Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of collagen types I, III, IV, and of fibronectin has been studied in the human dermis by light and electron-microscopic immunocytochemistry, using affinity purified primary antibodies and tetramethylrhodamine isothiocyanate-conjugated secondary antibodies. Type I collagen was present in all collagen fibers of both papillary and reticular dermis, but collagen fibrils, which could be resolved as discrete entities, were labeled with different intensity. Type III collagen codistributed with type I in the collagen fibers, besides being concentrated around blood vessels and skin appendages. Coexistence of type I and type III collagens in the collagen fibrils of the whole dermis was confirmed by ultrastructural double-labelling experiments using colloidal immunogold as a probe. Type IV collagen was detected in all basement membranes. Fibronectin was distributed in patches among collagen fibers and was associated with all basement membranes, while a weaker positive reaction was observed in collagen fibers. Ageing caused the thinning of collagen fibers, chiefly in the reticular dermis. The labeling pattern of both type I and III collagens did not change in skin samples from patients of up to 79 years of age, but immunoreactivity for type III collagen increased in comparison to younger skins. A loss of fibronectin, likely related to the decreased morphogenetic activity of tissues, was observed with age.
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PMID:Immunocytochemical localization of collagen types I, III, IV, and fibronectin in the human dermis. Modifications with ageing. 162 6

Amongst the uncommon forms of congenital severe colitis, we wish to draw attention to a peculiar and probably previously never described condition that we propose calling provisionally, epithelio-exfoliative colitis. This condition appears to be characterized by the following features: its early beginning within the first weeks of life; the smooth, glossy appearance of the mucosa, without ulcerations visible to the naked eye; the prevalent degenerative changes of the epithelial cells which become vacuolated, break away prematurely from the basement membrane and finally exfoliate within the glandular lumens; the distension and rupture of the glands, the mucous contents of which intrude into the lamina propria and induce a localized, mild and non suppurative inflammatory reaction; accessory reactive traits: intense mucus production actively regenerating epithelium (high mitotic activity, syncytial cells) and increase of the cholinergic fibers within the lamina propria. Although patchily distributed, these lesions involve the colon exclusively. The cause of epithelio-exfoliative colitis is unknown. However, the ultrastructural studies and immunocytochemical investigations using anti-collagen IV, antilaminin, anti-fibronectin antibodies disclose in some glands localized thinning and rupture of the basement membrane. These data suggest a primary disorder within the molecular arrangement of either the basement membrane itself or the proteins which anchor the glandular cells to the basement membrane.
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PMID:[Severe epithelio-exfoliative colitis in infants. Anatomical data]. 355 80

In this report, the authors describe a case of a 2-year, 11-month-old girl with glomerulonephritis and no family history of renal diseases and deafness. Immunofluorescent studies in the renal biopsy specimens with the use of anti-sera against human glomerular basement membrane (GBM) and P3 antigen (prepared from bovine GBM and inducible of Steblay's type nephritis in rats) demonstrated focal and segmental distribution of the GBM antigen(s). Electron microscopic examination revealed splitting and thinning of the GBM. Indirect immunofluorescence showed that there was no binding of Goodpasture's anti-GBM antibodies to the glomeruli. These findings are similar to those in patients with hereditary nephritis. The immunofluorescent examination of the fixation of the various anti-sera, including anti-types IV and V collagens, laminin, fibronectin, and actomyosin sera on the GBM, revealed normal reactivity. The abnormalities observed in this case may be a part of the spectrum of primary GBM defects.
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PMID:Glomerulonephritis with focal and segmental distribution of glomerular basement membrane antigen(s). 378 68

Striae distensae are characterized by a thinning of connective tissue stroma to produce linear, atrophic-appearing skin. Excessive adrenocortical activity, genetic factors and inherited defects of connective tissues, etc. are important causative factors in the formation of striae distensae, but the basic aetiology is not known. Total RNA was extracted from skin biopsies of five patients with striae distensae. The expression of genes coding for types I and III procollagen, elastin, fibronectin and beta-actin were studied and compared with those of four sex- and age-matched healthy individuals. The percentages of types I and III procollagen mRNA were 9.9 +/- 2.9% (mean +/- s.d.) and 10.6 +/- 1.6%, respectively, of the corresponding controls. The value for fibronectin mRNA in striae distensae was 7.3 +/- 1.8% of the control. The steady-state ratio fibronectin/type I procollagen mRNAs was 0.12 +/- 0.01 in striae distensae and 0.18 +/- 0.01 in the control. These observations suggest that expression of collagens, elastin and fibronectin genes are apparently decreased, and that there is a marked alteration of fibroblast metabolism, in striae distensae.
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PMID:Decreased expression of collagen and fibronectin genes in striae distensae tissue. 795 66

