MCP-1 neuroinflammatory processes are dependant on TNFR1. FOXO3a increases the activity of the TNFR2 promoter. Knock-down of the TNFR2 sensitizes microvascular endothelial cells to the activities of TNFR1 mediated apoptosis (programmed cell death). Endothelial dysfunction has been implicated as an important factor in the symptoms of many environmental diseases. FOXO3a is decreased in Nrf2 deficient cells. Other studies have identified FOXO3a as an important regulator of lifespan and aging. In ovarian cells, it has been shown that Nrf2 serves as a sensor and protects against harmful chemicals through a variety of ways including FOXO3a expression. Decreased Nrf2 will lead to a reduction of the FOXO3a modulation of TNFR2and consequentely may increase TNFR1-mediated apoptosis.
Ding, B., Kirkiles-Smith, N. C., and Pober, J. S. (2009). Foxo3a regulates oxygen-responsive expression of tumor necrosis factor receptor 2 in human dermal microvascular endothelial cells. J. Biol. Chem., 284(29):19331-19339. http://www.citeulike.org/user/HEIRS/article/5725120?updated=1252114581
GenAge for FOXO3.
Hu, X., Roberts, J. R., Apopa, P. L., Kan, Y. W., and Ma, Q. (2006). Accelerated ovarian failure induced by 4-vinyl cyclohexene diepoxide in nrf2 null mice. 3:940-954. http://www.citeulike.org/user/HEIRS/article/5725231
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