Smad anchor for receptor activation (SARA) is an important regulator of transforming growth factor β (TGF-β) signaling by recruiting Smad2/3 to TGF-β receptors. We recently demonstrated that the expressions of SARA and level of downstream phospho-Smad3 (p-Smad3) were upregulated in the brain in the epileptic rat model, but were never examined in patients with temporal lobe epilepsy (TLE). In this study, we examined the expressions of SARA and level of p-Smad3 in brain tissues of TLE patients using immunohistochemistry and western blot to demonstrate that SARA activation in neurons is sufficient to facilitate TGF- β pathway in patients to regulate epilepsy. We found that the expressions of SARA and level of p-Smad3 were significantly upregulated in neurons of the temporal cortex of TLE patients compared to controls. Moreover, SARA and p-Smad3 were strongly stained in the cytoplasm in the temporal cortex of TLE patients. Our results indicate that upregulation of SARA and p-Smad3 in cortex neurons might be involved in the development of intractable temporal lobe epilepsy.
Keywords: Patient; SARA; Seizure; Smad3; TGF-β; Temporal lobe epilepsy.