Secretoneurin promotes neuroprotection and neuronal plasticity via the Jak2/Stat3 pathway in murine models of stroke
J. Clin. Invest. Woei-Cherng Shyu, et al. 118:133 doi:10.1172/JCI32723 [Go to this article.]

Figure 2
Pretreatment with SN attenuates OGD-induced toxicity through a specific signaling pathway in PCCs. (A–C) Representative microscopic morphology of PCCs under various conditions (control, SN plus OGD, and OGD alone). (D) Cell death assessed by LDH activity in media of PCC cultures with or without 1 μg/l SN before exposure to OGD. SN pretreatment significantly attenuated OGD-induced cell death. (E) The density of MAP-2–immunreactive PCCs was significantly reduced by OGD, but returned to control levels with SN pretreatment. (F) Fluorimetric measurement under OGD. A significant reduction of caspase-3 activity was seen in the SN-pretreated PCCs. (G) A significant reduction of caspase-3⁺ immunofluorescent cells was observed in the SN-treated group. (H and I) Quantitation of Western blot in PCCs treated with SN under OGD showed significantly increased Bcl-2 expression. (J) Expression of p-Stat3, Stat3, p-Jak2, and Jak2. (K–M) The ratio of p-Stat3 and p-Jak2 to actin protein after SN treatment peaked at about a 2-fold increase in treated cells compared with control cells in a time- and dose-dependent manner. There was no statistically significant difference in Stat3 and Jak2 levels between treated and control cells. (N) Addition of AG490 to OGD-treated cells significantly reduced MAP-2–immunoreactive cell density in PCCs. Data are mean ± SEM. *P < 0.05, **P < 0.01 vs. control. Scale bar: 50 μm.