Factors inducing codistribution of marginal actin fibers and fibronectin in rat aortic endothelial cells

Abstract

Rat endothelial cells have a unique arrangement of actin fibers running with subendothelial fibronectin along the cell margins. The present study was conducted to identify the factors that are associated with codistribution of these actin fibers and fibronectin in fetal rat aortic endothelial cells, mainly using rheological techniques. Fluorescence histochemistry revealed that the codistribution pattern was established between gestational days 14 and 15. The endothelial cells changed from polygonal to spindle shaped during this gestational period. Although the aortic length remained almost unchanged during this period of gestation, both the diameter and expansion ratio of the aorta increased, by 9 and 10%, respectively. On the other hand, the wall shear rate increased rapidly during gestational days 13-16. These results indicate that the codistribution of actin fibers and subendothelial fibronectin along the margins of endothelial cells in fetal rat aorta occurs in association with a rise in stretch and shear stress and that the endothelial cells may require this change to maintain structural integrity.

Developmental Stage Dependent Expression of the Endothelial Stress Fibers and Organization of Fibronectin Fibrils in the Aorta of Chick Embryos

“…Since the fibronectin bundles widely superimposed on the stress fibers of overlaying endothelial cells in immunofluorescence images, the fibronectin's axial organization may possibly associate with the stress fiber expression. Similar colineage between the orientation of stress fiber and fibronectin fibrils was observed in rat aortae (Sugimoto et al , 1997) or in cultured cells (Burridge, 1986;Madri et al, 1983;Wechezak et al, 1985). In our previous study using the mesenteric artery of young chicks (Jinguji and Fujiwara, 1994), both the axial alignment of fibronectin fibrils and the expression of stress fibers were prominent as vessel diameter becomes larger and endothelial cells become longer.…”

“…Considerable evidences has been accumulated indicating that the endothelial cell elongation might be a cellular response to a high level of local fluid shear stress in vivo (Flaherty et al, 1972;Kim et al, 1989a) or in vitro (Franke et al, 1984;Levesque and Nerem, 1985). It has been also supposed that the cell elongation or the high blood shear stress could stimulate the stress fiber expression (White and Fujiwara,1986;Kim et al, 1989b;Sugimoto et al, 1997). The elongation of endothelial cells and the following expression of axially organized stress fibers, observed in the present study, might be induced by the increased blood shear stress in the processes of embryonic development.…”

In Development—A New Paradigm for Understanding Vascular Disease

“…Native endothelial cells normally reside on a matrix composed primarily of laminin and collagen IV (39). However, the subendothelial matrix in fetal or newborn arteries is enriched in fibronectin, with endothelial stress fibers connecting via focal adhesion complexes to fibronectin fibrils (3, 5, 6, 40). As endothelial cells mature during the immediate postnatal period, they reorganize their underlying matrix, decreasing the levels of fibronectin and increasing laminin and collagen IV (1, 3, 4, 40).…”

The atypical structure and function of newborn arterial endothelium is mediated by Rho/Rho kinase signaling

“…Indeed, endothelial adhesion to fibronectin stimulates stress fiber formation, which is prevented by inhibiting Rho kinase (9). The subendothelial matrix of endothelial cells lining fetal or newborn arteries is enriched in fibronectin, with endothelial stress fibers connecting via focal adhesion complexes to fibronectin fibrils (4,5,14,23). As endothelial cells mature during the immediate postnatal period, they reorganize their underlying matrix, decreasing the levels of fibronectin and generating a normal subendothelial matrix (4,5,15,16).…”

“…Endothelial cells lining fetal or newborn arteries are highly unusual, displaying prominent stress fibers (15,16,23) and reduced endothelial nitric oxide (NO)-mediated dilatation (1,3,8,27). Although common in cultured cells, arterial endothelial cells in vivo generally lack stress fibers, and F-actin is restricted to a faint cortical network at the cell periphery (7,10,15,16).…”