| Literature DB >> 29501959 |
Ingrid González-Casacuberta1, Constanza Morén1, Diana-Luz Juárez-Flores1, Anna Esteve-Codina2, Cristina Sierra3, Marc Catalán-García1, Mariona Guitart-Mampel1, Ester Tobías1, José César Milisenda1, Claustre Pont-Sunyer4, María José Martí4, Francesc Cardellach1, Eduard Tolosa4, Rafael Artuch5, Mario Ezquerra6, Rubén Fernández-Santiago7, Glòria Garrabou8.
Abstract
Mutations in the parkin gene (PRKN) are the most common cause of autosomal-recessive juvenile Parkinson's disease (PD). PRKN encodes an E3 ubiquitin ligase that is involved in multiple regulatory functions including proteasomal-mediated protein turnover, mitochondrial function, mitophagy, and cell survival. However, the precise molecular events mediated by PRKN mutations in PRKN-associated PD (PRKN-PD) remain unknown. To elucidate the cellular impact of parkin mutations, we performed an RNA sequencing study in skin fibroblasts from PRKN-PD patients carrying different PRKN mutations (n = 4) and genetically unrelated healthy subjects (n = 4). We identified 343 differentially expressed genes in PRKN-PD fibroblasts. Gene ontology and canonical pathway analysis revealed enrichment of differentially expressed genes in processes such as cell adhesion, cell growth, and amino acid and folate metabolism among others. Our findings indicate that PRKN mutations are associated with large global gene expression changes as observed in fibroblasts from PRKN-PD patients and support the view of PD as a systemic disease affecting also non-neural peripheral tissues such as the skin.Entities:
Keywords: Fibroblasts; Parkin; Parkinson's disease (PD); RNA sequencing (RNA-seq); Transcriptome
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Year: 2018 PMID: 29501959 DOI: 10.1016/j.neurobiolaging.2018.01.021
Source DB: PubMed Journal: Neurobiol Aging ISSN: 0197-4580 Impact factor: 4.673