Differences among 100-A filamentilament subunits from different cell types.

Bennett, Gudrun S.; Fellini, S A; Croop, James M.; Otto, Joann J.; Bryan, Joseph; Holtzer, H.

doi:10.1073/pnas.75.9.4364

Cited by 203 publications

(88 citation statements)

References 32 publications

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“…After prolonged treatment (24 h) of the cultures with 10-6M colcemid, juxtanuclear aggregates showing the characteristic caps and whorls of bundles of vimentin filaments were formed ( Fig. 5c; compare Osborn et al 1977;Bennett et al 1978;Franke et al 1978a, b;Hynes an Destree 1978).…”

Section: Resultsmentioning

confidence: 90%

Characterization of cells of amniotic fluids by immunological identification of intermediate-sized filaments: Presence of cells of different tissue origin

et al. 1981

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Section: Resultsmentioning

confidence: 90%

Characterization of cells of amniotic fluids by immunological identification of intermediate-sized filaments: Presence of cells of different tissue origin

et al. 1981

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“…A third type of filament, the intermediate filament (~10 nm in diameter), is also a component of the contractile system in smooth muscle cells. In visceral smooth muscle, intermediate filaments are composed primarily of desmin [11]; whereas in vascular smooth muscle they are composed primarily of vimentin [4,7,12,13]. Desmin is a prominent constituent of airway smooth muscle [14].…”

Section: Cellular Organization Of Contractile Apparatusmentioning

confidence: 99%

The contractile apparatus and mechanical properties of airway smooth muscle

Gunst¹,

Tang²

2000

Eur Respir J

146

122

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The functional properties of airway smooth muscle are fundamental to the properties of the airways in vivo. However, many of the distinctive characteristics of smooth muscle are not easily accounted for on the basis of molecular models developed to account for the properties of striated muscles. The specialized ultrastructural features and regulatory mechanisms present in smooth muscle are likely to form the basis for many of its characteristic properties.The molecular organization and structure of the contractile apparatus in smooth muscle is consistent with a model of force generation based on the relative sliding of adjacent actin and myosin filaments. In airway smooth muscle, actomyosin activation is initiated by the phosphorylation of the 20 kDa light chain of myosin; but there is conflicting evidence regarding the role of myosin light chain phosphorylation in tension maintenance. Tension generated by the contractile filaments is transmitted throughout the cell via a network of actin filaments anchored at dense plaques at the cell membrane, where force is transmitted to the extracellular matrix via transmembrane integrins. Proteins bound to actin and/or localized to actin filament anchorage sites may participate in regulating the shape of the smooth muscle cell and the organization of its contractile filament system. These proteins may also participate in signalling pathways that regulate the crossbridge activation and other functions of the actin cytoskeleton.The length-dependence of active force and the mechanical plasticity of airway smooth muscle may play an important role in determining airway responsiveness during lung volume changes in vivo. The molecular basis for the length-dependence of tension in smooth muscle differs from that in skeletal muscle, and may involve mechano-transduction mechanisms that modulate contractile filament activation and cytoskeletal organization in response to changes in muscle length. The reorganization of contractile filaments may also underlie the plasticity of the mechanical response of airway smooth muscle. Changes in the structural organization and signalling pathways of airway smooth muscle cells resulting form alterations in mechanical forces in the lung may be important factors in the development of pathophysiological conditions of chronic airway hyperresponsiveness. Eur Respir J 2000; 15: 600±616. The mechanical properties of airway smooth muscle are fundamental to the regulation of airway contractility and airway tone in vivo. These mechanical properties have traditionally been interpreted in terms of the "sliding filament model" of muscle contraction first proposed by HUXLEY and NIEDERGERKE [1] and HUXLEY and HANSON [2] to explain the contractile behaviour of skeletal muscle. Like other smooth muscles, airway smooth muscle exhibits the same hyperbolic force-velocity relationship that is characteristic of striated muscles, and the lengthtension relationship is also qualitatively similar to that of striated muscles [3]. The qualitative similarities be...

