An ancient control of epithelial barrier formation and wound healing

BioEssays ◽  
2005 ◽  
Vol 27 (10) ◽  
pp. 987-990 ◽  
Author(s):  
Bernard Moussian ◽  
Anne E. Uv
Keyword(s):  
Wound Healing ◽  
Epithelial Barrier ◽  
Barrier Formation

scholarly journals A Novel Pharmacological Approach to Enhance the Integrity and Accelerate Restitution of the Intestinal Epithelial Barrier

2020 ◽  
Vol 26 (9) ◽  
pp. 1340-1352
Author(s):  
Xuelei Cao ◽  
Lei Sun ◽  
Susana Lechuga ◽  
Nayden G Naydenov ◽  
Alex Feygin ◽  
...  
Keyword(s):  
Wound Healing ◽  
Epithelial Cell ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Cell Monolayers ◽  
Barrier Disruption ◽  
Epithelial Cell Monolayers ◽  
Immunofluorescence Labeling ◽  
E Cadherin

Abstract Background Disruption of the gut barrier is an essential mechanism of inflammatory bowel diseases (IBDs) contributing to the development of mucosal inflammation. A hallmark of barrier disruption is the disassembly of epithelial adherens junctions (AJs) driven by decreased expression of a major AJ protein, E-cadherin. A group of isoxazole compounds, such as E-cadherin-upregulator (ECU) and ML327, were previously shown to stimulate E-cadherin expression in poorly differentiated human cancer cells. This study was designed to examine whether these isoxazole compounds can enhance and protect model intestinal epithelial barriers in vitro. Methods The study was conducted using T84, SK-CO15, and HT-29 human colonic epithelial cell monolayers. Disruption of the epithelial barrier was induced by pro-inflammatory cytokines, tumor necrosis factor-α, and interferon-γ. Barrier integrity and epithelial junction assembly was examined using different permeability assays, immunofluorescence labeling, and confocal microscopy. Epithelial restitution was analyzed using a scratch wound healing assay. Results E-cadherin-upregulator and ML327 treatment of intestinal epithelial cell monolayers resulted in several barrier-protective effects, including reduced steady-state epithelial permeability, inhibition of cytokine-induced barrier disruption and junction disassembly, and acceleration of epithelial wound healing. Surprisingly, these effects were not due to upregulation of E-cadherin expression but were mediated by multiple mechanisms including inhibition of junction protein endocytosis, attenuation of cytokine-induced apoptosis, and activation of promigratory Src and AKT signaling. Conclusions Our data highlight ECU and ML327 as promising compounds for developing new therapeutic strategies to protect the integrity and accelerate the restitution of the intestinal epithelial barrier in IBD and other inflammatory disorders.

scholarly journals Laminin-driven Epac/Rap1 regulation of epithelial barriers on decellularized matrix

2019 ◽  
Author(s):  
Bethany M. Young ◽  
Keerthana Shankar ◽  
Cindy K. Tho ◽  
Amanda R. Pellegrino ◽  
Rebecca L. Heise
Keyword(s):  
Barrier Function ◽  
Cellular Response ◽  
Alveolar Epithelium ◽  
Epithelial Barrier ◽  
Epithelial Barrier Function ◽  
Main Challenge ◽  
Barrier Formation ◽  
Epithelial Barriers ◽  
Molecular Therapeutic

ABSTRACTDecellularized tissues offer a unique tool for developing regenerative biomaterials orin vitroplatforms for the study of cell-extracellular matrix (ECM) interactions. One main challenge associated with decellularized lung tissue is that ECM components can be stripped away or altered by the detergents used to remove cellular debris. Without characterizing the composition of lung decellularized ECM (dECM) and the cellular response caused by the altered composition, it is difficult to utilize dECM for regeneration and specifically, engineering the complexities of the alveolar-capillary barrier. This study takes steps towards uncovering if dECM must be enhanced with lost ECM proteins to achieve proper epithelial barrier formation. To achieve this, epithelial barrier function was assessed on dECM coatings with and without the systematic addition of several key basement membrane proteins. After comparing barrier function on collagen, fibronectin, laminin, and dECM in varying combinations as anin vitrocoating, the alveolar epithelium exhibited superior barrier function when dECM was supplemented with laminin as evidenced by trans-epithelial electrical resistance (TEER) and permeability assays. Increased barrier resistance with laminin addition was associated with upregulation of Claudin-18, E- cadherin, and junction adhesion molecule (JAM)-A, and stabilization of zonula occludens (ZO)-1 at junction complexes. The Epac/Rap1 pathway was observed to play a role in the ECM-mediated barrier function determined by protein expression and Epac inhibition. These findings reveal potential ECM coatings and molecular therapeutic targets for improved regeneration with decellularized scaffolds or edema related pathologies.

scholarly journals Activated Protein C in Cutaneous Wound Healing: From Bench to Bedside

