1,721,133 research outputs found
CYTOSKELETAL AND CONTRACTILE PROTEINS IN COELOMIC, UNFERTILIZED AND FERTILIZED EGGS OF DISCOGLOSSUS PICTUS (ANURA).
No full textCYTOSKELETAL AND CONTRACTILE PROTEINS IN COELOMIC, UNFERTILIZED AND FERTILIZED EGGS OF DISCOGLOSSUS PICTUS (ANURA).
No full textCYTOSKELETAL AND CONTRACTILE PROTEINS IN COELOMIC, UNFERTILIZED AND FERTILIZED EGGS OF DISCOGLOSSUS PICTUS (ANURA).
No full textMotile properties and localization of contractile proteins in the spermatozoon of Discoglossus Pictus.
No full textAnti-spectrin antibodies stain the oocyte nucleus and the site of fertilization channels in the egg of Discoglossus pictus (Anura)
No full textThe expression of alpha 2 beta 1 integrin and alpha smooth muscle actin in fibroblasts grown on collagen
No full textAnti-spectrin antibodies stain the oocyte nucleus and the site of fertilization channels in the egg of Discoglossus pictus (Anura)
No full textThe expression of α2β1 integrin and α smooth muscle actin in fibroblasts grown on collagen
No full textThe maturation of connective tissue involves the organization of collagen fibres by resident fibroblasts. Fibroblast attachment to collagen has been demonstrated to involve cell surface receptors, integrins of the β1 family. Integrins are associated with cytoplasmic actin of microfilaments either directly or through focal adhesions. The major actin isoform of fibroblast microfilaments is β actin and to a lesser extent α smooth muscle (α SM) actin. Cultured human dermal fibroblasts derived from adult dermis, newborn foreskin or keloid scar were grown on either uncoated or collagen-coated surfaces. The expression and synthesis of both α2β1 integrin and α SM actin were followed by immunohistology and immunoprecipitation. Fibroblasts on uncoated surfaces expressed little α2β1 integrin on their surface, while 20 per cent of them demonstrated α SM actin within microfilaments. Fibroblasts grown on a collagen-coated surface minimally expressed α SM actin in microfilament structures and a majority of the cells were positive for α2β1 integrin on their membranes. Using [35S]-methionine incorporation and immunoprecipitation, it was shown that fibroblasts grown in uncoated dishes synthesized more α SM actin than fibroblasts grown on collagen-coated dishes. In contrast, fibroblasts grown on collagen coated dishes synthesized more α2β1 integrin compared to the same cells grown on uncoated dishes. Fibroblasts maintained on a type I collagen upregulate the expression and synthesis of α2β1 integrin, and downregulate the expression and synthesis of α SM actin
PROLIFERATIVE ACTIVITY AND ALPHA-SMOOTH MUSCLE ACTIN EXPRESSION IN CULTURED RAT AORTIC SMOOTH-MUSCLE CELLS ARE DIFFERENTLY MODULATED BY TRANSFORMING GROWTH-FACTOR-BETA-1 AND HEPARIN
No full textLocally liberated cytokines and extracellular matrix components influence the proliferation and differentiation of arterial smooth muscle cells (SMC), thus playing a role in the development of the atheromatous plaque. It has been proposed that the response of SMC to these factors is influenced by their own phenotype. We have tested the effects of transforming growth factor-beta 1 (TGF-beta 1) and heparin on proliferation and expression of alpha-smooth muscle (SM) actin, a well-established SMC differentiation marker, by cultured rat SMC obtained from the normal aorta of young or old rats and from the intimal thickening developed 15 days after endothelial denudation in young rats; these SMC are known to express different phenotypic features. Heparin and TGF-beta 1 reduced serum-induced proliferation in SMC from young and old rats. Heparin increased the expression of alpha-SM actin protein and mRNA in SMC from young and old rats, while TGF-beta 1 exerted the opposite action. Moreover, TGF-beta 1 induced the appearance of an elongated shape in SMC from both young and old rats. In SMC cultured from intimal thickening, heparin induced a reduction of cell proliferation without modifying their characteristic epithelioid shape; TGF-beta 1 increased the proliferative activity and induced an elongated cell shape as well as a ''hills and valleys'' growth pattern similar to that observed in control medial SMC; both heparin and TGF-beta 1 induced an increase of alpha-SM actin expression. Our results show that TGF-beta 1 and heparin exert different effects on the same SMC, suggesting that these substances act at least in part independently. They are also compatible with the view that the action of cytokines and of extracellular matrix components depends on the phenotype of target SMC. (C) 1994 Academic Press, Inc
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