AI Article Synopsis
- The study investigates how circadian clock genes, specifically PER2 and PER3, may influence inflammation in a mouse model of experimental dry eye (EDE).
- RNA sequencing and various laboratory techniques were used to analyze gene expression and the effects of silencing these genes on inflammatory responses.
- Results indicated that changes in DNA methylation heightened the expression of PER2 and PER3, which subsequently contributed to increased inflammation during EDE.
Article Abstract
Purpose: To explore whether circadian clock genes contribute to elicit inflammation in experimental dry eye (EDE).
Methods: RNA sequencing analyzed mRNA expression patterns in EDE model. RT-qPCR and/or Western blot determined the expression of inflammatory factors and circadian genes during EDE. MethylTarget™ assays determined the promoter methylation levels of Per genes in vivo. Per2 or Per3 knockdown assessed their effects on inflammatory factors in vitro.
Results: We utilized an intelligently controlled environmental system (ICES) to establish a mouse EDE model. The significant upregulated genes were enriched for circadian rhythms. Therein lied oscillatory and time-dependent upregulation of PER2 and PER3, as well as their promoter hypomethylation during EDE. Silencing PER2 or PER3 significantly decreased inflammatory factor expression and also reversed such increased inflammatory response in azacitidine (AZA) treatment in vitro model.
Conclusions: Our findings suggest that DNA methylation mediated the upregulation of PER2 and PER3, leading to inflammatory response in EDE.
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| http://dx.doi.org/10.1080/09273948.2023.2205525 | DOI Listing |
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