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We investigated the effects of smoking and aging on proteins involved in the forkhead box O3 (FOXO3) signaling pathways in the lungs. Sixteen senescence-accelerated mouse-resistant 1 (SAMR1) and senescence-accelerated mouse-prone 8 (SAMP8) mice at 3 months of age were divided into a normally aged, smoke-exposed group (4 SAMR1 mice), a normally aged, air-exposed group (4 SAMR1 mice), an aging-accelerated, smoke-exposed group (4 SAMP8 mice), and an aging-accelerated, air-exposed group (4 SAMP8 mice). Expression of genes and proteins related to the FOXO3 signaling pathways in each group was examined by western blot analysis and immunohistochemistry. FOXO3a expression was significantly increased in the normally aged, air-exposed group compared with the aging-accelerated, air-exposed group. FOXO3a expression was significantly reduced in the aging-accelerated, smoke-exposed group compared with the aging-accelerated, air-exposed group. Sirtuin 1, manganese superoxide dis-mutase, and phosphatidylinositol 3-kinase (PI3K)/Akt expression decreased significantly in the smoke-exposed groups compared with the air-exposed groups and in the aging-accelerated groups compared with the normally aged groups. Signal transduction pathways mediated by the transcription factor FOXO3a (such as the PI3K/Akt pathway) may be involved in the accelerated aging of lung tissues in chronic obstructive pulmonary disease. Smoking inactivates the transcription factor FOXO3, thus accelerating lung tissue aging during chronic obstructive pulmonary disease.

Smoking, aging, and expression of proteins related to the FOXO3 signaling pathway in lung tissues