title: Gene expression profiling analysis of the putamen for the investigation of compensatory mechanisms in Parkinson's disease.
abstract: BACKGROUND
  Parkinson's disease (PD) is affecting 5 million people worldwide, but the response mechanisms of the striatum are still unclear. Therefore, identification of gene expression alterations in the striatum will greatly assist the development of novel therapy strategies.
  
  
  METHODS
  We performed a comprehensive gene expression analysis in 15 PD patients and 15 normal controls to identify differentially expressed genes (DEGs) using the expression profile GSE20291 from Gene Expression Omnibus (GEO). Gene Ontology (GO) analysis and Kyoto Encyclopedia of Gene and Genome (KEGG) pathway enrichment analysis were used to define functions and pathways altered in PD. Protein-protein interaction network was constructed to find out the modules with close interactions.
  
  
  RESULTS
  Total715 DEGs including 268 up-regulated and 447 down-regulated genes were obtained. GO functional enrichment analysis indicated that the genes related with neurons function and cell morphogenesis might be changed upon PD. KEGG pathway enrichment analysis showed that most of the genes were enriched in the nodes of Gap junction, calcium signaling pathway, phosphatidylinositol signaling system, long-term potentiation, Alzheimer's disease and GnRH signaling pathway. Protein-protein interaction network and module analysis suggested that some apoptosis related genes, such as PRKCA, CDC42 and BCL2 may play critical roles in striatal neurons growth.
  
  
  CONCLUSIONS
  Intrinsic striatal tyrosine hydroxylase interneurons growth may be promoted by changes in several genes expression and thus reduce the functional excitatory synapses.
authors.affiliation: Department of Neurology, the Fourth Affiliated Hospital of China Medical University, NO,4 chongshan Road, huanggu Area, Shenyang 110032, Liaoning, China. gaolbdoc@163.com.
authors.forename: Lianbo
authors.initials: L
authors.lastname: Gao
authors.forename: Honghua
authors.initials: H
authors.lastname: Gao
authors.forename: Huan
authors.initials: H
authors.lastname: Zhou
authors.forename: Yanyuan
authors.initials: Y
authors.lastname: Xu
mesh_terms: D005260:Female; D017629:Gap Junctions / Q000378:metabolism; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation / Q000502:physiology*; D053263:Gene Regulatory Networks; D016678:Genome; D006801:Humans; D008297:Male; D009474:Neurons / Q000378:metabolism; D020411:Oligonucleotide Array Sequence Analysis; D010300:Parkinson Disease / Q000473:pathology*; D060066:Protein Interaction Maps / Q000235:genetics; D051571:Protein Kinase C-alpha / Q000235:genetics / Q000378:metabolism; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D011699:Putamen / Q000378:metabolism* / Q000473:pathology; D015398:Signal Transduction / Q000235:genetics; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D014446:Tyrosine 3-Monooxygenase; D017346:Protein Serine-Threonine Kinases; C496628:PRKCA protein, human; D051571:Protein Kinase C-alpha