Figures & data
Figure 1. Arrangement of intestinal epithelial cells and intercellular junctions between epithelial cells. The apical junctions are composed of tight junctions and adherens junctions.
Figure 2. AMP-activated protein kinase (AMPK) activation accelerates the assembly of epithelial apical junctions. The apical side of epithelial cells is linked with adjacent epithelial cells through tight junctions (TJs) and adherens junctions (AJs). The primary constituents of TJs include transmembrane proteins, claudins, occludin, and junctional adhesion molecules (JAMs), which are stabilized by intracellular scaffolding protein zona occludens (ZO). AJs consist of two groups of transmembrane proteins, cadherins and nectins. Cadherins and nectins bind to the cytoskeleton by catenin-anchor proteins and afadin, respectively. AMPK activation accelerates TJ assembly stabilizes and maintains apical junctions, most likely through phosphorylation of TJ proteins and their associated proteins. In addition, AMPK enhances the expression of CDX2, which promotes epithelial differentiation and TJ protein expression.
Figure 3. AMP-activated protein kinase (AMPK) structure and activation. AMPK is structurally composed of catalytic α subunit, docking β subunit and regulatory γ subunit. AMPK is phosphorylated/activated by LKB1, CaMKKβ, TAK1 and other kinases. CaMKKβ: calmodulin-mediated kinase kinase β; LKB1: liver kinase B1; PP-2Cα: protein phosphatase 2C alpha; TAK1: transforming growth factor-β activated kinase 1.
Figure 4. Immunofluorescent staining of ZO-1 in jejunum tissues of wild-type (WT) and AMPK VilCre knock out male mice at age of 10-week. Arrows indicate ZO-1 at the border of villus. Scale bar is 200 μm. Adopted from Sun et al., 2017 published in Cell Death & Differentiation.Citation8
Figure 5. Physiological, nutritional and pharmacological factors regulate the activity of AMP-activated protein kinase (AMPK). AICAR: 5-aminoimidazole-4-carboxamide ribonucleoside; EGGC: Epigallocatechin gallate.
