PMID- 31309116 OWN - NLM STAT- MEDLINE DCOM- 20191219 LR - 20211204 IS - 2314-6141 (Electronic) IS - 2314-6133 (Print) VI - 2019 DP - 2019 TI - MicroRNA Expression Profiling Screen miR-3557/324-Targeted CaMK/mTOR in the Rat Striatum of Parkinson's Disease in Regular Aerobic Exercise. PG - 7654798 LID - 10.1155/2019/7654798 [doi] LID - 7654798 AB - This study aimed to screen the target miRNAs and to investigate the differential miR-3557/324-targeted signal mechanisms in the rats' model of Parkinson's disease (PD) with regular aerobic exercise. Rats were divided into sedentary control PD group (SED-PD, n = 18) and aerobic exercise PD group (EX-PD, n = 22). After 8 weeks of regular aerobic exercise, a 6-hydroxydopamine- (6-OHDA-) induced PD lesion model was constructed. Preregular aerobic exercises enhanced the injury resistance of rats with 6-OHDA-induced PD. The rotational behavior after injection of apomorphine hydrochloride was alleviated. Under the scanning electron microscopy, we found the neurons, axons, and villi of the striatum were clearly and tightly arranged, and neurons and axons significantly becoming larger. Tyrosine hydroxylase (TH) was increased significantly and alpha-synuclein protein expression was reduced in the EX-PD group compared to the SED-PD group. Screening from miRNA microarray chip, we further found upregulation of miR-3557 and downregulation of miR-324 were closely related to the calcium-modulating signaling pathway, remitting the progress of Parkinson's disease on aerobic exercise. Compared to the SED-PD group, Ca(2+)/calmodulin dependent protein kinase II (CaMK2alpha) was upregulated, but CaMKV and voltage-dependent anion-selective channel protein 1 (Vdac1) were significantly downregulated in the EX-PD group. Additionally, phosphatidylinositol-3-kinase (PI3K)/mammalian target of rapamycin (mTOR) expression were activated, and ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) expression was upregulated in the EX-PD group. Conclusions: the adaptive mechanism of regular aerobic exercise delaying neurodegenerative diseases and lesions was that miR-3557/324 was activated to regulate one of its targets CaMKs signaling pathways. CaMKs, coordinated with mTOR pathway-related gene expression, improved UCH-L1 level to favor for delaying neurodegeneration or improving the pathogenesis of PD lesions. FAU - Liu, Wenfeng AU - Liu W AUID- ORCID: 0000-0001-5641-3670 AD - Hunan Provincial Key Laboratory of Physical Fitness and Sports Rehabilitation, Hunan Normal University, Changsha, Hunan, 410012, China. AD - Department of Experimental and Clinical Pharmacology, University of Minnesota, Minneapolis, MN 55455, USA. AD - The Key Laboratory of Protein Chemistry and Developmental Biology of Ministry of Education, Hunan Normal University, Changsha, Hunan, 410081, China. FAU - Li, Li AU - Li L AUID- ORCID: 0000-0001-5902-9762 AD - School of Health & Kinesiology, Georgia Southern University, Statesboro, GA 30460, USA. FAU - Liu, Shaopeng AU - Liu S AD - Hunan Provincial Key Laboratory of Physical Fitness and Sports Rehabilitation, Hunan Normal University, Changsha, Hunan, 410012, China. FAU - Wang, Zhiyuan AU - Wang Z AD - Hunan Provincial Key Laboratory of Physical Fitness and Sports Rehabilitation, Hunan Normal University, Changsha, Hunan, 410012, China. FAU - Kuang, Heyu AU - Kuang H AD - Hunan Provincial Key Laboratory of Physical Fitness and Sports Rehabilitation, Hunan Normal University, Changsha, Hunan, 410012, China. FAU - Xia, Yan AU - Xia Y AD - Hunan Provincial Key Laboratory of Physical Fitness and Sports Rehabilitation, Hunan Normal University, Changsha, Hunan, 410012, China. FAU - Tang, Changfa AU - Tang C AUID- ORCID: 0000-0002-8104-7753 AD - Hunan Provincial Key Laboratory of Physical Fitness and Sports Rehabilitation, Hunan Normal University, Changsha, Hunan, 410012, China. FAU - Yin, Dazhong AU - Yin D AUID- ORCID: 0000-0002-6481-640X AD - The Key Laboratory of Protein Chemistry and Developmental Biology of Ministry of Education, Hunan Normal University, Changsha, Hunan, 410081, China. AD - Qingyuan People's Hospital, The Sixth Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511500, China. LA - eng PT - Journal Article DEP - 20190612 PL - United States TA - Biomed Res Int JT - BioMed research international JID - 101600173 RN - 0 (Calmodulin-Binding Proteins) RN - 0 (Camkv protein, rat) RN - 0 (MIRN324 microRNA, rat) RN - 0 (MicroRNAs) RN - 0 (Nerve Tissue Proteins) RN - EC 2.7.1.1 (mTOR protein, rat) RN - EC 2.7.11.1 (TOR Serine-Threonine Kinases) RN - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2) RN - EC 2.7.11.17 (Camk2a protein, rat) SB - IM MH - Animals MH - Calcium-Calmodulin-Dependent Protein Kinase Type 2/*biosynthesis MH - Calmodulin-Binding Proteins/*biosynthesis MH - Corpus Striatum/*metabolism/pathology/physiopathology MH - Gene Expression Profiling MH - *Gene Expression Regulation MH - Male MH - MicroRNAs/*biosynthesis MH - Nerve Tissue Proteins/*biosynthesis MH - Parkinson Disease, Secondary/*metabolism/pathology/physiopathology MH - *Physical Conditioning, Animal MH - Rats MH - Rats, Sprague-Dawley MH - *Signal Transduction MH - TOR Serine-Threonine Kinases/*metabolism PMC - PMC6594308 EDAT- 2019/07/17 06:00 MHDA- 2019/12/20 06:00 PMCR- 2019/06/12 CRDT- 2019/07/17 06:00 PHST- 2018/11/12 00:00 [received] PHST- 2019/05/13 00:00 [revised] PHST- 2019/05/22 00:00 [accepted] PHST- 2019/07/17 06:00 [entrez] PHST- 2019/07/17 06:00 [pubmed] PHST- 2019/12/20 06:00 [medline] PHST- 2019/06/12 00:00 [pmc-release] AID - 10.1155/2019/7654798 [doi] PST - epublish SO - Biomed Res Int. 2019 Jun 12;2019:7654798. doi: 10.1155/2019/7654798. eCollection 2019.