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肿瘤坏死因子(TNF)与源自莫氏矛头蝮蛇毒的锌金属蛋白酶BmooMP-Alpha-I之间的相互作用促进了该细胞因子的直接蛋白水解:分子建模与对接概述

Interaction between TNF and BmooMP-Alpha-I, a Zinc Metalloprotease Derived from Bothrops moojeni Snake Venom, Promotes Direct Proteolysis of This Cytokine: Molecular Modeling and Docking at a Glance.

作者信息

Silva Maraisa Cristina, Lopes Silva Tamires, Silva Murilo Vieira, Mota Caroline Martins, Santiago Fernanda Maria, Fonseca Kelly Cortes, Oliveira Fábio, Mineo Tiago Wilson Patriarca, Mineo José Roberto

机构信息

Institute of Biomedical Sciences, Laboratory of Immunoparasitology "Dr. Mario Endsfeldz Camargo", Federal University of Uberlândia, Av. Pará 1720, Uberlândia 38400-902, Brazil.

Institute of Biomedical Sciences, Laboratory of Biophysics, Federal University of Uberlândia, Av. Pará 1720, Uberlândia 38400-902, Brazil.

出版信息

Toxins (Basel). 2016 Jul 20;8(7):223. doi: 10.3390/toxins8070223.

Abstract

Tumor necrosis factor (TNF) is a major cytokine in inflammatory processes and its deregulation plays a pivotal role in several diseases. Here, we report that a zinc metalloprotease extracted from Bothrops moojeni venom (BmooMP-alpha-I) inhibits TNF directly by promoting its degradation. This inhibition was demonstrated by both in vitro and in vivo assays, using known TLR ligands. These findings are supported by molecular docking results, which reveal interaction between BmooMP-alpha-I and TNF. The major cluster of interaction between BmooMP-alpha-I and TNF was confirmed by the structural alignment presenting Ligand Root Mean Square Deviation LRMS = 1.05 Å and Interactive Root Mean Square Deviation IRMS = 1.01 Å, this result being compatible with an accurate complex. Additionally, we demonstrated that the effect of this metalloprotease on TNF is independent of cell cytotoxicity and it does not affect other TLR-triggered cytokines, such as IL-12. Together, these results indicate that this zinc metalloprotease is a potential tool to be further investigated for the treatment of inflammatory disorders involving TNF deregulation.

摘要

肿瘤坏死因子(TNF)是炎症过程中的一种主要细胞因子,其失调在多种疾病中起着关键作用。在此,我们报告从矛头蝮蛇毒液中提取的一种锌金属蛋白酶(BmooMP-alpha-I)通过促进TNF的降解直接抑制TNF。使用已知的Toll样受体(TLR)配体,通过体外和体内试验均证实了这种抑制作用。分子对接结果支持了这些发现,该结果揭示了BmooMP-alpha-I与TNF之间的相互作用。通过结构比对证实了BmooMP-alpha-I与TNF之间相互作用的主要簇,呈现出配体均方根偏差(LRMS)= 1.05 Å和相互作用均方根偏差(IRMS)= 1.01 Å,该结果与精确复合物相符。此外,我们证明这种金属蛋白酶对TNF的作用独立于细胞毒性,并且不影响其他TLR触发的细胞因子,如白细胞介素-12。总之,这些结果表明这种锌金属蛋白酶是一种潜在的工具,有待进一步研究用于治疗涉及TNF失调的炎症性疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/242d/4963855/7d56ab9aa985/toxins-08-00223-g001.jpg

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