In order to analyse the incorporation pattern of synthetic prosthesis made of Teflon and Dacron in the arterial system, 21 prostheses removed surgically and seven prostheses obtained from autopsies were examined; the duration of the implantation periods ranged from 30 min up to 10 years. Essentially the early phase of prosthetic incorporation (phase I) includes exudative inflammatory reactions as part of acute inflammatory processes. The degree of order within the tissue architecture and the mutual influence of matrix and cells in the reaction appeared to be slight. The cellular infiltrate found on the outer prosthetic surface is of local origin whereas the inner prosthetic lining contains cells of haematogenous origin. The organisation phase (phase II), which is comparable to the reparative-proliferative phase of an inflammatory reaction, showed activation of the reticulo-endothelial system together with the start of phagocytosis and a thinning of the prosthetic structures. Collagen type I and type III and fibronectin served both as a guidance and a growth tract for the cells during the cellular permeation of the prosthesis. Fibronectin and collagen type III have a special "catalytic" function. Collagen type I causes the firm anchoring of the vascular prosthesis in the periprosthetic tissue. The loss of stability of the prosthesis due to phagocytosis of fibres is balanced by the newly formed connective tissue within the wall of the vessel. The fibroblasts involved in the organisation must be derived from the flowing blood and from local mesenchymal cells. A chronic inflammatory reaction persisted during the late phase. In some cases increased proliferation of the inner mesenchymal lining of the prosthesis was observed together with regressive changes. The lack of a continuous surrounding stromal architecture on the luminal side of the vessel can be regarded as the main reason for this proliferation. Transformation of haematogenous cells into angioblasts or endothelial cells was not seen. Small endothelialised areas were only seen in the vicinity of anastomoses and following transprosthetic permeation by capillaries.
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PMID:The pathology of vascular grafts. 816 12

A mouse model for the autosomal form of Alport syndrome was produced. These mice develop a progressive glomerulonephritis with microhematuria and proteinuria, consistent with the human disease. End-stage renal disease develops at approximately 14 weeks of age. TEM analysis of the glomerular basement membranes (GBM) during development of renal pathology revealed focal multilaminated thickening and thinning beginning in the external capillary loops at 4 weeks and spreading throughout the GBM by 8 weeks. By 14 weeks, half of the glomeruli were fibrotic with collapsed capillaries. Immunofluorescence analysis of the GBM showed the absence of type IV collagen alpha-3, alpha-4, and alpha-5 chains and a persistence of alpha-1 and alpha-2 chains (these chains normally localize to the mesangial matrix). Northern blot analysis using probes specific for the collagen chains illustrate the absence of COL4A3 in the knockout, whereas mRNAs for the remaining chains are unchanged. An accumulation of fibronectin, heparan sulfate proteoglycan, laminin-1, and entactin was observed in the GBM of the affected animals. The temporal and spatial pattern of accumulation was consistent with that for thickening of the GBM as observed by TEM. Thus, expression of these basement membrane-associated proteins may be involved in the progression of Alport renal disease pathogenesis. The levels of mRNAs encoding the basement membrane-associated proteins at 7 weeks were unchanged.
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PMID:Collagen COL4A3 knockout: a mouse model for autosomal Alport syndrome. 895 99

Lung epithelial and mesenchymal cells are separated by a basement membrane. At late fetal gestation, this basement membrane in fenestrated, allowing epithelial cytoplasmic extensions to reach in close proximity of the interstitial fibroblast. The enzymes responsible for this focal basement membrane remodelling, and their cellular origin, remains to be defined. Basement membrane remodelling generally involves a special class of matrix-degrading enzymes, called metalloproteinases. Herein, we report that fetal lung cells originating from both tissue layers, mesoderm and endoderm, express the metalloproteinase genes, MMP-1 or interstitial collagenase, and MMP-3 or stromelysin. The inhibitor of metalloproteinases, TIMP-1, is mainly expressed in fetal lung fibroblasts. During late fetal development, MMP-1 mRNA expression in both cell types increases close to term (day 21, term = 22 days), while that of stromelysin and TIMP-1 remain constant. Both fibroblasts and epithelial cells express fibronectin (FN) mRNA. The expression of the FN gene in epithelial cells decreases slightly at the canalicular stage of lung development (days 19-20), whereas FN expression in fibroblasts is not changed with advancing gestation. Procollagen alpha 1 (I) mRNA is predominantly detected in fibroblasts whereas message for laminin B1 chain is primarily found in epithelial cells. Expression of procollagen alpha 1 (I) mRNA decreases in fibroblasts during the canalicular stage of fetal lung development compared to the pseudoglandular stage (day 18) but increases thereafter at the saccular stage (day 21) of development. Laminin B1 expression in epithelial cells declines with advancing gestation. These data are consistent with a process of basement membrane thinning during the canalicular stage, followed by metalloproteinase-mediated penetration. Further, a progressive reduction in laminin expression is consistent with progressive epithelial differentiation.
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PMID:Ontogeny of extracellular matrix gene expression by rat lung cells at late fetal gestation. 948 4