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“…Recent studies have shown that the major component ofthe intermediate filaments in muscle is a protein of 50,000-55,000 mol wt (15). In nonmuscle cells, other than nerve, a related protein of slightly higher mass (55,000-58,000 daltons) forms the 10-nm filaments, although the two proteins may also coexist in the same cell (5,20,24). A marked increase in the number of intermediate filaments, frequently in the form ofcables, can be induced in muscle and in other cells by drugs such as cytochalasin B and Colcemid (CIBA Pharmaceutical Co., Summit, N.…”

mentioning

confidence: 99%

Hypertrophy-induced increase of intermediate filaments in vascular smooth muscle.

Berner¹,

Somlyo²,

Somlyo³

1981

The Journal of Cell Biology

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The distribution of filaments was studied in hypertrophied rabbit vascular smooth muscle . Hypertrophy was induced by partial ligation of the portal-anterior mesenteric vein . 14 d after ligation, there was an approximately threefold increase in the number of intermediate filaments per cross-sectional area, as compared to control values . The actin :intermediate:myosin filament ratio was 15 :1 .1 :1 in control and 15 :3 .5 :0 .5 in hypertrophied portal-anterior mesentric vein vascular smooth muscle . Comparison of the filament ratios with the increase in volume density of the hypertrophied cells suggests that the number of myosin filaments per cell profile remained approximately the same as in controls, whereas the number of actin filaments increased in proportion to the increase in cell volume .Intermediate (10 nm diameter) filaments are ubiquitous components ofmost, if not all, eukaryotic cells (see reference 39 for review) . In nonneural tissue, they were first described by Ishikawa et al. (35) in cultured cells and distinguished from actin filaments through the difference in size and the failure of the 10-nm filaments to bind the heavy meromyosin subfragment of myosin. Recent studies have shown that the major component ofthe intermediate filaments in muscle is a protein of 50,000-55,000 mol wt (15). In nonmuscle cells, other than nerve, a related protein of slightly higher mass (55,000-58,000 daltons) forms the 10-nm filaments, although the two proteins may also coexist in the same cell (5,20,24). A marked increase in the number of intermediate filaments, frequently in the form ofcables, can be induced in muscle and in other cells by drugs such as cytochalasin B and Colcemid (CIBA Pharmaceutical Co., Summit, N. J.) (4,29,33,34,38,55,56) .In normal adult mammalian smooth muscle, intermediate filaments generally surround dense bodies on which actin filaments insert (2) . Intermediate filaments are very numerous in cultured vascular (45-47) and other smooth muscles (11)(12)(13)60). In previous studies of normal adult vascular smooth muscle, occasional cells were found containing massive quantities ofintermediate filaments that appeared to displace the normal actin and myosin filament lattice (50, 52) . Although it was recognized that such proliferation of intermediate filaments in adult smooth muscle represented some form of cellular pathology, its specific cause was not known . We now show that a large increase in the number of intermediate filaments in vascular smooth muscle occurs during hypertrophy induced by increasing vascular distending pressure. In addition, we also 96 describe changes found in the number and distribution ofactin and myosin filaments of hypertrophied vascular smooth muscle . These studies are being pursued to enable us to eventually distinguish the secondary effects of increased pressure on vascular smooth muscle from possible primary pathology of cell organelles that may cause hypertension. MATERIALS AND METHODSNew Zealand white male rabbits (1 .8-2 .7 kg) were anesthetized w...

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Differences among 100-A filamentilament subunits from different cell types.

Abstract: The protein subunit of 100-A filaments constitutes approximately 50% of the cytoskeleton protein of chick fibroblasts.

Cited by 203 publications

References 32 publications

Characterization of cells of amniotic fluids by immunological identification of intermediate-sized filaments: Presence of cells of different tissue origin

Characterization of cells of amniotic fluids by immunological identification of intermediate-sized filaments: Presence of cells of different tissue origin

The contractile apparatus and mechanical properties of airway smooth muscle

Hypertrophy-induced increase of intermediate filaments in vascular smooth muscle.

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