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aerobic exercise. Rats were divided into sedentary control PD group (SED-PD,<jats:italic> n<\/jats:italic> = 18) and aerobic exercise PD group (EX-PD,<jats:italic> n<\/jats:italic> = 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 <jats:italic>\u03b1<\/jats:italic>-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\u2019s disease on aerobic exercise. Compared to the SED-PD group, Ca<jats:sup>2+<\/jats:sup>\/calmodulin dependent protein kinase II (<jats:italic>CaMK2<jats:italic>\u03b1<\/jats:italic><\/jats:italic>) was upregulated, but<jats:italic> CaMKV<\/jats:italic> and voltage-dependent anion-selective channel protein 1 (<jats:italic>Vdac1<\/jats:italic>) were significantly downregulated in the EX-PD group. Additionally, phosphatidylinositol-3-kinase (<jats:italic>PI3K<\/jats:italic>)\/mammalian target of rapamycin (<jats:italic>mTOR<\/jats:italic>) expression were activated, and ubiquitin carboxy-terminal hydrolase L1 (<jats:italic>UCH-L1<\/jats:italic>) 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.<\/jats:p>","DOI":"10.1155\/2019\/7654798","type":"journal-article","created":{"date-parts":[[2019,6,12]],"date-time":"2019-06-12T19:30:45Z","timestamp":1560367845000},"page":"1-12","source":"Crossref","is-referenced-by-count":15,"title":["MicroRNA Expression Profiling Screen miR-3557\/324-Targeted<i> CaMK\/mTOR<\/i> in the Rat Striatum of Parkinson\u2019s Disease in Regular Aerobic Exercise"],"prefix":"10.1155","volume":"2019","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5641-3670","authenticated-orcid":true,"given":"Wenfeng","family":"Liu","sequence":"first","affiliation":[{"name":"Hunan Provincial Key Laboratory of Physical Fitness and Sports Rehabilitation, Hunan Normal University, Changsha, Hunan, 410012, China"},{"name":"Department of Experimental and Clinical Pharmacology, University of Minnesota, 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