TY - JOUR
T1 - MicroRNA Expression Profiling Screen miR-3557/324-targeted CaMK/mTOR in the Rat Striatum of Parkinson's Disease in Regular Aerobic Exercise
AU - Liu, Wenfeng
AU - Li, Li
AU - Liu, Shaopeng
AU - Wang, Zhiyuan
AU - Kuang, Heyu
AU - Xia, Yan
AU - Tang, Changfa
AU - Yin, Dazhong
PY - 2019/6/12
Y1 - 2019/6/12
N2 - 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 α -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, Ca2+/calmodulin dependent protein kinase II ( CaMK2 α ) 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.
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 α -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, Ca2+/calmodulin dependent protein kinase II ( CaMK2 α ) 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.
UR - https://digitalcommons.georgiasouthern.edu/health-kinesiology-facpubs/181
M3 - Article
SN - 2314-6133
VL - 2019
JO - BioMed Research International
JF - BioMed Research International
ER -