| External factors: | Kallistatin |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| 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. |
| Target gene: | LET-7G |
| 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. |
| Regulatory pathway: | miR-34a-SIRT1-eNOS |
| R-EF-Pathway: | -- |
| 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. |
Annotation: