Next Article in Journal
Recent Developments in Using Drosophila as a Model for Human Genetic Disease
Next Article in Special Issue
Is TAK1 a Direct Upstream Kinase of AMPK?
Previous Article in Journal
Molecular Regulation of Nitrate Responses in Plants
Previous Article in Special Issue
Co-Expression Network Analysis of AMPK and Autophagy Gene Products during Adipocyte Differentiation
Article Menu
Issue 7 (July) cover image

Export Article

Open AccessReview
Int. J. Mol. Sci. 2018, 19(7), 2040;

Implications of AMPK in the Formation of Epithelial Tight Junctions

Groupe Interdisciplinaire de Génoprotéomique Appliquée (GIGA), Cardiovascular Sciences, University of Liège (ULiège), Avenue de L'Hôpital 11, 4000 Liège, Belgium
Department of Cellular and Molecular Physiology, Yale School of Medicine, New Haven, CT 06520, USA
Division of Nephrology, Centre Hospitalier Universitaire de Liège (CHU of Liège), University of Liège (CHU ULiège), 13-B4000 Liège, Belgium
Author to whom correspondence should be addressed.
Received: 12 June 2018 / Revised: 9 July 2018 / Accepted: 9 July 2018 / Published: 13 July 2018
(This article belongs to the Special Issue AMP-Activated Protein Kinase Signalling)
Full-Text   |   PDF [1039 KB, uploaded 13 July 2018]   |  


Tight junctions (TJ) play an essential role in the epithelial barrier. By definition, TJ are located at the demarcation between the apical and baso-lateral domains of the plasma membrane in epithelial cells. TJ fulfill two major roles: (i) TJ prevent the mixing of membrane components; and (ii) TJ regulate the selective paracellular permeability. Disruption of TJ is regarded as one of the earliest hallmarks of epithelial injury, leading to the loss of cell polarity and tissue disorganization. Many factors have been identified as modulators of TJ assembly/disassembly. More specifically, in addition to its role as an energy sensor, adenosine monophosphate-activated protein kinase (AMPK) participates in TJ regulation. AMPK is a ubiquitous serine/threonine kinase composed of a catalytic α-subunit complexed with regulatory β-and γ-subunits. AMPK activation promotes the early stages of epithelial TJ assembly. AMPK phosphorylates the adherens junction protein afadin and regulates its interaction with the TJ-associated protein zonula occludens (ZO)-1, thereby facilitating ZO-1 distribution to the plasma membrane. In the present review, we detail the signaling pathways up-and down-stream of AMPK activation at the time of Ca2+-induced TJ assembly. View Full-Text
Keywords: AMPK; tight junctions; epithelial cells; ZO-1; par complex; MDCK; nectin-afadin; adherent junctions AMPK; tight junctions; epithelial cells; ZO-1; par complex; MDCK; nectin-afadin; adherent junctions

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Share & Cite This Article

MDPI and ACS Style

Rowart, P.; Wu, J.; Caplan, M.J.; Jouret, F. Implications of AMPK in the Formation of Epithelial Tight Junctions. Int. J. Mol. Sci. 2018, 19, 2040.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top