| External factors: | Rapamycin |
| Aging type: | Prevent |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Chronic obstructive pulmonary disease |
| Experiment: | SA-β-gal activity assay |
| Description: | The PDL was lower for PA-SMCs and P-ECs from patients with COPD compared with those from controls. Rapamycin treatment consistently increased the PDLs of both PA-SMCs and P-ECs from patients with COPD and, to a lesser extent, from controls. Thus, PDLs for PA-SMCs and P-ECs from patients with COPD and controls no longer differed when both were treated with rapamycin. Rapamycin treatment also decreased the number of β-Gal–positive cells to similar values in the COPD and control groups.Rapamycin (10 nM) reduced IL-6, IL-8, and CCL2 levels in cells derived from COPD patients and from controls,although the effects varied among patients. |
| Regulatory pathway: | mTOR |
| R-EF-Pathway: | Downregulation |
| Official symbol(s): | MTOR |
| Pathway experiment: | Western blot//ELISA |
| Pathway description: | Rapamycin treatment increased the PDL in PA-SMCs from SM22-TSC1–/– mice, decreased the β-Gal–positive cell count, and inhibited mTOR activity . The increased mTOR signaling and higher cytokine levels measured 3 months after tamoxifen exposure in these mice returned to normal after rapamycin treatment. |
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