Research Article

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

Published: July 31, 2015
Genet. Mol. Res. 14 (3) : 8547-8554 DOI: https://doi.org/10.4238/2015.July.31.2
Cite this Article:
(2015). Smoking, aging, and expression of proteins related to the FOXO3 signaling pathway in lung tissues. Genet. Mol. Res. 14(3): gmr4814. https://doi.org/10.4238/2015.July.31.2
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Abstract

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 dis­mutase, 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.

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 dis­mutase, 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.