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Christopher Snyder, Kirk Mantione
(Neuroscience Research Institute, State University of New York at Old Westbury, Old Westbury, USA)
Med Sci Monit Basic Res 2014; 20:63-69
DOI: 10.12659/MSMBR.890557
Background:
Parkinson’s disease (PD) continues to be an important neurological disorder. It is caused by the loss of dopaminergic neurons in the substantia nigra. Dopamine, the neurotransmitter produced from dopaminergic neurons, is a major precursor of endogenous morphine. There are approximately 18 genes associated with PD; their roles have not yet been completely established. PARK2 is a gene that encodes for the protein parkin, and PINK1 is a gene that encodes for PTEN-induced putative kinase 1.
Material and Methods:
Our objective was to determine if morphine treatment of HTB-11 cells affects the expression of PINK1 and PARK2. HTB-11 cells were treated with 10–7 M morphine for 2 h and a microarray analysis was conducted. To verify the microarray analysis, 3 Q-PCR trials were run using 10–6 M naloxone, morphine (10–7 M), or a naloxone/morphine mix.
Results:
In both the microarray analysis and the Q-PCR analysis, PARK2 was up-regulated and PINK1 was down-regulated.
Conclusions:
Morphine can affect the expression of PD-associated genes.
Keywords: Cell Line, Gene Expression Regulation - drug effects, Morphine - pharmacology, Oligonucleotide Array Sequence Analysis, Parkinson Disease - genetics, Protein Kinases - metabolism, Real-Time Polymerase Chain Reaction, Ubiquitin-Protein Ligases - metabolism