{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T11:30:08Z","timestamp":1789471808242,"version":"build-2803163510"},"reference-count":48,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2015,6,11]],"date-time":"2015-06-11T00:00:00Z","timestamp":1433980800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"crossref","award":["81371397"],"award-info":[{"award-number":["81371397"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Brain Pathology"],"published-print":{"date-parts":[[2016,3]]},"abstract":"Abstract<\/jats:title>P<\/jats:styled-content>arkinson's disease (PD<\/jats:styled-content>) is the most prevalent movement disorder characterized by selective loss of midbrain dopaminergic (DA<\/jats:styled-content>) neurons. MicroRNA<\/jats:styled-content>\u2010124 (miR<\/jats:styled-content>\u2010124) is abundantly expressed in the DA<\/jats:styled-content> neurons and its expression level decreases in the 1\u2010methyl\u20104\u2010pheny\u20101, 2, 3, 6\u2010tetrahydropyridine (MPTP<\/jats:styled-content>) model of PD<\/jats:styled-content>. However, whether the upregulation of miR\u2010124 could attenuate neurodegeneration remains unknown. Here, we employed miR\u2010124 agomir and miR\u2010124 mimics to upregulate miR<\/jats:styled-content>\u2010124 expression in MPTP<\/jats:styled-content>\u2010treated mice and MPP<\/jats:styled-content>+<\/jats:sup>\u2010intoxicated SH<\/jats:styled-content>\u2010SY5Y<\/jats:styled-content> cells, respectively. We found that loss of DA<\/jats:styled-content> neurons and striatal dopamine in MPTP<\/jats:styled-content>\u2010treated mice was significantly reduced by upregulating miR<\/jats:styled-content>\u2010124. In addition, we identified a target of miR<\/jats:styled-content>\u2010124, B<\/jats:styled-content>im that mediated the neuroprotection of miR<\/jats:styled-content>\u2010124. Indeed, treatment of miR<\/jats:styled-content>\u2010124 agomir in MPTP<\/jats:styled-content>\u2010treated mice inhibited B<\/jats:styled-content>im expression, thus suppressing B<\/jats:styled-content>ax translocation to mitochondria. Moreover, impaired autophagy process in MPTP<\/jats:styled-content>\u2010treated mice and MPP<\/jats:styled-content>+<\/jats:sup>\u2010intoxicated SH<\/jats:styled-content>\u2010SY5Y<\/jats:styled-content> cells characterized as autophagosomes (AP<\/jats:styled-content>) accumulation and lysosomal depletion were alleviated by the upregulation of miR\u2010124. Taken together, these results indicate that upregulation of miR<\/jats:styled-content>\u2010124 could regulate apoptosis and impaired autophagy process in the MPTP<\/jats:styled-content> model of PD<\/jats:styled-content>, thus reducing the loss of DA<\/jats:styled-content> neurons.<\/jats:p>","DOI":"10.1111\/bpa.12267","type":"journal-article","created":{"date-parts":[[2015,5,15]],"date-time":"2015-05-15T10:51:55Z","timestamp":1431687115000},"page":"167-176","source":"Crossref","is-referenced-by-count":173,"title":["MiR<\/scp>\u2010124 Regulates Apoptosis and Autophagy Process in MPTP<\/scp> Model of P<\/scp>arkinson's Disease by Targeting to B<\/scp>im"],"prefix":"10.1111","volume":"26","author":[{"given":"Huiqing","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Neurosurgery Zhujiang Hospital Southern Medical University Guangzhou China"},{"name":"The National Key Clinic Specialty The Neurosurgery Institute of Guangdong Province Guangdong Provincial Key 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Provincial Key Laboratory on Brain Function Repair and Regeneration Southern Medical University Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haoyuan","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery Zhujiang Hospital Southern Medical University Guangzhou China"},{"name":"The National Key Clinic Specialty The Neurosurgery Institute of Guangdong Province Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration Southern Medical University Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xin","family":"Gong","sequence":"additional","affiliation":[{"name":"The National Key Clinic Specialty The Neurosurgery Institute of Guangdong Province Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration Southern Medical University Guangzhou China"},{"name":"Department of Neurosurgery Hunan Provincial People's Hospital Changsha 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Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration Southern Medical University Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shizhong","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Neurosurgery Zhujiang Hospital Southern Medical University Guangzhou China"},{"name":"The National Key Clinic Specialty The Neurosurgery Institute of Guangdong Province Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration Southern Medical University Guangzhou 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