The aberrantly expressed long non‐coding RNA RNA in?the substantia nigra and corpus striatum of Nrf2‐knockout mice

摘要

Abstract Nuclear factor erythroid 2 like 2 (Nrf2) functions as a neuroprotective agent in Parkinson's disease ( PD ). This study aimed to investigate the key long non‐coding RNA s (lnc RNA s) correlated with Nrf2, which might provide valuable information for the exploration of pathogenesis of PD . The lnc RNA and mRNA expression profiling of substantia nigra and corpus striatum of Nrf2 (?/?) mice model was obtained from microarray analysis. The animal experiments conducted for this study were approved by the ethics committee of Hebei Medical University. Bioinformatics analyses were conducted, including differentially expressed lnc RNA s/ mRNA (differentially expressed lncRNA, DEL /differentially expressed mRNA, DEM ) identification, DEL ‐ DEM coexpression network construction, and biological functions prediction. Quantitative real‐time polymerase chain reaction ( qRT ‐ PCR ) was subjected to validate abnormally expressed DEL s and DEM s in the substantia nigra and corpus striatum of Nrf2 (?/?) mice model. A total of 48 DEL s (37 down‐regulated and 11 up‐regulated) were identified both in Nrf2 (?/?) substantia nigra and corpus striatum; 96 DEM s and 643 DEM s were identified in the substantia nigra and corpus striatum, respectively. DEL ‐ DEM coexpressed network was constructed. Lnc RNA AK 076880, AK 036620, and AK 020330 had high connectivity with DEM s both in the substantia nigra and corpus striatum. These DEM s were significantly enriched in signaling pathways such as the calcium signaling pathway, Huntington's disease, Alzheimer's disease, mitogen‐activated protein kinase ( MAPK ) signaling pathway, and the Wnt signaling pathway. Generally, qRT ‐ PCR validation results of selected DEM s and DEL s were consistent with microarray data. The dysregulated DEL s and DEM s in the substantia nigra and corpus striatum of Nrf2?(?/?) mice were identified. Our results might provide useful information for further exploring the pathogenesis mechanism of PD.