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Kim, Ji-Eun,Kang, Tae-Cheon Elsevier/North Holland 2017 Brain research Vol.1672 No.-
<P><B>Abstract</B></P> <P>Status epilepticus (SE, a prolonged seizure activity) is a high risk factor of developing vasogenic edema, which leads to secondary complications following SE. In the present study, we investigated whether transient receptor potential canonical channel-3 (TRPC3) may link vascular endothelial growth factor (VEGF) pathway to NFκB/ET<SUB>B</SUB> receptor axis in the rat piriform cortex during vasogenic edema formation. Following SE, TRPC3 and ET<SUB>B</SUB> receptor independently activated phosphatidylinositol 3 kinase (PI3K)/AKT/eNOS signaling pathway. SN50 (a NFκB inhibitor) attenuated the up-regulations of eNOS, TRPC3 and ET<SUB>B</SUB> receptor expressions following SE, accompanied by reductions in PI3K/AKT phosphorylations. Inhibition of SE-induced VEGF over-expression by leptomycin B also abrogated PI3K and AKT phosphorylations, but not TRPC3 expression. Wortmannin (a PI3K inhibitor) and 3CAI (an AKT inhibitor) effectively inhibited up-regulation of eNOS expressions and vasogenic edema lesion following SE. These findings indicate that PI3K/AKT may be common down-stream molecules for TRPC3- and ET<SUB>B</SUB> receptor signaling pathways during vasogenic edema formation. In addition, the present data demonstrate for the first time that TRPC3 may integrate VEGF- and NFκB-mediated vasogenic edema formation following SE. Thus, we suggest that PI3K/AKT signaling pathway may be one of considerable therapeutic targets for vasogenic edema.</P> <P><B>Highlights</B></P> <P> <UL> <LI> SE increases TRPC3-mediated PI3K/AKT phosphorylation in the PC. </LI> <LI> ET<SUB>B</SUB> receptor also increases SE-induced PI3K/AKT phosphorylation. </LI> <LI> NFκB inhibitor abolishes both TRPC3- and ET<SUB>B</SUB> receptor-mediated PI3K/AKT phosphorylation. </LI> <LI> Inhibition of VEGF over-expression reduces TRPC3-mediated PI3K/AKT phosphorylation. </LI> <LI> PI3K/AKT inhibitors attenuates vasogenic edema by abrogating eNOS activation. </LI> </UL> </P>
손의동,Hyun Ju Song,민영실,Chang Yell Shin,정지훈 한국분자세포생물학회 2006 Molecules and cells Vol.22 No.1
We investigated the possible role of p38 MAPK and ETB receptors in ET-1 induction of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) in cultured feline esophageal smooth muscle cells (ESMC). Confluent layers of ESMC were stimulated with 10 nM ET-1 and expression of COX-1 and COX-2, involvement of receptors, and activation of p38 MAPK, were examined by Western blot analysis. Levels of PGE2 induced by ET-1 were measured by Elisa. Using ETA and ETB antagonists (BQ-123 and BQ-788, respectively), the contribution of the ET receptors to COX-1 and COX-2 expression induced by ET-1 was determined. Western blot analysis revealed that treatment of ESMC with ET-1 resulted in transient expression of COX-2 and activation of p38 MAPK. Activation of p38 MAPK was maximal after 1 h. SB202190, a p38 MAPK inhibitor, reduced expression of COX-2, but not COX-1. ET-1induced release of PGE2 was also blocked by SB202190. COX-2 expression was upregulated only via the ETB receptor, and COX-1 expression was not affected by either antagonist. Taken together, our data suggest that ET-1 causes p38 MAPK-dependent expression of COX-2 by interacting with ETB receptors on ESMC