2019 ◽  
Vol 20 (4) ◽  
pp. 903 ◽  
Author(s):  
Ruilong Zhao ◽  
Haiyan Lin ◽  
Lara Bereza-Malcolm ◽  
Elizabeth Clarke ◽  
Christopher Jackson ◽  
...  
Keyword(s):  
Wound Healing ◽  
Clinical Studies ◽  
Protein C ◽  
Activated Protein C ◽  
Epithelial Barrier ◽  
Cutaneous Wound Healing ◽  
Cutaneous Wound ◽  
Beneficial Effects ◽  
The Past ◽  
Complex Process

Independent of its well-known anticoagulation effects, activated protein C (APC) exhibits pleiotropic cytoprotective properties. These include anti-inflammatory actions, anti-apoptosis, and endothelial and epithelial barrier stabilisation. Such beneficial effects have made APC an attractive target of research in a plethora of physiological and pathophysiological processes. Of note, the past decade or so has seen the emergence of its roles in cutaneous wound healing—a complex process involving inflammation, proliferation and remodelling. This review will highlight APC’s functions and mechanisms, and detail its pre-clinical and clinical studies on cutaneous wound healing.

T1820 Enteric Glial Cells Promote Wound Healing of Intestinal Epithelial Barrier in Part Via a FAK-Dependent Pathway

2008 ◽  
Vol 134 (4) ◽  
pp. A-570
Author(s):  
Laurianne Van Landeghem ◽  
Pascal Derkinderen ◽  
Philippe Aubert ◽  
Hervé Enslen ◽  
Isabelle Guisle-Marsollier ◽  
...  
Keyword(s):  
Wound Healing ◽  
Glial Cells ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Promote Wound Healing ◽  
Enteric Glial Cells ◽  
Dependent Pathway

scholarly journals Epithelial barrier formation by airway basal cells

Thorax ◽  
1997 ◽  
Vol 52 (3) ◽  
pp. 213-217 ◽  
Author(s):  
J. S. Erjefalt ◽  
F. Sundler ◽  
C. G. Persson
Keyword(s):  
Epithelial Barrier ◽  
Basal Cells ◽  
Barrier Formation

scholarly journals Circulating Ouabain Modulates Expression of Claudins in Rat Intestine and Cerebral Blood Vessels

2020 ◽  
Vol 21 (14) ◽  
pp. 5067
Author(s):  
Alexander G. Markov ◽  
Arina A. Fedorova ◽  
Violetta V. Kravtsova ◽  
Anastasia E. Bikmurzina ◽  
Larisa S. Okorokova ◽  
...  
Keyword(s):  
Tight Junction ◽  
Blood Vessels ◽  
Barrier Properties ◽  
Transepithelial Resistance ◽  
Epithelial Barrier ◽  
Cerebral Blood Vessels ◽  
Down Regulation ◽  
Barrier Formation ◽  
Tight Junction Permeability

The ability of exogenous low ouabain concentrations to affect claudin expression and therefore epithelial barrier properties was demonstrated previously in cultured cell studies. We hypothesized that chronic elevation of circulating ouabain in vivo can affect the expression of claudins and tight junction permeability in different tissues. We tested this hypothesis in rats intraperitoneally injected with ouabain (1 μg/kg) for 4 days. Rat jejunum, colon and brain frontal lobes, which are variable in the expressed claudins and tight junction permeability, were examined. Moreover, the porcine jejunum cell line IPEC-J2 was studied. In IPEC-J2-cells, ouabain (10 nM, 19 days of incubation) stimulated epithelial barrier formation, increased transepithelial resistance and the level of cSrc-kinase activation by phosphorylation, accompanied with an increased expression of claudin-1, -5 and down-regulation of claudin-12; the expression of claudin-3, -4, -8 and tricellulin was not changed. In the jejunum, chronic ouabain increased the expression of claudin-1, -3 and -5 without an effect on claudin-2 and -4 expression. In the colon, only down-regulation of claudin-3 was observed. Chronic ouabain protected the intestine transepithelial resistance against functional injury induced by lipopolysaccharide treatment or by modeled acute microgravity; this regulation was most pronounced in the jejunum. Claudin-1 was also up-regulated in cerebral blood vessels. This was associated with reduction of claudin-3 expression while the expression of claudin-5 and occludin was not affected. Altogether, our results confirm that circulating ouabain can functionally and tissue-specifically affect barrier properties of epithelial and endothelial tissues via Na,K-ATPase-mediated modulation of claudins expression.

scholarly journals Calmodulin 4 is dispensable for epidermal barrier formation and wound healing in mice

2014 ◽  
Vol 24 (1) ◽  
pp. 55-57 ◽  
Author(s):  
Juliane C. Lessard ◽  
Alexandr Kalinin ◽  
Paul W. Bible ◽  
Maria I. Morasso
Keyword(s):  
Wound Healing ◽  
Epidermal Barrier ◽  
Barrier Formation
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