Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2021 Feb:19:10-16.
doi: 10.1016/j.cophys.2020.06.012. Epub 2020 Jun 30.

Actin cytoskeleton dynamics during mucosal inflammation: a view from broken epithelial barriers

Susana Lechuga  1 , Andrei I Ivanov  1
Affiliations

Actin cytoskeleton dynamics during mucosal inflammation: a view from broken epithelial barriers

Susana Lechuga et al. Curr Opin Physiol. 2021 Feb.

Abstract

Disruption of epithelial barriers is a key pathogenic event of mucosal inflammation: It ignites the exaggerated immune response and accelerates tissue damage. Loss of barrier function is attributed to the abnormal structure and permeability of epithelial adherens junctions and tight junctions, driven by inflammatory stimuli through a variety of cellular mechanisms. This review focuses on roles of the actin cytoskeleton in mediating disruption of epithelial junctions and creation of leaky barriers in inflamed tissues. We summarize recent advances in understanding the role of cytoskeletal remodeling driven by actin filament turnover and myosin II-dependent contractility in the homeostatic regulation of epithelial barriers and barrier disruption during mucosal inflammation. We also discuss how the altered biochemical and physical environment of the inflamed tissues could affect the dynamics of the junction-associated actomyosin cytoskeleton, leading to the disruption of epithelial barriers.

Keywords: actin turnover; adherens junctions; cytoskeletal forces; non-muscle myosin II; permeability; tight junctions.

PubMed Disclaimer

Conflict of interest statement

Conflict of interest: None declared.

Figures

Figure 1.
Figure 1.
Organization of the actin cytoskeleton and cytoskeleton-generated forces at epithelial junctions. a. A diagram depicts different fractions of the actin cytoskeleton associated with the apical junctions and lateral contacts of adjacent columnar epithelial cells. b. A putative spatial organization of the actomyosin cytoskeleton at epithelial apicaljunctions. Red arrows indicate directionality of forces generated by the perijunctional cytoskeleton.
Figure 2.
Figure 2.
Multiple mechanisms affecting the organization and dynamics of the epithelial actin cytoskeleton during mucosal inflammation. The diagram presents most likely mechanisms by which inflammatory environment can alter the structure and remodeling of the perijunctional actomyosin cytoskeleton in epithelial cells, resulting in breakdown of epithelial barriers.
See this image and copyright information in PMC

References

    1. Rubsam M, Broussard JA, Wickstrom SA, Nekrasova O, Green KJ, Niessen CM: Adherens Junctions and Desmosomes Coordinate Mechanics and Signaling to Orchestrate Tissue Morphogenesis and Function: An Evolutionary Perspective. Cold Spring Harb Perspect Biol 2018, 10:a02907. - PMC - PubMed
    1. Van Itallie CM, Anderson JM: Architecture of tight junctions and principles of molecular composition. Semin Cell Dev Biol 2014, 36:157–165. - PMC - PubMed
    1. Charras G, Yap AS: Tensile Forces and Mechanotransduction at Cell-Cell Junctions. Curr Biol 2018, 28:R445–R457. - PubMed
    1. Citi S: The mechanobiology of tight junctions. Biophys Rev 2019, 11:783–793. - PMC - PubMed
    1. Varadarajan S, Stephenson RE, Miller AL: Multiscale dynamics of tight junction remodeling. J Cell Sci 2019, 132:jcs229286. - PMC - PubMed

LinkOut - more resources