| External factors: | Kynurenine |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Osteoporosis |
| Experiment: | SA-β-gal activity assay//Western blot |
| Description: | In the present study, we tested the idea that kynurenine induces the cell-function inhibitor and antiproliferation process of senescence in BMSCs.Treatment of BMSCs with KYN for 24hr significantly increased SA-β-galactosidase activity,a hallmark of senescence.Additionally, the expression levels of the Cyclin D kinase (CDK) inhibitor,p21 was significantly elevated under kynurenine treatment while the level of another CDK inhibitor, p16 remained unchanged.These data suggest that treatment with KYN promotes senescence in BMSCs. |
| Regulatory pathway: | AhR |
| R-EF-Pathway: | Upregulation |
| Official symbol(s): | AHR |
| Pathway experiment: | SA-β-gal activity assay//Western blot |
| Pathway description: | Treatment of BMSCs with different doses of kynurenine resulted in elevated immunofluorescent AhR nuclear staining.inhibition of AhR by CH-223191 and 3’4’-DMF,also affected senescence. CH-223191 treatment prevented the increase of kynurenine-induced SA-beta-galactosidase activity.Treatment of BMSCs with 3’4’-DMF inhibited kynurenine-induced overexpression of senescence marker, p21. Additionally, AhR inhibition by DMF prevented the formation of senescence-associated chromatin foci. Together,these data support that KYN upregulates senescence and suppresses autophagy in BMSC through the AhR pathway. |
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