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Puslapis 1 nuo 1389 rezultatus
Vascular smooth muscle caldesmon.
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Caldesmon, a major actin- and calmodulin-binding protein, has been identified in diverse bovine tissues, including smooth and striated muscles and various nonmuscle tissues, by denaturing polyacrylamide gel electrophoresis of tissue homogenates and immunoblotting using rabbit anti-chicken gizzard
Properties of smooth muscle vinculin.
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Vinculin, isolated from turkey gizzard smooth muscle, was purified by chromatography on CM-cellulose after isolation from a DEAE-cellulose column. Two-dimensional gel electrophoretic analysis of crude muscle fractions demonstrated that: 1) much of the approximately 130,000-dalton protein present in
Plasmin induces smooth muscle cell proliferation.
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BACKGROUND
Plasminogen activators are routinely used for thrombolysis. They lead to the generation of the protease, plasmin, which can induce smooth muscle cell proliferation and may thus promote further intimal hyperplasia in the thrombolysed vessel. The signaling pathways used by plasmin are not
Targeted expression of a protease-resistant IGFBP-4 mutant in smooth muscle of transgenic mice results in IGFBP-4 stabilization and smooth muscle hypotrophy.
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The insulin-like growth factor-binding protein 4 (IGFBP-4), the most abundant IGF-binding protein produced by rodent smooth muscle cells (SMC), is degraded by specific protease(s) potentially releasing IGF-I for local bioactivity. IGFBP-4 protease(s) recognizes basic residues within the midregion of
Modulation of smooth muscle responses by serine proteases and related enzymes.
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Standard isolated smooth muscle tissue preparations were used to screen the musculotropic actions of serine proteases and other substances that are generated during hemostatic activation. Sera obtained from human, rabbit, and guinea pigs produced a dose-dependent contraction of these isolated tissue
Mechanisms of smooth muscle responses to inflammation.
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BACKGROUND
Inflammation-induced changes in smooth muscle may be the consequence of changes in the properties of smooth muscle itself, in the control by nerves and hormones, in the microenvironment, or in the balance of constitutive or induced mediators. A general concept is that the specific
Loss of the serine protease HTRA1 impairs smooth muscle cells maturation.
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Vascular smooth muscle cell (VSMC) dysfunction is a hallmark of small vessel disease, a common cause of stroke and dementia. Two of the most frequently mutated genes in familial small vessel disease are HTRA1 and NOTCH3. The protease HTRA1 cleaves the NOTCH3 ligand JAG1 implying a mechanistic link
Mechanisms of airway remodeling. Airway smooth muscle.
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The airway smooth muscle cell can contract; relax; participate in allergic and inflammatory responses by expressing adhesion molecules, releasing cytokines, and producing matrix proteins and proteases; and, as has been reported, undergo migration. These properties enable the muscle cell to be a key
Endothelin degradation by vascular smooth muscle cells.
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The mechanism(s) of degradation of the potent vasoconstrictor endothelin-1 (ET-1) by rat vascular smooth muscle A-10 cells, which possess the ETA receptor subtype, was investigated by incubating [125I]ET-1 (0.1 nM) with cells for 0-4 h at 37 degrees C in the presence and absence of lysosomal enzyme
Elastase-like proteases in rat aorta smooth muscle cells and fibroblasts.
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Conformation-dependent proteolysis of smooth-muscle myosin.
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The folded 10 S conformation of turkey gizzard myosin is more resistant to proteolysis by papain than the extended 6 S conformation. These findings confirm those of Onishi and Watanabe (Onishi, H., and Watanabe, S. (1984) J. Biochem. (Tokyo) 95, 899-902). In addition, we suggest that the effect of
Protease-susceptible sites and properties of fragments of aortic smooth-muscle myosin.
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We have examined the protease susceptibility of aortic myosin, the thermal unfolding profiles of myosin rod and light meromyosin (LMM) and the solubility properties of the LMM fragments. Two major protease-susceptible sites were found, located at the head-rod junction and the heavy meromyosin
Protease activated receptor-2 expression and function in asthmatic bronchial smooth muscle.
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Asthmatic bronchial smooth muscle (BSM) is characterized by structural remodeling associated with mast cell infiltration displaying features of chronic degranulation. Mast cell-derived tryptase can activate protease activated receptor type-2 (PAR-2) of BSM cells. The aims of the present study were
Intracellular localization of Cthrc1 characterizes differentiated smooth muscle.
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OBJECTIVE
We recently reported expression of collagen triple helix repeat containing-1 (Cthrc1) in injured arteries and proteolytic cleavage of Cthrc1 in smooth muscle cells in vitro. The present study characterizes Cthrc1 processing and determines its biological
The calpain-calpastatin system in vascular smooth muscle.
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Vascular smooth muscle contains large amounts of the Ca(2+)-dependent protease calpain II. In this study, we compared bovine aortic muscle (muscle phenotype) to cultured bovine aortic cells of smooth muscle origin (modulated phenotype) with respect to major constituents of the calpain-calpastatin
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