Phenotype modulation in primary cultures of rat aortic smooth muscle cells
Identifieur interne : 003065 ( Main/Exploration ); précédent : 003064; suivant : 003066Phenotype modulation in primary cultures of rat aortic smooth muscle cells
Auteurs : Johan Thyberg [Suède] ; Karin Blomgren [Suède]Source :
- Virchows Archiv B [ 0340-6075 ] ; 1990-12-01.
English descriptors
- KwdEn :
- Teeft :
- Actin, Actin filaments, Aortic, Biol, Bottger, Carboxylic ionophore monensin, Cell size, Chloroquine, Cisterna, Colchicine, Contractile, Cytochalasin, Cytoskeleton, Degraded material, Electron micrograph, Electron microscopy, Endoplasmic, Endoplasmic reticulum, Extracellular matrix, Fibronectin, Filament, Gabbiani, Golgi, Growth factor, Hedin, Large golgi, Lysosomal, Matrix, Microtubule, Modulation, Monensin, Muscle cells, Myofilament bundles, Nocodazole, Other hand, Phenotype, Phenotype modulation, Phenotypic, Phenotypic modulation, Primary culture, Primary cultures, Proc natl acad, Reticulum, Rough endoplasmic reticulum, Skalli, Smooth muscle cell, Smooth muscle cells, Stacks, Synthetic phenotype, Thyberg, Vacuole.
Abstract
Summary: The transition of adult rat aortic smooth muscle cells from a contractile to a synthetic phenotype during the first week of primary culture on a substrate of fibronectin in serumfree medium was studied by light and electron microscopy. The weak base chloroquine and the carboxylic ionophore monensin were both found to inhibit the spreading of the cells and the accompanying changes in cellular fine structure. The exchange of myofilament bundles for a prominent rough endoplasmic reticulum and Golgi complex was delayed and vacuoles filled with incompletely degraded material accumulated in the cytoplasm. The microtubuledisruptive drugs colchicine and nocodazole likewise opposed the spreading and fine structural reorganization of the cells. Most typically, the Golgi stacks were small and widely dispersed. In addition, vacuoles of the type mentioned above increased in number. On the other hand, there was surprisingly little effect of cytochalasin B, a drug that is supposed to interfere with the assembly of actin filaments. The observations suggest that the phenotypic modulation of arterial smooth muscle cells is dependent on: (a) lysosomal degradation of discarded cellular constituents, (b) active vesicular transport along the exocytic pathway to provide the expanding cell surface with new membrane, and (c) a normal microtubular cytoskeleton to ensure the establishment of a new and functionally efficient intracellular organization.
Url:
DOI: 10.1007/BF02899380
Affiliations:
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matrix</term><term>Fibronectin</term><term>Filament</term><term>Gabbiani</term><term>Golgi</term><term>Growth factor</term><term>Hedin</term><term>Large golgi</term><term>Lysosomal</term><term>Matrix</term><term>Microtubule</term><term>Modulation</term><term>Monensin</term><term>Muscle cells</term><term>Myofilament bundles</term><term>Nocodazole</term><term>Other hand</term><term>Phenotype</term><term>Phenotype modulation</term><term>Phenotypic</term><term>Phenotypic modulation</term><term>Primary culture</term><term>Primary cultures</term><term>Proc natl acad</term><term>Reticulum</term><term>Rough endoplasmic reticulum</term><term>Skalli</term><term>Smooth muscle cell</term><term>Smooth muscle cells</term><term>Stacks</term><term>Synthetic phenotype</term><term>Thyberg</term><term>Vacuole</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: The transition of adult rat aortic smooth muscle cells from a contractile to a synthetic phenotype during the first week of primary culture on a substrate of fibronectin in serumfree medium was studied by light and electron microscopy. The weak base chloroquine and the carboxylic ionophore monensin were both found to inhibit the spreading of the cells and the accompanying changes in cellular fine structure. The exchange of myofilament bundles for a prominent rough endoplasmic reticulum and Golgi complex was delayed and vacuoles filled with incompletely degraded material accumulated in the cytoplasm. The microtubuledisruptive drugs colchicine and nocodazole likewise opposed the spreading and fine structural reorganization of the cells. Most typically, the Golgi stacks were small and widely dispersed. In addition, vacuoles of the type mentioned above increased in number. On the other hand, there was surprisingly little effect of cytochalasin B, a drug that is supposed to interfere with the assembly of actin filaments. The observations suggest that the phenotypic modulation of arterial smooth muscle cells is dependent on: (a) lysosomal degradation of discarded cellular constituents, (b) active vesicular transport along the exocytic pathway to provide the expanding cell surface with new membrane, and (c) a normal microtubular cytoskeleton to ensure the establishment of a new and functionally efficient intracellular organization.</div></front></TEI><affiliations><list><country><li>Suède</li></country><region><li>Svealand</li></region><settlement><li>Stockholm</li></settlement></list><tree><country name="Suède"><region name="Svealand"><name sortKey="Thyberg, Johan" sort="Thyberg, Johan" uniqKey="Thyberg J" first="Johan" last="Thyberg">Johan Thyberg</name></region><name sortKey="Blomgren, Karin" sort="Blomgren, Karin" uniqKey="Blomgren K" first="Karin" last="Blomgren">Karin Blomgren</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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