Response of the endothelial cell transcriptome to supraphysiological laminar shear stress

White, Simon; Hayes, Elaine; Lehoux, Stéphanie; Jeremy, Jamie Y.; Horrevoets, Anton J.G.; Newby, Andrew C.

doi:10.1016/j.atherosclerosis.2010.08.010

Cited by 1 publication

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“…Particularly in the vasculature, the two types of biomechanical stimuli, such as frictional force known as shear stress (SS), or wall shear stress (WSS) that acts tangentially to the vessel, could determinate dysregulation of the cellular redox status, that in turn could have effects on intracellular signaling pathways involved in disease progression [33]. For example, exposure of endothelial cells to laminar SS can induce a suppression of ROS levels [34,35]. Conversely, exposure of endothelial cells to WSS using an irregular flow induces an increase of ROS levels and a reduced bioavailability of the vasodilator molecule NO [36], which is involved in preventing the activation and adhesion of platelets and leukocytes to the wall of the injured vessel [37].…”

Section: Smoke Oxidative Stress and Fibrosis In Lung Pathogenesismentioning

confidence: 99%

InnovativeIn VitroModels for the Study of Lung Diseases

Picchio¹,

Cammisotto²,

Pagano³

et al. 2021

Cell Interaction - Molecular and Immunological Basis for Disease Management

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Basic and translational research on lung biology and pathology can greatly benefit from the development of 3D in vitro models with physiological relevance. Lung organoids and lungs-on-chip allow the creation of different kinds of in vitro microenvironments, that can be useful for the elucidation of novel pathogenetic pathways, for example concerning tissue fibrosis in chronic diseases. Moreover, they represent important translational models for the identification of novel therapeutic targets, and for preliminary testing of new drugs. In this chapter, we provide a selected overview of recent studies on innovative 3D in vitro models that have enhanced our knowledge on chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF), particularly concerning oxidative stress and pro-fibrotic pathogenetic mechanisms. Despite several limitations, these complex models must be considered as complementary in all respects to in vivo studies on animal models and clinical research.

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