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. Author manuscript; available in PMC: 2019 Jun 24.
Published in final edited form as: Eur J Neurosci. 2018 Nov 29;49(1):27–39. doi: 10.1111/ejn.14223

FIGURE 8.

FIGURE 8

Graphic summary of protective roles potential mechanisms of CaMKK in endothelial cells and BBB under ischemic conditions. In brain endothelial cells after stroke, CaMKK β activates SIRT1 by phosphorylation, which subsequently produces anti-oxidative effect and enhances eNOS signaling. eNOS signaling then produces pleiotropic effects including endothelial cell protection and inhibiting inflammation by reducing VCAM-1, ICAM-1, E-selectins and leukocytes extravasation. STO-609 and EX-527 are pharmacological inhibitors of CaMKK and SIRT1, respectively. BBB: blood–brain barrier; CaMKK β: Calcium/Calmodulin-Dependent Protein Kinase Kinase β; eNOS: endothelial nitric oxide synthase; ICAM-1: intercellular adhesion molecule −1; SIRT1: sirtuin 1; VCAM-1: vascular cell adhesion molecule-1. [Colour figure can be viewed at wileyonlinelibrary.com]