2. Academic Validation
  3. Pramipexole attenuates neuronal injury in Parkinson's disease by targeting miR-96 to activate BNIP3-mediated mitophagy

Pramipexole attenuates neuronal injury in Parkinson's disease by targeting miR-96 to activate BNIP3-mediated mitophagy

  • Neurochem Int. 2021 Jun;146:104972. doi: 10.1016/j.neuint.2021.104972.
Dong-Xin Wang 1,  Ying Yang 2,  Xiao-Song Huang 2,  Jia-Yu Tang 2,  Xi Zhang 3,  Hong-Xing Huang 4,  Bin Zhou 4,  Bo Liu 4,  Hui-Qiong Xiao 5,  Xiao-Hui Li 2,  Ping Yang 6,  Shu-Cheng Zou 4,  Kun Liu 4,  Xiao-Ye Wang 7,  Xiao-Song Li 8
Affiliations

Affiliations

  • 1 The Research Institute of Mentality and Sanitation, Hunan Provincial Brain Hospital, Changsha, 410007, Hunan Province, PR China.
  • 2 Medical Department of Neurology, Hunan Provincial Brain Hospital, Changsha, 410007, Hunan Province, PR China.
  • 3 Clinical Medical School, Hunan Traditional Chinese Medicine University, Changsha, 410006, Hunan Province, PR China.
  • 4 Department of Neurosurgery, Hunan Provincial Brain Hospital, Changsha, 410007, Hunan Province, PR China.
  • 5 Department of Scientific Research, Hunan Provincial Brain Hospital, Changsha, 410007, Hunan Province, PR China.
  • 6 Department of Psychology, Hunan Provincial Brain Hospital, Changsha, 410007, Hunan Province, PR China.
  • 7 The Institution of Clinical Trials on Drugs, Hunan Provincial Brain Hospital, Changsha, 410007, Hunan Province, PR China. Electronic address: 1821192004@qq.com.
  • 8 The Research Institute of Mentality and Sanitation, Hunan Provincial Brain Hospital, Changsha, 410007, Hunan Province, PR China. Electronic address: 68872731@qq.com.
PMID: 33493581 DOI: 10.1016/j.neuint.2021.104972
Abstract

Background: Parkinson's disease is a common neurodegenerative problem. Pramipexole (PPX) plays protective role in Parkinson's disease. Nevertheless, the mechanism of PPX in Parkinson's disease-like neuronal injury is largely uncertain.

Methods: 1-methyl-4-phenylpyridinium (MPP+)-stimulated neuronal cells and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mice were used as the model of Parkinson's disease. MPP+-induced neuronal injury was assessed via cell viability, lactic dehydrogenase (LDH) release and Apoptosis. microRNA-96 (miR-96) and BCL2/adenovirus E1B 19 kDa interacting protein 3 (BNIP3) abundances were examined by quantitative reverse transcription polymerase chain reaction (qRT-PCR) or Western blotting. Mitophagy was tested by Western blotting and immunofluorescence staining. MPTP-induced neuronal injury in mice was investigated via behavioral tests and TUNEL.

Results: PPX alleviated MPP+-induced neuronal injury via increasing cell viability and decreasing LDH release and Apoptosis. PPX reversed MPP+-induced miR-96 expression and inhibition of Mitophagy. miR-96 overexpression or BNIP3 interference weakened the suppressive role of PPX in MPP+-induced neuronal injury. miR-96 targeted BNIP3 to inhibit PTEN-induced putative kinase 1 (PINK1)/Parkin signals-mediated Mitophagy. miR-96 overexpression promoted MPP+-induced neuronal injury via decreasing BNIP3. PPX weakened MPTP-induced neuronal injury in mice via regulating miR-96/BNIP3-mediated Mitophagy.

Conclusion: PPX mitigated neuronal injury in MPP+-induced cells and MPTP-induced mice by activating BNIP3-mediated Mitophagy via directly decreasing miR-96.

Keywords

BNIP3; Mitophagy; Parkinson's disease; Pramipexole; miR-96.

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