First Author | Costain WJ | Year | 2003 |
Journal | Peptides | Volume | 24 |
Issue | 1 | Pages | 137-46 |
PubMed ID | 12576095 | Mgi Jnum | J:81953 |
Mgi Id | MGI:2450436 | Doi | 10.1016/s0196-9781(02)00286-3 |
Citation | Costain WJ, et al. (2003) PLG regulates hnRNP-L expression in the rat striatum and pre-frontal cortex: identification by ddPCR. Peptides 24(1):137-46 |
abstractText | Central dopaminergic systems are implicated in schizophrenia and Parkinson's disease, and are known to be modulated by the endogenous tripeptide Pro-Leu-Gly-NH(2) (PLG or MIF-1, melanocyte-stimulating hormone release inhibiting factor-1). Differential display polymerase chain reaction (ddPCR) was utilized to identify genes that are regulated by protracted PLG treatment (20mg/kg, i.p. for 28 days) in male Sprague-Dawley rats. A total of 2400 genes were screened and 3 down-regulated bands were identified in the PLG-treated samples. Sequencing analysis revealed a total of six unique cDNA species. One fragment possessed a high degree of homology with Mus musculus hnRNP-L (protein L) mRNA (GenBank #AB009392) (termed PRG1: PLG regulated gene 1). Elongation of the PRG1 cDNA, by RACE-PCR, provided an 835bp sequence with 95% homology to AB009392 over a 743bp span. Open reading frame analysis provided a putative amino acid sequence consistent with the identity of PRG1 as rat hnRNP-L. Northern hybridization experiments with PRG1 revealed a 2.3kb mRNA species that was decreased by 65% in the PLG-treated tissue. Western blot analysis revealed significantly decreased hnRNP-L levels in the striatum and pre-frontal cortex (but not the nucleus accumbens) by 71 and 61%, respectively of PLG-treated animals. The identification of altered expression of hnRNP-L following PLG treatment provides insight into the long-term effects of PLG and may provide insight into its molecular mechanism of action. |