External factors
| External factors: |
Kallistatin |
| Category: |
Chemical compounds |
| Experiment: |
SA-β-gal activity assay//qRT-PCR//Telomerase activity assay |
| Description: |
Representative images showed that H2O2treatment induced pronounced cellular senescence in HUVECs,while purified recombinant human kallistatin pretreatment reversed the effec.Kallistatin blocked H2O2-induced p16INK4A and PAI-1 expression,and prevented H2O2-mediated inhibition of telomerase activity. |
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Regulatory relationship
| R-EF-Target gene:
|
Upregulation |
| Official symbol(s): |
LET-7G |
| Target gene experiment: |
qRT-PCR |
| Target gene description: |
Kallistatin treatment significantly increased Let-7g synthesis, whereas genistein, a tyrosine kinase inhibitor, blocked kallistatin’s effect. |
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| Regulatory pathway:
|
miR-34a-SIRT1-eNOS |
| Pathway experiment: |
qRT-PCR//Western blot |
| Pathway description: |
The effects of kallistatin on the regulation of SIRT1, eNOS, catalase and SOD-2 were determined. Kallistatin treatment not only markedly enhanced SIRT1, eNOS, catalase and SOD-2 expression,but also prevented H2O2-mediated inhibition of these antioxidant genes.Let-7g inhibitor (Let-7g anti-sense RNA) blocked kallistatin’s inhibition of miR-34a synthesis .Let-7g inhibitor abolished kallistatin induced SIRT1 and eNOS mRNA levels, and blocked kallistatin-mediated elevation of SIRT1 and eNOS levels by western blot. |
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.
Pathway view
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