Apical cytoskeletons and junctional complexes as a combined system in epithelial cell sheets

Abstract

Epithelial cell sheet formation is central to many aspects of vertebrate development and function. For example, it is a major principle of differentiation in embryogenesis and regeneration, enables the compartmentalization of tissues, and is the basis for the maintenance of homeostasis throughout the body. A key characteristic of biologically functional epithelial cell sheets is a clear difference between the top and bottom sides owing to the apicobasal polarity of the cells in the sheet, as seen in the simple polar epithelia. Epithelial cell sheets are formed by cell-cell adhesion conferred by junctional complexes, in particular via tight junctions (TJs), which thus create a paracellular barrier. This review focuses on the apical side of the sheet, which serves as the front line. The apical membranes and TJs of the various tissues have specific characteristics that enable them to function and adapt to their biological context: each system must be robust, but also dynamic and flexible to maintain homeostasis. Here, we describe various apical cytoskeletal structures that are critical to the integrity of epithelial cell sheets. We also discuss the association of apical cytoskeletal networks with TJs, which thus forms a combined system, tentatively termed the TJ-apical complex.

Pharmacological activation of ERβ by arctigenin maintains the integrity of intestinal epithelial barrier in inflammatory bowel diseases

“…45 The interaction between TJ proteins and the actin cytoskeleton predominantly maintains the TJ structure and allows the cytoskeletal regulation of TJ barrier integrity. 46 In this study, arctigenin ameliorated the abnormal distribution of F-actin skeleton myofilament induced by TNF-α and IL-1β in Caco-2 and HT-29 cells, suggesting that TJ might be implicated in the protection of arctigenin on the intestinal epithelial barrier. Given that TJ works depending on the protein expression level and membrane distribution, 47 the effect of arctigenin on the expression and the location of CLDN1, ZO-1, and occludin in the intestinal epithelial cells were evaluated.…”

Epidermal barrier disruption by 9‐hydroxy‐10E,12Z‐octadecadienoic acid in human keratinocytes

“…6 Actin filaments, which directly bind to tight junctions, are involved in the formation, function and maintenance of the epidermal barrier. 4,5 There-fore, the dysfunction of tight junctions including redundant actin rearrangement induces the loss of water from the body and excessive percutaneous sensitization. This tight junction instability is known to cause allergic skin or inflammatory bowel diseases.…”

“…We next examined the level of filamentous actin (F-actin) using flow cytometry because cytoskeletal rearrangement regulates the integration of cell-cell adhesion. 4 Actually, enhancement of F-actin content elicited by increases in cytosolic calcium concentration and myosin light chain phosphorylation decreased TER. 5 9-HODE differ in having their hydroxy residues in the S or R configuration.…”

“…This result confirmed a potential barrier‐attenuating effect of 9‐HODE on NHEK. We next examined the level of filamentous actin (F‐actin) using flow cytometry because cytoskeletal rearrangement regulates the integration of cell–cell adhesion . Actually, enhancement of F‐actin content elicited by increases in cytosolic calcium concentration and myosin light chain phosphorylation decreased TER .…”

“…Notably, the 9‐HODE signal via the G2A activates guanosine 5′‐O‐(γ‐thio)triphosphate binding, intracellular calcium mobilization, a mitogen‐activated protein kinase and c‐Jun N‐terminal kinase, which are signals upstream of actin rearrangement . Actin filaments, which directly bind to tight junctions, are involved in the formation, function and maintenance of the epidermal barrier . Therefore, the dysfunction of tight junctions including redundant actin rearrangement induces the loss of water from the body and excessive percutaneous sensitization.…”