Endothelial Cell Biomechanical Responses are Dependent on Both Fluid Shear Stress and Tensile Strain

Meza, Daphne; Musmacker, Bryan; Steadman, Elisabeth; Stransky, Thomas; Rubenstein, David A.

doi:10.1007/s12195-019-00585-0

Cited by 31 publications

(23 citation statements)

References 85 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As the diaphragm contracts, a negative intrapleural pressure expands the lungs. Concurrent fluid shear stress and tensile strain have been shown to influence cell area, PECAM‐1 phosphorylation, and ICAM‐1 expression 48 . CEC and LEC response to shear stress was also significantly regulated by the type of coating used.…”

Section: Discussionmentioning

confidence: 99%

Cardiac and lung endothelial cells in response to fluid shear stress on physiological matrix stiffness and composition

et al. 2020

View full text Add to dashboard Cite

Objective Preconditioning of endothelial cells from different vascular beds has potential value for re‐endothelialization and implantation of engineered tissues. Understanding how substrate stiffness and composition affects tissue‐specific cell response to shear stress will aid in successful endothelialization of engineered tissues. We developed a platform to test biomechanical and biochemical stimuli. Methods A novel polydimethylsiloxane‐based parallel plate flow chamber enabled application of laminar fluid shear stress of 2 dynes/cm2 for 12 hours to microvascular cardiac and lung endothelial cells cultured on cardiac and lung‐derived extracellular matrix. Optical imaging of cells was used to quantify cell changes in cell alignment. Analysis of integrin expression was performed using flow cytometry. Results Application of fluid shear stress caused the greatest cell alignment in cardiac endothelial cells seeded on polystyrene and lung endothelial cells on polydimethylsiloxane. This resulted in elongation of the lung endothelial cells. αv and β3 integrin expression decreased after application of shear stress in both cell types. Conclusion Substrate stiffness plays an important role in regulating tissue‐specific endothelial response to shear stress, which may be due to differences in their native microenvironments. Furthermore, cardiac and lung endothelial cell response to shear stress was significantly regulated by the type of coating used.

show abstract

Section: Discussionmentioning

confidence: 99%

Cardiac and lung endothelial cells in response to fluid shear stress on physiological matrix stiffness and composition

et al. 2020

View full text Add to dashboard Cite

show abstract

“…As an efficient signaling molecule, PECAM-1 has diverse vascular biology roles, including angiogenesis, platelet function, thrombosis, mechanosensing of fluid shear stress, and regulating leukocyte migration ( Woodfin et al, 2007 ). Five percent CS alone did not cause any significant changes in cell area and cell aspect ratio compared to untreated control cells, but cell area increased significantly in response to concurrent shear stress and CS ( Meza et al, 2019 ). Upon CS, the cytoplasmic domain of PECAM-1 is unfolded and exposes a phosphorylation site, allowing the rapid PECAM-1 phosphorylation, transforming a mechanical signal into a biochemical signal ( Snyder et al, 2017 ).…”

Section: Dysfunction Of Pulmonary Microvascular Endothelial Barriermentioning

confidence: 90%

Mechanisms of Mechanical Force Induced Pulmonary Vascular Endothelial Hyperpermeability

Lai

Huang

2021

Front. Physiol.

View full text Add to dashboard Cite

Mechanical ventilation is a supportive therapy for patients with acute respiratory distress syndrome (ARDS). However, it also inevitably produces or aggravates the original lung injury with pathophysiological changes of pulmonary edema caused by increased permeability of alveolar capillaries which composed of microvascular endothelium, alveolar epithelium, and basement membrane. Vascular endothelium forms a semi-selective barrier to regulate body fluid balance. Mechanical ventilation in critically ill patients produces a mechanical force on lung vascular endothelium when the endothelial barrier was destructed. This review aims to provide a comprehensive overview of molecular and signaling mechanisms underlying the endothelial barrier permeability in ventilator-induced lung jury (VILI).

show abstract

“…These findings underline that mechanotransduction depends on a complex interplay of diverse forces. Meza et al [ 43 ] also analyzed the effects of pulsatile shear stress and cyclic tensile strain on ECs and found that both forces, but not synergistically, increased effects on EC morphology and activation, indicated by the phosphorylation of platelet endothelial cell adhesion molecule (PECAM)-1 and increased surface expression of ICAM-1.…”

Section: In Vitro Systems To Model Flow Dynamics and Endothelial Wall Shear Stress (Wss)mentioning

confidence: 99%

Investigation of Wall Shear Stress in Cardiovascular Research and in Clinical Practice—From Bench to Bedside

Urschel

Tauchi

Achenbach

et al. 2021

IJMS

View full text Add to dashboard Cite

In the 1900s, researchers established animal models experimentally to induce atherosclerosis by feeding them with a cholesterol-rich diet. It is now accepted that high circulating cholesterol is one of the main causes of atherosclerosis; however, plaque localization cannot be explained solely by hyperlipidemia. A tremendous amount of studies has demonstrated that hemodynamic forces modify endothelial athero-susceptibility phenotypes. Endothelial cells possess mechanosensors on the apical surface to detect a blood stream-induced force on the vessel wall, known as “wall shear stress (WSS)”, and induce cellular and molecular responses. Investigations to elucidate the mechanisms of this process are on-going: on the one hand, hemodynamics in complex vessel systems have been described in detail, owing to the recent progress in imaging and computational techniques. On the other hand, investigations using unique in vitro chamber systems with various flow applications have enhanced the understanding of WSS-induced changes in endothelial cell function and the involvement of the glycocalyx, the apical surface layer of endothelial cells, in this process. In the clinical setting, attempts have been made to measure WSS and/or glycocalyx degradation non-invasively, for the purpose of their diagnostic utilization. An increasing body of evidence shows that WSS, as well as serum glycocalyx components, can serve as a predicting factor for atherosclerosis development and, most importantly, for the rupture of plaques in patients with high risk of coronary heart disease.

show abstract

Endothelial Cell Biomechanical Responses are Dependent on Both Fluid Shear Stress and Tensile Strain

Abstract: Associate Editor William H. Guilford oversaw the review of this article.

Cited by 31 publications

References 85 publications

Cardiac and lung endothelial cells in response to fluid shear stress on physiological matrix stiffness and composition

Cardiac and lung endothelial cells in response to fluid shear stress on physiological matrix stiffness and composition

Mechanisms of Mechanical Force Induced Pulmonary Vascular Endothelial Hyperpermeability

Investigation of Wall Shear Stress in Cardiovascular Research and in Clinical Practice—From Bench to Bedside

Contact Info

Product

Resources

About