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Role of Stress on Driving the Intestinal Paracellular Permeability

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CURRENT ISSUES IN MOLECULAR BIOLOGY
卷 45, 期 11, 页码 9284-9305

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MDPI
DOI: 10.3390/cimb45110581

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gut epithelium; paracellular permeability; claudins; occludin; stress; corticosterone

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The gut epithelium controls intestinal permeability through tight junction proteins. Stress disrupts this control by affecting the binding of stress hormones to receptors. Studying the neuroendocrine effects of stress and intestinal permeability is important for the treatment of related diseases.
The gut epithelium is a polarized monolayer that exhibits apical and basolateral membrane surfaces. Monolayer cell components are joined side by side via protein complexes known as tight junction proteins (TJPs), expressed at the most apical extreme of the basolateral membrane. The gut epithelium is a physical barrier that determinates intestinal permeability, referred to as the measurement of the transit of molecules from the intestinal lumen to the bloodstream or, conversely, from the blood to the gut lumen. TJPs play a role in the control of intestinal permeability that can be disrupted by stress through signal pathways triggered by the ligation of receptors with stress hormones like glucocorticoids. Preclinical studies conducted under in vitro and/or in vivo conditions have addressed underlying mechanisms that account for the impact of stress on gut permeability. These mechanisms may provide insights for novel therapeutic interventions in diseases in which stress is a risk factor, like irritable bowel syndrome. The focus of this study was to review, in an integrative context, the neuroendocrine effects of stress, with special emphasis on TJPs along with intestinal permeability.

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