External factors
| External factors: |
Kynurenine |
| Category: |
Chemical compounds |
| 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. |
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Regulatory relationship
| R-EF-Pathway:
|
Upregulation |
| Official symbol(s): |
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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. |
Aging network
Annotation:
The green line represents Upregulation.
The purple line represents Downregulation.
The orange line represents Activation.
The yellow line represents Inhibition.
The gray line represents Unclear.