Proteomic Profiling of Iron Overload-Induced Human Hepatic Cells Reveals Activation of TLR2-Mediated Inflammatory Response.
Proteomic Profiling of Iron Overload-Induced Human Hepatic Cells Reveals Activation of TLR2-Mediated Inflammatory Response.
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铁过载诱导的人肝细胞的蛋白质组学分析揭示了 TLR2 介导的炎症反应的激活。
DOI：
10.3390/molecules21030322
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发表时间：
2016-03-17
期刊：
影响因子：
--
通讯作者：
Zhou X
中科院分区：
文献类型：
--
作者：
Li X;Li S;Lu M;Yang G;Shen Y;Zhou X
Background: Hepatic iron overload is common in patients who have undergone hematopoietic cell transplantation (HCT) and may predispose to peri- and post-HCT toxicity. To better reveal more molecules that might be involved in iron overload-induced liver injury, we utilized proteomics to investigate differentially expressed proteins in iron overload-induced hepatocytes vs. untreated hepatocytes. Methods and Results: HH4 hepatocytes were exposed to ferric ammonium citrate (FAC) to establish an in vitro iron overload model. Differentially expressed proteins initiated by the iron overload were studied by two-dimensional liquid chromatography tandem mass spectrometry (2D-LC-MS) analysis. We identified 93 proteins whose quantity statistically significantly changes under excess hepatocyte iron conditions. Gene Ontology (GO) analysis showed that these differentially expressed proteins in HH4 cells are involved in various biological process including endocytosis, response to wounding, di-, trivalent inorganic cation homeostasis, inflammatory response, positive regulation of cytokine production, and etc. Meanwhile, proteomics data revealed protein level of TLR2 and IL6ST significantly increased 7 times and 2.9 times, respectively, in iron overloaded HH4 cells. Our subsequent experiments detected that FAC-treated HH4 cells can activate IL6 expression through TLR2-mediated inflammatory responses via the NF-κB pathway. Conclusions: In this study, we demonstrated that iron overload induced hepatocytes triggering TLR2-mediated inflammatory response via NF-κB signaling pathway in HH4 cells.
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哺乳动物细胞和秀丽隐杆线虫中的生化和功能比较揭示了EHD蛋白的共享和不同作用。
影响因子：
--
作者：
George, Manju;Ying, GuoGuang;Rainey, Mark A.;Solomon, Aharon;Parikh, Pankit T.;Gao, Qingshen;Band, Vimla;Band, Hamid
通讯作者：
Band, Hamid
影响因子：
4.3
作者：
Platzbecker, Uwe;Bornhaeuser, Martin;Germing, Ulrich;Stumpf, Julian;Scott, Bart L.;Kroeger, Nicolaus;Schwerdtfeger, Rainer;Boehm, Alexandra;Kobbe, Guido;Theuser, Catrin;Rabitsch, Werner;Valent, Peter;Sorror, Mohamed L.;Ehninger, Gerhard;Deeg, H. Joachim
通讯作者：
Deeg, H. Joachim
DOI：
10.3324/haematol.10075
发表时间：
2007-01-01
期刊：
HAEMATOLOGICA-THE HEMATOLOGY JOURNAL
影响因子：
--
作者：
Locasciulli, Anna;Oneto, Rosi;Fuhrer, Monika
通讯作者：
Fuhrer, Monika
影响因子：
4.3
作者：
Rajamani U;Jialal I
通讯作者：
Jialal I
影响因子：
4.4
作者：
Cox, Juergen;Neuhauser, Nadin;Mann, Matthias
通讯作者：
Mann, Matthias