跨膜蛋白 TMEM230,胶质瘤和胶质病中金属蛋白和运动蛋白的调节器。

3区 生物学 Q1 Biochemistry, Genetics and Molecular Biology
Cinzia Cocola, Edoardo Abeni, Valentina Martino, Eleonora Piscitelli, Stefano Morara, Paride Pelucchi, Ettore Mosca, Alice Chiodi, Tasnim Mohamed, Mira Palizban, Giuseppina De Petro, Giovanni Porta, Burkhard Greve, Alessio Noghero, Valerio Magnaghi, Gianfranco Bellipanni, James Kehler, Martin Götte, Federico Bussolino, Luciano Milanesi, Ileana Zucchi, Rolland Reinbold
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引用次数: 0

摘要

神经胶质细胞通过分泌可溶性因子、不溶性支架和囊泡,为神经元和神经组织的细胞外区提供物理和化学支持与保护。此外,神经胶质细胞还具有再生能力,可重塑其物理微环境并改变其附近不同细胞类型的生理特性。各种类型的异常神经胶质细胞和巨噬细胞与人类疾病、失调和恶性肿瘤有关。我们曾证实,跨膜蛋白 TMEM230 能够分泌促血管生成因子和金属蛋白酶,诱导内皮细胞萌发和通道形成,从而具有组织血管再造和再生能力。在健康的正常神经组织中,TMEM230 主要表达于神经胶质细胞和嗜髓鞘细胞,这表明它在神经组织稳态中发挥着重要作用。TMEM230与RNASET2(溶酶体、线粒体和囊泡)和STEAP家族成员(高尔基复合体)的共同表达支持了TMEM230对内膜系统的调控。神经胶质细胞成分的细胞内转运和细胞外分泌与运动蛋白介导的内吞、外吞和吞噬作用有关。被转运的成分包括金属蛋白、金属蛋白酶、聚糖、糖结合体加工和消化酶,它们在吞噬体和囊泡中发挥作用,调节正常的神经组织微环境、平衡、应激反应以及神经组织损伤或变性后的修复。TMEM230 的持续异常高水平会促进金属蛋白的表达、贩运和分泌,从而导致肿瘤相关浸润和高肿瘤等级胶质瘤的血管过度扩张。中枢神经系统或外周系统损伤后,TMEM230 的转录调控上调通过激活胶质细胞和巨噬细胞产生的微通道/微管(称为血管模拟)以及血管萌发和分支,促进组织伤口愈合、重塑和血管再通。我们的研究结果表明,TMEM230 可能是胶质瘤和胶质病中一大类金属蛋白由运动蛋白介导的转运和分区的主调控因子。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Transmembrane protein TMEM230, regulator of metalloproteins and motor proteins in gliomas and gliosis.

Glial cells provide physical and chemical support and protection for neurons and for the extracellular compartments of neural tissue through secretion of soluble factors, insoluble scaffolds, and vesicles. Additionally, glial cells have regenerative capacity by remodeling their physical microenvironment and changing physiological properties of diverse cell types in their proximity. Various types of aberrant glial and macrophage cells are associated with human diseases, disorders, and malignancy. We previously demonstrated that transmembrane protein, TMEM230 has tissue revascularization and regenerating capacity by its ability to secrete pro-angiogenic factors and metalloproteinases, inducing endothelial cell sprouting and channel formation. In healthy normal neural tissue, TMEM230 is predominantly expressed in glial and marcophate cells, suggesting a prominent role in neural tissue homeostasis. TMEM230 regulation of the endomembrane system was supported by co-expression with RNASET2 (lysosome, mitochondria, and vesicles) and STEAP family members (Golgi complex). Intracellular trafficking and extracellular secretion of glial cellular components are associated with endocytosis, exocytosis and phagocytosis mediated by motor proteins. Trafficked components include metalloproteins, metalloproteinases, glycans, and glycoconjugate processing and digesting enzymes that function in phagosomes and vesicles to regulate normal neural tissue microenvironment, homeostasis, stress response, and repair following neural tissue injury or degeneration. Aberrantly high sustained levels TMEM230 promotes metalloprotein expression, trafficking and secretion which contribute to tumor associated infiltration and hypervascularization of high tumor grade gliomas. Following injury of the central nervous or peripheral systems, transcient regulated upregulation of TMEM230 promotes tissue wound healing, remodeling and revascularization by activating glial and macrophage generated microchannels/microtubules (referred to as vascular mimicry) and blood vessel sprouting and branching. Our results support that TMEM230 may act as a master regulator of motor protein mediated trafficking and compartmentalization of a large class of metalloproteins in gliomas and gliosis.

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来源期刊
Advances in protein chemistry and structural biology
Advances in protein chemistry and structural biology BIOCHEMISTRY & MOLECULAR BIOLOGY-
CiteScore
7.40
自引率
0.00%
发文量
66
审稿时长
>12 weeks
期刊介绍: Published continuously since 1944, The Advances in Protein Chemistry and Structural Biology series has been the essential resource for protein chemists. Each volume brings forth new information about protocols and analysis of proteins. Each thematically organized volume is guest edited by leading experts in a broad range of protein-related topics.
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