External factors
| External factors: |
Kallistatin |
| Category: |
Chemical compounds |
| 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. |
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Regulatory relationship
| 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 |
| Official symbol(s): |
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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. |
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.
Related pathway view