Gene name: | IGF1 |
Aging type: | Prevent |
Aging characteristic: |
Tissue type: | -- |
Cell name: | Aortic endothelial cell |
Gene ID: | 3479 |
Category: | protein coding |
Phenotype: | Atherosclerosis |
Experimental category: | L |
PMID: | 23261989 |
Experiment: | SA-β-gal activity assay |
Description: | Incubation with 100 ng/mL IGF-1 for 24 h prior to hydrogen peroxide exposure significantly reduced expression of β-galactosidase activity, indicating that the enhanced antioxidant activity in response to IGF-1 counteracted oxidative stress induced premature cell senescence. |
Target gene: | GPX1 |
Official symbol(s): | GPX1 |
R-AG-Target gene: | Upregulation |
Subcategory: | Unclear |
Target gene experiment: | Western blot//Enzyme activity assay//Immunostaining |
Target gene description: | Conversely,glutathione peroxidase (GPX) activity was upregulated in a dose-dependent and time-dependent manner.We further assessed GPX1 and GPX4 expressions by Western blot analysis. IGF-1 upregulated GPX1 (2.6-fold increase, 100 ng/mL IGF-1 vs 0 ng/mL IGF-1).Pre-exposure to IGF-1 dose-dependently suppressed ROS levels in both basal and oxidized LDL-stimulated cells. IGF-1's antioxidant effect was also time-dependent, since the ROS suppression by IGF-1 was more pronounced after 24 h exposure than at 1 h. |
Regulatory pathway: | PI3K |
R-AG-Pathway: | -- |
Official symbol(s): | PIK3CA |
Pathway experiment: | Western blot//GPX activity assay |
Pathway description: | The phosphatidylinositide 3-kinase (PI3k) inhibitor, LY294002, significantly suppressed IGF-1 upregulation of GPX1. IGF-1 upregulation of GPX activity was also significantly suppressed by LY294002 but not by PD98059 or SB202190, confirming that IGF-1 regulation of GPX was PI3k dependent. |
Annotation:
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