Therapeutic protocols based on photobiomodulation (PBM) have been used for treatment of clinical conditions, such as wounds, pain, and inflammation processes. Existent data indicates that PBM is capable of altering reactive oxygen species (ROS) production. High levels of ROS can cause shortening and dysfunctional telomeres. Therefore, a better understanding of the effects induced by PBM on telomere maintenance is needed. This study aimed to assess the expression of genes related to telomere maintenance in Saccharomyces cerevisiae after irradiation with low-power red laser and ultraviolet A LED. Cultures of S. cerevisiae were exposed to low-power red laser (660 nm, 21.2 J/cm2, 205 s, 99 mW) and ultraviolet A LED (390 nm, 6 J/cm2, 205 s, 7 mW), incubated for 1 h in rich medium, total mRNA was extracted, cDNA was synthetized, and RAP1, RIF1, RIF2, STN1 and TEN1 mRNA levels in S. cerevisiae FF18733 cells were evaluated by real-time quantitative polymerase chain reaction. The results indicated that, at the fluences evaluated, exposure to low-power red laser does not induce changes on genes expression but exposure to ultraviolet A LED alone, and to simultaneous ultraviolet A LED and low-power red laser significantly (p < 0.05) reduce STN1 and TEN1 mRNA levels in S. cerevisiae. Exposure to low-power red laser could not affect mRNA telomere maintenance genes but exposure to ultraviolet A LED, and simultaneous low-power red laser and ultraviolet A LED, could decrease gene expression of telomere maintenance genes in S. cerevisiae. Our results could be taken into account for irradiation conditions carried out in current clinical protocols based on low-power lasers and LEDs as well as for developing new clinical protocols targeting telomere maintenance involved in PBM-induced therapeutic effects.
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Evidence ID | Analyze ID | Gene/Complex | Systematic Name/Complex Accession | Qualifier | Gene Ontology Term ID | Gene Ontology Term | Aspect | Annotation Extension | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Phenotype | Experiment Type | Experiment Type Category | Mutant Information | Strain Background | Chemical | Details | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Disease Ontology Term | Disease Ontology Term ID | Qualifier | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Regulator | Regulator Systematic Name | Target | Target Systematic Name | Direction | Regulation of | Happens During | Regulator Type | Direction | Regulation Of | Happens During | Method | Evidence | Strain Background | Reference |
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Site | Modification | Modifier | Source | Reference |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Allele | Assay | Annotation | Action | Phenotype | SGA score | P-value | Source | Reference | Note |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Assay | Annotation | Action | Modification | Source | Reference | Note |
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Complement ID | Locus ID | Gene | Species | Gene ID | Strain background | Direction | Details | Source | Reference |
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Evidence ID | Analyze ID | Dataset | Description | Keywords | Number of Conditions | Reference |
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