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. Author manuscript; available in PMC: 2015 Mar 1.
Published in final edited form as: Brain Behav Immun. 2013 Dec 29;37:187–196. doi: 10.1016/j.bbi.2013.12.018

Figure 6.

Figure 6

TGFβ1-Smad3 pathway and activation of aging microglia. LPS increased the expression of Smad3 and pSmad3 in young mice. TGFβ1 was able to decrease the production of NO induced by LPS, an effect that was independent of Smad3. TGFβ1 induced Aβ uptake by a Smad3-dependent manner. In adult mice, basal levels of Smad3 and pSmad3 were elevated. However, they were not further induced by administration of LPS. TGFβ1 inhibited production of ROS induced by LPS at least partially in a Smad3-dependent manner. Basal levels of Aβ uptake were increased in microglia obtained from adult animals compared with those of young mice, but TGFβ1 did not induce further uptake of Aβ. Increased TGFβ1-Smad3 activity on microglia associated with aging appears to impair the beneficial effect of TGFβ1, favoring cytotoxicity depending on the increased production of ROS and the accumulation of Aβ secondary to its decreased removal.