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SYNCRIP controls miR-137 and striatal learning in animal models of methamphetamine abstinence

Acta Pharmaceutica Sinica B 2022年第8期12卷 3281-3297页

作者： Baeksun Kim Sung Hyun Tag Eunjoo Nam suji ham sujin Ahn Juhwan Kim Doo-Wan Cho Sangjoon Lee Young-Su Yang Seung Eun Lee Yong Sik Kim Il-Joo Cho Kwang Pyo Kim Su-Cheol Han Heh-In Im Convergence Research Center for Diagnosis Treatment and Care System of Dementia(DTC)Korea Institute of Science and Technology(KIST)Seoul 02792Republic of Korea Division of Bio-Medical Science&Technology KIST SchoolKorea University of Science and Technology(UST)Seoul 02792Republic of Korea Center for Neuroscience KISTSeoul 02792Republic of Korea Animal Model Research Center Jeonbuk Department of Inhalation ResearchKorea Institute of Toxicology(KIT)Korea Research Institute of Chemical Technology(KRICT)Jeongeup 56212Republic of Korea Research Animal Resource Center KISTSeoul 02792Republic of Korea Department of Pharmacology Seoul National University College of MedicineSeoul 03080Republic of Korea Center for BioMicrosystems KISTSeoul 02792Republic of Korea Department of Applied Chemistry Kyung Hee UniversityGyeonggi-do 17104Republic of Korea

Abstinence from prolonged psychostimulant use prompts stimulant withdrawal *** adaptations within the dorsal striatum have been considered the main hallmark of stimulant abstinence. Here we explored striatal miRNA-target interaction and its impact on circulating miRNA marker as well as behavioral dysfunctions in methamphetamine(MA) abstinence. We conducted miRNA sequencing and profiling in the nonhuman primate model of MA abstinence, followed by miRNA qPCR,LC-MS/MS proteomics, immunoassays, and behavior tests in mice. In nonhuman primates, MA abstinence triggered a lasting upregulation of miR-137 in the dorsal striatum but a simultaneous downregulation of circulating miR-137. In mice, aberrant increase in striatal miR-137-dependent inhibition of SYNCRIP essentially mediated the MA abstinence-induced reduction of circulating miR-137. Pathway modeling through experimental deduction illustrated that the MA abstinence-mediated downregulation of circulating miR-137 was caused by reduction of SYNCRIP-dependent miRNA sorting into the exosomes in the dorsal striatum. Furthermore, diminished SYNCRIP in the dorsal striatum was necessary for MA abstinence-induced behavioral bias towards egocentric spatial learning. Taken together, our data revealed circulating miR-137 as a potential blood-based marker that could reflect MA abstinence-dependent changes in striatal miR-137/SYNCRIP axis, and striatal SYNCRIP as a potential therapeutic target for striatum-associated cognitive dysfunction by MA withdrawal syndrome.

关键词： Methamphetamine Abstinence Withdrawal Striatum miR-137 SYNCRIP Biomarker Behavior

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Bee venom phospholipase A2 ameliorates amyloidogenesis and neuroinflammation through inhibition of signal transducer and activator of transcription-3 pathway in Tg2576 mice

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Translational Neurodegeneration 2019年第1期8卷 317-332页

作者： Hyeon Joo ham Sang-Bae Han Jaesuk Yun In Jun Yeo Young Wan ham Se Hyun Kim Pil-Hoon Park Dong-Young Choi Jin Tae Hong College of Pharmacy and Medical Research Center Chungbuk National UniversityOsongsaengmyeong 1-roOsong-eupHeungdeok-guCheongjuChungbuk 28160Republic of Korea Department of Chemistry Utah Valley University800 W University PkwyOremUT 84058USA INISTst Co. LTD767Sinsu-roSuji-guYongin-si 16827Gyeonggi-doRepublic of Korea College of Pharmacy Yeungnam University280 Daehak RoadGyeonsanGyeongbuk 38541Republic of Korea

Background:Neuroinflammation and accumulation ofβ-amyloid(Aβ)play a significant role in the onset and progression of Alzheimer’s disease(AD).Our previous study demonstrated that signal transducer and activator of transcription-3(STAT3)plays a major role in neuroinflammation and ***:In the present study,we investigated the inhibitory effect of bee venom phospholipase A2(bvPLA2)on memory deficiency in Tg2576 mice,which demonstrate genetic characteristics of AD and the mechanism of its action at the cellular and animal *** in vivo study,we examined the effect of bvPLA2 on improving memory by conducting several behavioral tests with the administration of bvPLA2(1 mg/kg)to Tg2576 *** in vitro study,we examined the effect of bvPLA2 on amyloidogenesis and neuroinflammation by treating bvPLA2 on LPSactivated BV2 ***:We found that bvPLA2 alleviated memory impairment in Tg2576 mice,as demonstrated in the behavioral tests assessing *** the bvPLA2-treated group,Aβ,amyloid precursor protein(APP),and β-secretase 1(BACE1)levels and β-secretase activity were significantly *** of pro-inflammatory cytokines and inflammation-related proteins decreased in the brain of bvPLA2-treated group,whereas anti-inflammatory cytokines *** addition,bvPLA2 reduced STAT3 phosphorylation in the brains of the bvPLA2-treated *** the cellular level,bvPLA2 inhibits production of nitric oxide,pro-inflammatory cytokines,and inflammation-related proteins including ***,bvPLA2 inhibits the production of Aβin cultured BV-2 *** from the docking experiment,pull-down assay,and the luciferase assay show that bvPLA2 directly binds STAT3 and,thus,regulates gene expression ***,when the STAT3 inhibitor and bvPLA2 were administered together,the anti-amyloidogenic and anti-inflammatory effects were further enhanced than when they were administered ***:These results suggest that bvPLA2 could r

关键词： Bee venom phospholipase A2 Alzheimer’s disease Amyloidogenesis Neuroinflammation STAT3

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