Spreading of vascular endothelial cells in culture: Spatial reorganization of cytoplasmic fibers and organelles

Ausprunk, Dianna H.; Berman, Herbert J.

doi:10.1016/0040-8166(78)90057-5

Cited by 15 publications

(8 citation statements)

References 24 publications

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“…Mitotic cells, at least in vitro, show lessened ability to adhere (29). This could be particularly critical for the endothelium because the lining of the aorta is subject to focal shear forces as high as 200 dynes/cm (19).…”

Section: Discussionmentioning

confidence: 99%

Organization of actin cytoskeleton in normal and regenerating arterial endothelial cells.

Gabbiani¹,

Gabbiani²,

Lombardi³

1983

Proc. Natl. Acad. Sci. U.S.A.

106

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The distribution of actin stress fibers in normal and regenerating (after endothelial denudation by means of a balloon catheter) rabbit aortic endothelial cells has been studied by means of immunofluorescence with human actin autoantibodies on enface endothelial cell preparations. Our results show that: (i) under normal conditions actin is accumulated as a network at the periphery of endothelial cells. Stress fibers are present only in endothelial cells located immediately below intercostal artery branches; (ii) stress fibers develop in endothelial cells early during regeneration and persist after the end of endothelial mitotic and motile activities; and (iii) the orientation of stress fibers within the cytoplasm follows the direction of blood flow, with the exception of stress fibers situated in cells at the edge of the wound, when endothelial cell progression toward the denuded area as well as mitotic activity have ceased. We conclude that stress fibers are an organelle present in endothelial cells in vivo and that they reorganize during endothelial cell adaptation to unfavorable or pathological situations.Endothelial continuity depends on the maintenance of an extremely thin single cell layer. When arterial endothelium is removed by mechanical abrasion, the wound is repaired by endothelial cell replication and movement (1). When the endothelial cell loss is small (few cells in width) repair is accomplished essentially by movement without replication (2). Cell movement results probably from the activity of cytoskeletal and cytocontractile elements (3), among which actin is the most abundant. Cellular actin (4, 5) is organized in the form of G actin, a microfilamentous network, and microfilamentous bundles or stress fibers, which are typical of most adherent cultured cells, including endothelial cells. Stress fibers have been shown to contain actin, myosin, and regulatory proteins (6-9). Little information is presently available on the distribution of stress fibers in vivo (5).We have studied the organization of stress fibers in endothelial cells of rabbit aorta and carotid artery under normal conditions and during regeneration after ballooning-induced endothelial denudation (10). For this purpose, we have developed a technique of immunofluorescent staining with antiactin antibodies (AAAbs) on en face endothelial cell preparations. Our results show that under normal conditions stress fibers are present only in some aortic endothelial cells-namely, those submitted to high shear stress; they become common in regenerating endothelial cells and persist long after motile and mitotic activities have ceased. MATERIALS AND METHODSMale rabbits, -3 kg of body weight, were used for the experiments. The endothelium was removed from the thoracic aorta or the left carotid artery by using the technique originally described by Baumgartner and Studer (10) with minor modifications. Evans blue (4 ml of a 1% solution in 0.9% NaCI) was injected intravenously 20 min prior to sacrifice to label denuded areas (blue areas). Tw...

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Section: Discussionmentioning

confidence: 99%

Organization of actin cytoskeleton in normal and regenerating arterial endothelial cells.

Gabbiani¹,

Gabbiani²,

Lombardi³

1983

Proc. Natl. Acad. Sci. U.S.A.

106

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“…As endothelial cells go from round to spread during substrate attachment there is a well-characterized effect on the size and shape of the nucleus, causing it to ''deform'' [17]. Additionally, during cell attachment, there are forces exerted by the cytoplasmic filaments that can cause the subcellular organelles to rearrange and/or redistribute [16]. These subcellular changes may give rise to light-scattering spectroscopic fingerprints that can be used to describe the degree of attachment of the cell population once calibrated against attachment standards.…”

Section: Discussionmentioning

confidence: 99%

“…Specifically, interactions during the process of cell attachment onto a substrate can be assessed through the possible detection of changes in cell shape [14,15], sub-cellular organelle distribution [16], nuclear deformation [17], focal adhesion complex formation [18][19][20], and the assembly of micro-filamentous stress fibers [18][19][20]. Interactions involved in phenotypic differentiation could be assessed through the possible detection of changes in organelle size, abundance, and distribution as well as the abundance of actin and myosin filaments [21][22][23][24][25][26].…”

Section: Introductionmentioning

confidence: 99%

Spectroscopic translation of cell–material interactions

et al. 2007

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“…1974;De Chastonay et al. 1983], as well as in cultured endothelial cells [Asprunk and Berman, 1978]. It is known that in rats exposed to hypobaric hypoxia, increased endothelial or intimal proliferation of the pulmonary trunk and artery begins at 3 days, lasts for 10 days, and declines thereafter Reid.…”

Section: Discussionmentioning

confidence: 99%

“…1983, clusters of microvilli-rich cells [Still and Dennison. 1974;Asprunk and Berman. 1978;Hazama et al.…”

Section: Discussionmentioning

confidence: 99%

Scanning Electron Microscopy of Pulmonary Vascular Endothelium in Rats with Hypoxia-Induced Hypertension

Hung¹,

McKenzie²,

Mattioli³

et al. 1986

Cells Tissues Organs

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Scanning electron microscopy was used to study the endothelial surface of the pulmonary trunk, artery, and vein in normobaric control rats as well as in rats exposed to hypobaric hypoxia for 7 and 21 days. The individual endothelial cells of the normobaric pulmonary trunk and hilar artery were flat and slightly elongated with elevated nuclear regions, and those of the intermediate-sized artery were more elongated and had more microvilli than the large arteries studied. Their endothelial cell boundaries were outlined by beaded cytoplasmic projections. The surfaces of the normobaric hilar and intermediate-sized veins were smooth and demonstrated numerous longitudinal streaks. These venous endothelial cells were elongated and their cell boundaries were outlined by low discontinuous marginal folds. Exposure to hypobaric hypoxia caused the following changes on the arterial surface: elevation of the endothelial cells; formation of microvilli-rich cell clusters; formation of hollow defects; and the attachment of leukocytes. Hypobaric hypoxia also caused the disappearance of the longitudinal streaks and the occurrence of microvilli-rich cells in the hilar veins. The endothelial surface modifications in the hypobaric rats could be related to thickening of the endothelium, intimal edema, increased intimal connective tissue, luminal invasion of leukocytes, and increased endothelial cell proliferation, known to occur in systemic arteries of hypertensive animals.

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Spreading of vascular endothelial cells in culture: Spatial reorganization of cytoplasmic fibers and organelles

Cited by 15 publications

References 24 publications

Organization of actin cytoskeleton in normal and regenerating arterial endothelial cells.

Organization of actin cytoskeleton in normal and regenerating arterial endothelial cells.

Spectroscopic translation of cell–material interactions

Scanning Electron Microscopy of Pulmonary Vascular Endothelium in Rats with Hypoxia-Induced Hypertension

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