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Mol Biol Cell. 1999 Mar;10(3):785-98.
Modulation of cell proliferation and differentiation through substrate-dependent changes in fibronectin conformation.
Garcia AJ, Vega MD, Boettiger D.
Department of Microbiology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. andres.garcie.gatech.edu
Integrin-mediated cell adhesion to extracellular matrices provides signals essential for cell cycle progression and differentiation. We demonstrate that substrate-dependent changes in the conformation of adsorbed fibronectin (Fn) modulated integrin binding and controlled switching between proliferation and differentiation. Adsorption of Fn onto bacterial polystyrene (B), tissue culture polystyrene (T), and collagen (C) resulted in differences in Fn conformation as indicated by antibody binding. Using a biochemical method to quantify bound integrins in cultured cells, we found that differences in Fn conformation altered the quantity of bound alpha5 and beta1 integrin subunits but not alphav or beta3. C2C12 myoblasts grown on these Fn-coated substrates proliferated to different levels (B > T > C). Immunostaining for muscle-specific myosin revealed minimal differentiation on B, significant levels on T, and extensive differentiation on C. Differentiation required binding to the RGD cell binding site in Fn and was blocked by antibodies specific for this site. Switching between proliferation and differentiation was controlled by the levels of alpha5beta1 integrin bound to Fn, and differentiation was inhibited by anti-alpha5, but not anti-alphav, antibodies, suggesting distinct integrin-mediated signaling pathways. Control of cell proliferation and differentiation through conformational changes in extracellular matrix proteins represents a versatile mechanism to elicit specific cellular responses for biological and biotechnological applications.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10069818&dopt=Abstract
Photochem Photobiol. 1999 Jan;69(1):41-6.
Alterations of hairless mouse skin exposed to chronic UV irradiation and its prevention by hydrocortisone.
Mitani H, Koshiishi I, Toyoda H, Toida T, Imanari T.
Sansho Seiyaku Co., Fukuoka, Japan.
Ultraviolet-induced alterations of skin were investigated in a murine animal model. Groups of hairless mice were exposed to UV (black light, lambda max 352 nm; UV distribution: 300-310 nm, 0.9%; 310-320 nm, 2.0%; 320-420 nm, 97.1%) for 20 weeks at a dose of 16.3 J/cm2 five times weekly on weekdays. At the end of 20 weeks irradiation, the dorsal skins were biochemically and histologically examined. Ultraviolet caused remarkable increases in amounts of hyaluronan, chondroitin sulfates and dermatan sulfates in skin (microgram/cm2). Interestingly, a significant change in a collagen content (hydroxyproline, microgram/g of dry powder) caused by UV irradiation was not observed, whereas the amount of collagen (hydroxyproline, microgram/cm2) increased remarkably. Histologically, no distinguishable thickening was observed in both upper dermis and lower dermis, but thickening of the epidermis was observed. Furthermore, the histological study indicated that UV irradiation caused a disappearance of crowds of adipocytes, alternative appearance of numerous fibroblasts and accumulation of collagen bundles and hyaluronan in lower dermis. Hydrocortisone, an anti-inflammatory agent, prevented both the fibrosis of lower dermis and the accumulation of the extracellular matrix components. Based on these results, it seems reasonable that UV penetrates into the lower dermis and causes fibrosis there, resulting from the inflammatory responses.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10063799&dopt=Abstract
J Biol Chem. 1999 Mar 12;274(11):7570-5.
Folding and assembly of type X collagen mutants that cause metaphyseal chondrodysplasia-type schmid. Evidence for co-assembly of the mutant and wild-type chains and binding to molecular chaperones.
McLaughlin SH, Conn SN, Bulleid NJ.
School of Biological Sciences, 2.205 Stopford Building, University of Manchester, Manchester, M13 9PT, United Kingdom.
