Abstract

The cytoskeletal components of endothelial cells in the renal artery were examined by analysis of en face preparations under confocal laser scanning microscopy. Renal arterial endothelial cells were shown to be elongated along the direction of blood flow, while stress fibers ran perpendicular to the flow in the basal portion. Focal adhesions were observed along the stress fibers in dot-like configurations. On the other hand, stress fibers in the apical portion of cells ran along the direction of flow. The localizations of stress fibers and focal adhesions in endothelial cells in the renal artery differed from those of unperturbed aortic and venous endothelial cells. Tyrosine-phosphorylated proteins were mainly detected at the sites of cell-to-cell apposition, but not in focal adhesions. Pulsatile pressure and fluid shear stress applied over endothelial cells in the renal artery induce stress fiber organization and localization of focal adhesions. These observations suggest that the morphological alignment of endothelial cells along the direction of blood flow and the organization of cytoskeletal components are independently regulated.

Highlights

  • The cytoskeletal components of endothelial cells play important roles in maintaining the fundamental structure of the thin inner layer of the blood vessels called the endothelium

  • When the focal plane was adjusted at the basal portion of the cell, stress fibers were shown to run perpendicular to the direction of blood flow (Figure 1(b); arrowheads)

  • In the apical portion of unperturbed endothelial cells located in the abdominal aorta, stress fibers were only observed along the direction of blood flow in both the apical and basal portions [14]

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Summary

Introduction

The cytoskeletal components of endothelial cells play important roles in maintaining the fundamental structure of the thin inner layer of the blood vessels called the endothelium. Endothelial cells form a single cell layer on the surfaces of blood vessels and are constantly subjected to both fluid shear stress and periodic strain caused by blood pressure induced by the pulsatile flow. Endothelial cells in culture are known to respond to cyclic stretching [10] and hyperosmotic shock [7]. Cyclic stretching applied to cells in culture is a model of pulsatile stretching induced by blood pressure in vivo, and the effects differ from those of fluid shear stress generated by the blood flow. Hemodynamic shear stress caused by blood flow occurs in combination with cyclic stretching caused by the pressure of pulsatile flow generated by blood pressure

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