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Transcriptomic Analysis of Long Noncoding RNA and mRNA Expression Profiles in the Amygdala of Rats with Bone Cancer Pain-Depression Comorbidity.

ABSTRACT: Bone cancer pain (BCP)-depression comorbidity has become a complex clinical problem during cancer treatment; however, its underlying molecular mechanisms have not been clarified. Several long noncoding RNAs (lncRNAs) have been demonstrated to be promising therapeutic targets in depression, but research on the role of lncRNAs in BCP-depression comorbidity has been limited. Therefore, high-throughput RNA sequencing was performed to detect differentially expressed profiles in the amygdala of a BCP-depression rat model in this study. We detected 330 differentially expressed mRNAs (DEmRNAs) and 78 differentially expressed lncRNAs (DElncRNAs) in the BCP-depression comorbidity model and then verified the expression of six DEmRNAs and six DElncRNAs with the greatest degrees of difference by RT-qPCR. Furthermore, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses revealed that differentially expressed genes were strongly enriched in inflammatory and immunologic systemic responses. Then the nuclear factor kappa B (NF-κB) signaling pathway and the Th17 differentiation pathway showed significant differences, as determined by Western blot analysis. Finally, we constructed a protein-protein interaction (PPI) network to explore the potential regulatory mechanism of DEmRNAs. In conclusion, our study reveals a new resource for the understanding of dysregulated lncRNAs and mRNAs in BCP-depression comorbidity and provides novel potential therapeutic targets for further approaches.

SUBMITTER: Wu S

PROVIDER: S-EPMC8400935 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Transcriptomic analysis of long noncoding RNAs and mRNAs expression profiles in the spinal cord of bone cancer pain rats.

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| S-EPMC9188197 | biostudies-literature

Comorbidity between Alzheimer’s disease and Major Depression: a behavioural and transcriptomic characterization study in mice

Project description:Background: Major Depression (MD) is the most prevalent psychiatric disease in the population and is considered a prodromal stage of the Alzheimer’s disease (AD). Despite both diseases having a robust genetic component, the common transcriptomic signature remains unknown. Method: In this regard, we investigated the cognitive and emotional behavioural responses in 3- (n=16 per group) and 6-month-old (n=14 per group) in APP/PSEN1-Tg mutant mice, before -amyloid plaques were detected in comparison with non-transgenic mice. Then, we studied the deregulation of genes and pathways in prefrontal cortex, striatum, hippocampus and amygdala of mice at both ages, using transcriptomic and functional data analysis. Results: We found that depressive-like and anxiety-like behaviours, as well as memory impairments are already present at 3-month-old APP/PSEN1-Tg mutant mice together with the deregulation of several genes such as Ciart, Chrm5, Aldh1a, Grin3b, Nr1d1 and Mc4r, and gene sets, including components of the circadian rhythms, electronic transport chain, neuroinflammation and neurotransmission. Then, we extended these results to human data performing GSEA analysis using DisGeNET database, which is specific for diseases and disease-related phenotypes and provides translational support for common deregulated gene sets related to MD and AD. Conclusion: The present study shed further light on the genetic bases shared between MD and AD, illustrating a wide characterization from the behavioural to transcriptomic level in APP/PSEN1-Tg mutant mouse model. These findings could indicate that late MD could be an early manifestation of AD.

2022-01-17 | GSE167739 | GEO

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