| Gene name: | GCG |
| Aging type: | Prevent |
| Aging characteristic: |
| Tissue type: | -- |
| Cell name: | HUVEC |
| Experiment: | SA-β-gal activity assay |
| Description: | Treatment of HUVECs with GLP-1 attenuated the increase of senescent cells in a dose-responsive manner. |
| Target gene: | DPP-4//CREB |
| Official symbol(s): | DPP4//CREB1 |
| R-AG-Target gene: | Upregulation//Activation |
| Subcategory: | Unclear |
| Target gene experiment: | Western blot |
| Target gene description: | Treatment of the ZDF animals with vildagliptin resulted in a significant reduction of DPP-4 activity and an almost 6-fold increase of GLP-1 plasma levels.The vildagliptin treatment did, however, decrease cellular senescence in these animals, to levels almost comparable to those of lean rats (2.6±0.6% versus 2.3±0.5%). This suggests that increased GLP-1 levels by DPP-4 inhibition have a protective effect on the vasculature.Western blot analysis using an anti phosphorylated CREB antibody showed that GLP-1 treatment increased relative phosphorylated CREB levels by 52% compared with the control. |
| Regulatory pathway: | CAMP-PKA |
| R-AG-Pathway: | -- |
| Official symbol(s): | CAMP-PRKACA |
| Pathway experiment: | Premature senescence assay |
| Pathway description: | PKA inhibition by H89 was also sufficient to block the GLP-1-mediated protective effect on HUVECs. H89 inhibition showed a dose response effect on cellular senescence in combination with GLP-1, with a complete abolishment of the GLP-1 protective effect at a concentration of 1 umol/L H89. Similar results were obtained with another PKA inhibitor KT5720. |
Annotation:
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