| External factors: | Kallistatin |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Aging |
| Experiment: | SA-β-gal activity assay//RT-PCR |
| Description: | Exposure of EPCs to TNF-a for 6 days markedly increased SA-β-gal-positive cell numbers compared with the control group, whereas preincubation with purified human kallistatin significantly reduced TNF-a induced SA-β-gal-positive cells. Moreover, kallistatin markedly reduced the expression of p16INK4a, a cyclin-dependent kinase inhibitor known to be a senescence-associated inducer of cell cycle arrest. |
| Target gene: | MIR-21 |
| R-EF-Target gene: | Downregulation |
| Official symbol(s): | MIR-21 |
| Target gene experiment: | qRT-PCR |
| Target gene description: | Kallistatin also antagonized TNF-a induced miR-21 synthesis. |
| Regulatory pathway: | miR-34a-SIRT1 |
| R-EF-Pathway: | -- |
| Official symbol(s): | MIR34A-SIRT1 |
| Pathway experiment: | Western blot//qRT-PCR |
| Pathway description: | Furthermore, STZ induced a significant increase of miR-34a and miR-21 synthesis, as well as reduced SIRT1, eNOS, and catalase mRNA levels in aortas of diabetic mice compared to control mice, while kallistatin administration reversed STZ-mediated effect.Kallistatin treatment increased SIRT1 protein levels, as determined by Western blot. |
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