Complement Factor H Displays Opposite Expression Patterns Under Two Situations of Methamphetamine Administration: Acute
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LETTER TO THE EDITOR
Complement Factor H Displays Opposite Expression Patterns Under Two Situations of Methamphetamine Administration: Acute Exposure and Chronic Dependence Ming Lin1,2 • Jiamin Xu1,2 Xiaoping Pu1,2
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Zhimin Liu3 • Liang Qin4,5 • Xiaodong Wang4,5
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Received: 8 April 2020 / Accepted: 9 June 2020 Ó Shanghai Institutes for Biological Sciences, CAS 2020
Dear Editor, Methamphetamine (METH) is a highly addictive central nervous system stimulant that has severe physical and psychological side-effects, including loss of appetite, hyperactivity, dysphoria, and depression [1]. Due to its illegal production, distribution, sale, and possession it has become a worldwide burden. METH is directly toxic to dopaminergic and serotoninergic neurons, resulting in excitotoxicity, oxidative stress, and other processes [2]. Research on biomolecules associated with these processes will be useful for identifying potential markers, exploring the mechanism of METH dependence, and even developing prevention and treatment strategies.
The authors Ming Lin and Jiamin Xu are co-first authors and contributed equally to this work.
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s12264-020-00576-6) contains supplementary material, which is available to authorized users. & Xiaodong Wang [email protected] & Xiaoping Pu [email protected] 1
National Key Research Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing 100191, China
2
Department of Molecular and Cellular Pharmacology, School of Pharmaceutical Sciences, Peking University, Beijing 100191, China
3
National Institute on Drug Dependence, Peking University, Beijing 100191, China
4
Centre for Imaging and Systems Biology, Minzu University of China, Beijing 100081, China
5
College of Life and Environmental Sciences, Minzu University of China, Beijing 100081, China
Complement factor H (CFH) is one of these potential METH-dependence-related molecules; it is a 155-kDa glycoprotein comprised of 20 contiguous complement control protein modules [3]. It can be secreted by several types of cells, including monocytes, fibroblasts, endothelial cells, platelets, and retinal pigment epithelial cells, but it is mainly secreted by the liver [3]. CFH is the major soluble regulator of the complement alternative pathway due to its ability to recognize related biomolecules to inhibit the activation and amplification of the complement system on host surfaces. Mutations of CFH can lead to autoimmune inflammatory and thrombotic disorders, such as age-related macular degeneration and atypical hemolytic uremic syndrome [3]. Our previous studies found that CFH is strongly associated with METH administration. Using two-dimensional gel electrophoresis to investigate protein expression in METH abusers and control serum, CFH has been found to be stably up-regulated after chronic METH abuse/ dependence [4]. Moreover, the up-regulation of CFH has also been reported in the serum and the ventr
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