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Matrix-driven cell size change modulates aortic endothelial cell proliferation and sheet migration.

Joseph A. Madri, Bruce M. Pratt, Judith Yannariello‐Brown

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Abstract

Current hypotheses suggest that the extracellular matrix modulates cellular function in physiologic homeostasis and during injury and repair and that selected cellular functions are cell and nuclear size dependent. For elucidation of the role of extracellular matrix-driven cell size changes in the modulation of endothelial cell proliferation and sheet migration an in vitro model system was used that allows for the culture of bovine aortic endothelial cells (BAEC) on various purified extracellular matrix components. BAEC exhibited distinct patterns in rates of attachment, spreading, migration, and proliferation when cultured on the selected extracellular matrix components laminin, types I and III collagen, type IV collagen, and fibronectin. In addition, there was a correlation between cell and nuclear size (on the various matrices tested) and rates of cell attachment and spreading. In contrast, an inverse correlation was noted between cell and nuclear size (on the various matrices tested) and proliferation and sheet migration. These data demonstrate that endothelial cells respond to matrix components in specific but complex fashions, mediated, in part, by changes in cell and nuclear size.

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What this paper is about

Current hypotheses suggest that the extracellular matrix modulates cellular function in physiologic homeostasis and during injury and repair and that selected cellular functions are cell and nuclear size dependent. For elucidation of the role of extracellular matrix-driven cell size changes in the modulation of endothelial cell proliferation and sheet migration an in vitro model system was used that allows for the culture of bovine aortic endothelial cells (BAEC) on various purified extracellular matrix components. BAEC exhibited distinct patterns in rates of attachment, spreading, migration, and proliferation when cultured on the selected extracellular matrix components laminin, types I and III collagen, type IV collagen, and fibronectin. In addition, there was a correlation between cell and nuclear size (on the various matrices tested) and rates of cell attachment and spreading. In contrast, an inverse correlation was noted between cell and nuclear size (on the various matrices tested) and proliferation and sheet migration. These data demonstrate that endothelial cells respond to matrix components in specific but complex fashions, mediated, in part, by changes in cell and nuclear size.

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Available abstract

Current hypotheses suggest that the extracellular matrix modulates cellular function in physiologic homeostasis and during injury and repair and that selected cellular functions are cell and nuclear size dependent. For elucidation of the role of extracellular matrix-driven cell size changes in the modulation of endothelial cell proliferation and sheet migration an in vitro model system was used that allows for the culture of bovine aortic endothelial cells (BAEC) on various purified extracellular matrix components. BAEC exhibited distinct patterns in rates of attachment, spreading, migration, and proliferation when cultured on the selected extracellular matrix components laminin, types I and III collagen, type IV collagen, and fibronectin. In addition, there was a correlation between cell and nuclear size (on the various matrices tested) and rates of cell attachment and spreading. In contrast, an inverse correlation was noted between cell and nuclear size (on the various matrices tested) and proliferation and sheet migration. These data demonstrate that endothelial cells respond to matrix components in specific but complex fashions, mediated, in part, by changes in cell and nuclear size.

Key concepts: Extracellular matrix, Fibronectin, Cell biology, Cell growth, Biology, Laminin, Endothelial stem cell, Extracellular

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Matrix-driven cell size change modulates aortic endothelial cell proliferation and sheet migration. — Research Paper | ScholarLens