Schmid metaphyseal chondrodysplasia results from mutations within the COOH-terminal globular domain (NC1) of type X collagen, a short chain collagen expressed in the hypertrophic region of the growth plate cartilage. Previous in vitro studies have proposed that mutations prevent the association of the NC1 domain of constituent chains of the trimer based upon a lack of formation of a trimeric structure that is resistant to dissociation with sodium dodecyl sulfate. To examine the effect of mutations on folding and assembly within a cellular context, bovine type X cDNAs containing analogous disease causing mutations Y598D, N617K, W651R, and wild-type were expressed in semi-permeabilized cells. We assessed trimerization of the mutant chains by their ability to form a collagen triple helix. Using this approach, we demonstrate that although there is an apparent lower efficiency of association of the mutant NC1 domains, they can drive the formation of correctly aligned triple helices with the same thermal stability as the wild-type collagen. When epitope-tagged mutant and wild-type collagen were co-expressed, heterotrimers could be detected by sequential immunoprecipitation. Both wild-type and mutant type X chains were found in association with the molecular chaperones protein disulfide isomerase and Hsp 47. The implications of these findings on the likely mechanism of Schmid metaphyseal chondrodysplasia will be discussed.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10066825&dopt=Abstract
Biochem Biophys Res Commun. 1999 Mar 5;256(1):114-20.
Signal transduction pathways mediated by glycoprotein Ia/IIa in human platelets: comparison with those of glycoprotein VI.
Inoue K, Ozaki Y, Satoh K, Wu Y, Yatomi Y, Shin Y, Morita T.
Department of Clinical and Laboratory Medicine, Yamanashi Medical University, Shimokato 1110 Tamaho, Yamanashi, Nakakoma, 409-3898, Japan.
Human platelets were activated either by glycoprotein (GP) Ia/IIa agonist (rhodocytin) or by a GPVI agonist (collagen-related peptide, CRP), and the intracellular signal transduction pathways were compared in the presence of various inhibitors. Rhodocytin isolated from Calloselasma rhodostoma venom was verified as a GPIa/IIa agonist, based on the inhibitory effects of three mAbs directed against GPIa. Platelet activation mediated by GPIa/IIa led to overt platelet aggregation, elevation of intracellular Ca2+, and tyrosine phosphorylation of several proteins, similar to that of GPVI. p72(syk) and phospholipase Cgamma2 (PLCgamma2) tyrosine phosphorylation were also observed with GPIa/IIa-mediated platelet aggregation, although they peaked slightly later than that of GPVI. In contrast to GPVI-mediated platelet activation, most of these phenomena induced by GPIa/IIa activation were markedly suppressed by acetylsalicylic acid (ASA) or cytochalasin D. These findings suggest that the requirements for thromboxane A2 (TXA2) production and actin polymerization, which are the characteristics of collagen-induced platelet activation, are derived from the GPIa/IIa-mediated signal transduction, but not from that of GPVI. 1999 Academic Press.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10066433&dopt=Abstract
J Cardiovasc Pharmacol. 1999 Mar;33(3):485-91.
Lacidipine prevents the hypertension and renal and cardiac changes induced by high-fructose diet in WKY rats.
Cosenzi A, Sacerdote A, Seculin P, Odoni G, Plazzotta N, Bernobich E, Bellini G.
Istituto di Medicina Clinica, University of Trieste, Italy.
Normotensive rats fed a high-fructose diet (HFD) develop hypertriglyceridemia, hyperinsulinemia, and hypertension. The glomerular changes observed in the kidneys of these animals are similar to those observed in diabetic rats. The aim of this study was to evaluate whether lacidipine, a calcium antagonist, could have a protective effect with this animal model. Forty male Wistar-Kyoto (WKY) rats were divided into four groups treated with HFD + placebo; HFD + lacidipine, 0.3 mg/kg/day; HFD + lacidipine, 3 mg/kg/day; or standard diet + placebo for 4 weeks. Urinary excretion of the stable metabolic products of nitric oxide (NO) was determined, because this vasoactive agent has been found to cause hemodynamic changes in the diabetic kidney. Glomerular size was determined by means of morphometric analysis. The results of this study show that lacidipine prevents (a) the HFD-induced increase in blood pressure in a dose-dependent manner; (b) the HFD-induced increase in glomerular size and fibronectin synthesis; and (c) the increase of collagen III synthesis in the heart. The drug had no effect on the increased urinary excretion of the stable metabolic products of NO. These data suggest that lacidipine might be useful in preventing the renal and cardiac damage caused by hypertension and non-insulin-dependent diabetes mellitus.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10069686&dopt=Abstract
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