| External factors: | IR |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Other |
| Phenotype: | Aging |
| Experiment: | SA-β-gal activity assay |
| Description: | IR induced SA-β-gal activity in CCR6 +Th17, CCR6 neg Th and Treg, but SA-β-gal activity dose-response was significantly higher for CCR6 +Th17 compared to CCR6 neg Th and Treg.Interestingly, irradiated CCR6 +Th17 secreted larger amounts of VEGF-A and IL-8 compared to irradiated CCR6 neg Th. |
| Target gene: | H2A.J |
| R-EF-Target gene: | Upregulation |
| Official symbol(s): | H2A.J |
| Target gene experiment: | γH2AX staining//qRT-PCR//Immunofluorescence |
| Target gene description: | We thus investigated DSB repair by enumerating γH2AX foci in sorted, resting CCR6 +Th17, CCR6 neg Th and Treg lymphocytes at different time points after 2Gy IR. IR-induced γH2AX foci peaked around 15-30 min post-IR in the three T-lymphocyte subsets which showed similar repair kinetics, but the number of γH2AX foci at 30min after 2Gy IR was higher in CCR6 +Th17 compared to CCR6 neg Th and Treg. H2A.J expression increased 72 hours after a 2Gy IR of CCR6 +Th17 and CCR6 neg Th, but this increased expression was higher in CCR6 +Th17. |
| Regulatory pathway: | ROS-MAPKs-mTOR |
| R-EF-Pathway: | Activation |
| Pathway experiment: | qRT-PCR |
| Pathway description: | Pretreatment with NAC, rapamycin, and the three MAPKinase pathway inhibitors prevented the IR-induced upregulation of p16 Ink4a expression and SA-β-Gal activity in both CCR6 +Th17 and CCR6 neg Th, whereas pretreatment with the ATM inhibitor did not. Conversely, IR-induced H2A.J expression was not prevented by pretreatment with NAC, rapamycin and p38-MAPK inhibitor, whereas pretreatment with the ATM inhibitor or MEK1/2 and JNK inhibitors did prevent its expression. |
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