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Integrated insight into the molecular mechanisms of selenium modulates MPP+ induced cytotoxicity in Parkinson’s disease model

ABSTRACT: Parkinson’s disease (PD) is a common neurodegenerative disease, which associated with oxidative stress. Due to the antioxidant function of Selenium (Se), it may have a neuroprotective function in PD. Nevertheless, the Se involved and its role in the protective function is still unclear. 1-methyl-4-phenylpyridinium (MPP+), which inhibits mitochondrial respiration, is usually used to produce a reliable PD cellular model. In this study, we discovered that Se could modulate cytotoxicity in MPP+ induced PD model and used genome wide high throughput sequencing to capture the gene expression profiles of MPP+ treatment PC12 cells with or without Se. We identified 351 differentially expressed mRNAs (DEGs) and 14 differentially expressed long non-coding RNAs (DELs) in MPP+ group vs. normal control group, 244 DEGs and 27 DELs in Se + MPP+ group vs. MPP+ group. Functional annotation analysis of DEGs and DELs cis-target genes revealed that they were enriched in reactive oxygen species (ROS) metabolic process and mitochondrial control of apoptosis. Our data suggests that DEGs, Txnrd1, siglec1 and Klf2, and the DEL AABR07044454.1 cis-acting on target gene Cdkn1a, may act a protective function in PD model. For the first time, our study systematically demonstrated that mRNAs and lncRNAs induced by Se involved in neuroprotection in PD and provided new insight into how Se modulates cytotoxicity in MPP+ induced PD model.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE186702 | GEO | 2024/10/27

REPOSITORIES: GEO

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Project description:Background: Peripheral T‐cell lymphomas (PTCLs) are a heterogeneous group of neoplasms characterized by a poor prognosis. Histone deacetylase (HDAC) inhibitors have emerged as novel therapeutic agents for PTCLs. In this study, we aimed to explore the immunomodulatory effect of the HDAC inhibitor chidamide on circulating PD-1(+) cells from patients with PTCL, as well as its correlation with treatment response. Methods: We enrolled newly diagnosed patients with PTCLs treated with a combination of chidamide and chemotherapy. Gene expression profile analysis was performed on peripheral blood PD-1(+) cells, both at baseline and at the end of treatment. A list of differentially expressed genes (DEGs) was identified. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed to annotate the biological implications of the DEGs. A gene concept network was constructed to identify the key DEGs for further PCR verification. Results: A total of 302 DEGs were identified in the complete remission (CR) group, including 162 upregulated and 140 downregulated genes. In contrast, only 12 DEGs were identified in the non-CR group. GO analysis revealed that these upregulated DEGs were mainly involved in chemokine activity, cell chemotaxis, and cellular response to interleukin-1 and interferon-γ. Furthermore, KEGG pathway analysis showed that these DEGs were enriched in cytokine-cytokine receptor interaction and chemokine signaling pathways. The innate immune signaling pathways, including the Toll-like and NOD-like receptor signaling pathways, were also influenced. The gene concept network revealed that the key upregulated genes belonged to the C-C chemokine family. Conclusion: Our results showed that chidamide treatment notably enhanced the expression of genes associated with chemokine activity and chemotaxis function of circulating PD-1(+) cells. By recruiting immune cells and improving the innate immune function of PD-1(+) cells, chidamide may reshape the tumor microenvironment to an anti-tumor phenotype and synergize with checkpoint inhibitors.

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Integrated insight into the molecular mechanisms of selenium modulates MPP+ induced cytotoxicity in Parkinson’s disease model

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