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碱性成纤维细胞生长因子2诱导的蛋白质组变化支持海马神经元中的路易体病理。

Basic Fibroblast Growth Factor 2-Induced Proteome Changes Endorse Lewy Body Pathology in Hippocampal Neurons.

作者信息

Kumar Rohit, Donakonda Sainitin, Müller Stephan A, Lichtenthaler Stefan F, Bötzel Kai, Höglinger Günter U, Koeglsperger Thomas

机构信息

German Center for Neurodegenerative Diseases (DZNE), 81337 Munich, Germany; Faculty of Medicine, Klinikum rechts der Isar, Technical University of Munich, 81675 Munich, Germany; Department of Neurology, Ludwig Maximilian University, 81377 Munich, Germany.

Institute of Immunology and Experimental Oncology, Technical University of Munich, 81675 Munich, Germany.

出版信息

iScience. 2020 Aug 21;23(8):101349. doi: 10.1016/j.isci.2020.101349. Epub 2020 Jul 9.

DOI:10.1016/j.isci.2020.101349
PMID:32707433
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7381695/
Abstract

Hippocampal Lewy body pathology (LBP) is associated with changes in neurotrophic factor signaling and neuronal energy metabolism. LBP progression is attributed to the aggregation of α-synuclein (α-Syn) and its cell-to-cell transmission via extracellular vehicles (EVs). We recently discovered an enhanced EV release in basic fibroblast growth factor (bFGF)-treated hippocampal neurons. Here, we examined the EV and cell lysate proteome changes in bFGF-treated hippocampal neurons. We identified n = 2,310 differentially expressed proteins (DEPs) induced by bFGF. We applied weighted protein co-expression network analysis (WPCNA) to generate protein modules from DEPs and mapped them to published LBP datasets. This approach revealed n = 532 LBP-linked DEPs comprising key α-Syn-interacting proteins, LBP-associated RNA-binding proteins (RBPs), and neuronal ion channels and receptors that can impact LBP onset and progression. In summary, our deep proteomic analysis affirms the potential influence of bFGF signaling on LBP-related proteome changes and associated molecular interactions.

摘要

海马体路易体病理（LBP）与神经营养因子信号传导和神经元能量代谢的变化有关。LBP的进展归因于α-突触核蛋白（α-Syn）的聚集及其通过细胞外囊泡（EVs）的细胞间传递。我们最近发现，在碱性成纤维细胞生长因子（bFGF）处理的海马神经元中，EV释放增强。在此，我们研究了bFGF处理的海马神经元中EV和细胞裂解物蛋白质组的变化。我们鉴定出由bFGF诱导的n = 2310个差异表达蛋白（DEP）。我们应用加权蛋白质共表达网络分析（WPCNA）从DEP生成蛋白质模块，并将其映射到已发表的LBP数据集。这种方法揭示了n = 532个与LBP相关的DEP，包括关键的α-Syn相互作用蛋白、LBP相关的RNA结合蛋白（RBP）以及可能影响LBP发生和进展的神经元离子通道和受体。总之，我们的深度蛋白质组学分析证实了bFGF信号传导对LBP相关蛋白质组变化和相关分子相互作用的潜在影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a081/7381695/840288872cb6/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a081/7381695/8c5ebeb5b09f/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a081/7381695/3241a317ca7d/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a081/7381695/91166c6a09eb/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a081/7381695/eba2632a75d7/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a081/7381695/1456e7f829ea/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a081/7381695/7dd8e8698386/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a081/7381695/840288872cb6/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a081/7381695/8c5ebeb5b09f/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a081/7381695/3241a317ca7d/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a081/7381695/91166c6a09eb/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a081/7381695/eba2632a75d7/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a081/7381695/1456e7f829ea/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a081/7381695/7dd8e8698386/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a081/7381695/840288872cb6/gr6.jpg

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