.

出版信息

Biology (Basel). 2025 Apr 3;14(4):369. doi: 10.3390/biology14040369.

DOI:10.3390/biology14040369
PMID:40282234
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12024758/
Abstract

The TULP family was first identified in progressively obese mice, and , as a member of its family, has been much studied in tumor cells, but studies on its role in adipocytes have not yet been reported. This study found that the expression of showed an increasing trend in the differentiation of 3T3-L1 cells, and overexpression of enhanced the proliferation and differentiation capacity of the cells, while inhibition caused the opposite result. is a negative regulator of the Hedgehog signaling pathway, which can control lipid metabolism in adipose tissues, but whether can play a role in adipose tissues through the Hedgehog signaling pathway is not yet known. It was experimentally found that could promote adipogenic differentiation of precursor adipocytes by inhibiting the activity of the Hedgehog signaling pathway. Our results elucidate the role of TULP3 in the generation of precursor adipocytes and provide useful information for a deeper understanding of the molecular mechanisms of adipocytogenesis, which will contribute to the improvement of the treatment of adipose tissue dysfunction or uncontrolled adipogenesis-related diseases.

摘要

TULP家族最初是在进行性肥胖小鼠中被鉴定出来的,作为该家族的一员,它在肿瘤细胞中已得到广泛研究,但关于其在脂肪细胞中的作用尚未见报道。本研究发现,[具体蛋白名称]在3T3-L1细胞分化过程中的表达呈上升趋势,过表达[具体蛋白名称]可增强细胞的增殖和分化能力,而抑制则产生相反的结果。[具体蛋白名称]是Hedgehog信号通路的负调节因子,可控制脂肪组织中的脂质代谢,但[具体蛋白名称]是否能通过Hedgehog信号通路在脂肪组织中发挥作用尚不清楚。实验发现,[具体蛋白名称]可通过抑制Hedgehog信号通路的活性来促进前体脂肪细胞的成脂分化。我们的研究结果阐明了TULP3在前体脂肪细胞生成中的作用,并为更深入了解脂肪细胞生成的分子机制提供了有用信息,这将有助于改善脂肪组织功能障碍或脂肪生成失控相关疾病的治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ee/12024758/5884a4eca6cb/biology-14-00369-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ee/12024758/6128ec7a78a1/biology-14-00369-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ee/12024758/078bd86651af/biology-14-00369-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ee/12024758/05cd32b1e5b2/biology-14-00369-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ee/12024758/ca89a9b200c0/biology-14-00369-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ee/12024758/5884a4eca6cb/biology-14-00369-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ee/12024758/6128ec7a78a1/biology-14-00369-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ee/12024758/078bd86651af/biology-14-00369-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ee/12024758/05cd32b1e5b2/biology-14-00369-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ee/12024758/ca89a9b200c0/biology-14-00369-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/42ee/12024758/5884a4eca6cb/biology-14-00369-g005.jpg

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本文引用的文献

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Nature. 2024 Dec 18. doi: 10.1038/s41586-024-08348-2.
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TULP3 silencing suppresses cell proliferation, migration and invasion in gastric cancer via the PTEN/Akt/Snail pathway.TULP3基因沉默通过PTEN/Akt/Snail信号通路抑制胃癌细胞的增殖、迁移和侵袭。
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Suppression of Adipogenesis and Fat Accumulation by Vitexin Through Activation of Hedgehog Signaling in 3T3-L1 Adipocytes.
毛蕊花糖苷通过激活 3T3-L1 脂肪细胞中的 Hedgehog 信号通路抑制脂肪生成和脂肪积累。
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Primary Cilia Are Critical Regulators of White Adipose Tissue Expansion.初级纤毛是白色脂肪组织扩张的关键调节因子。
Front Physiol. 2021 Oct 25;12:769367. doi: 10.3389/fphys.2021.769367. eCollection 2021.
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Caudatin suppresses adipogenesis in 3T3-L1 adipocytes and reduces body weight gain in high-fat diet-fed mice through activation of hedgehog signaling.白花前胡丙素通过激活 Hedgehog 信号通路抑制 3T3-L1 脂肪细胞的脂肪生成,并减少高脂饮食喂养小鼠的体重增加。
Phytomedicine. 2021 Nov;92:153715. doi: 10.1016/j.phymed.2021.153715. Epub 2021 Aug 19.
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