A method for the wet extrusion of human plasma-derived fibronectin-fibrinogen cables is described. Solutions of fibronectin and fibrinogen with and without sodium alginate and carboxymethylcellulose (CMC) are tested. The rheological properties of the protein solutions changed from Newtonian to shear thinning non-Newtonian in the presence of small quantities of these additives, the apparent viscosity increased, and the extrusion properties of the protein solutions improved. Cables were prepared using a capillary with a diameter of 1 mm and overall length of 18 mm. Cable diameter was reduced to about 0.5 mm by drawing using a series of rollers. Cables prepared with sodium alginate were found to have suitable properties, and those made with CMC were sticky and difficult to handle. Solutions containing no sodium alginate required a minimum total protein concentration of about 70 mg/mL for extrusion. Extruded cables were prepared with solutions containing 140 mg/mL total protein with 12.9 mg/mL alginate (high protein), and 46 mg/mL total protein with 47.6 mg/mL of sodium alginate (high alginate). The mechanical strength of the extruded cables was within the range suitable for application in tissue engineering. Extrusion of the protein solutions into cables was achieved in a coagulation bath. Cables with a mechanical strength of approximately 30 N/mm(2), suitable for wound repair and nerve regeneration applications, were prepared with a coagulation bath containing 0.25 M HCl, 2% CaCl(2) at a pH of <0.9. These cables also had a large average elongation at break of 52%, and showed an increase in cable length after breakage (permanent set) of 20%, demonstrating the potential for drawing the cables down to a fine diameter.
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PMID:Wet extrusion of fibronectin-fibrinogen cables for application in tissue engineering. 1128 12

Fibronectin (FN) is reported to be important for early morphogenetic movements in a variety of vertebrate embryos, but the cellular basis for this requirement is unclear. We have used confocal and digital time-lapse microscopy to analyze cell behaviors in Xenopus gastrulae injected with monoclonal antibodies directed against the central cell-binding domain of fibronectin. Among the defects observed is a disruption of fibronectin matrix assembly, resulting in a failure of radial intercalation movements, which are required for blastocoel roof thinning and epiboly. We identified two phases of FN-dependent cellular rearrangements in the blastocoel roof. The first involves maintenance of early roof thinning in the animal cap, and the second is required for the initiation of radial intercalation movements in the marginal zone. A novel explant system was used to establish that radial intercalation in the blastocoel roof requires integrin-dependent contact of deep cells with fibronectin. Deep cell adhesion to fibronectin is sufficient to initiate intercalation behavior in cell layers some distance from the substrate. Expression of a dominant-negative beta1 integrin construct in embryos results in localized depletion of the fibronectin matrix and thickening of the blastocoel roof. Lack of fibronectin fibrils in vivo is correlated with blastocoel roof thickening and a loss of deep cell polarity. The integrin-dependent binding of deep cells to fibronectin is sufficient to drive membrane localization of Dishevelled-GFP, suggesting that a convergence of integrin and Wnt signaling pathways acts to regulate radial intercalation in Xenopus embryos.
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PMID:Regulation of cell polarity, radial intercalation and epiboly in Xenopus: novel roles for integrin and fibronectin. 1156 66

Previous experiments showed that transgenic mice expressing a secreted self-activating transforming growth factor (TGF) -beta1 did not show a phenotype in the lens and cornea until postnatal day 21, when anterior subcapsular cataracts, sporadic thickening of the corneal stroma, and thinning of the corneal epithelium were noted (Srinivasan et al., 1998). To examine the effects of higher concentrations of TGF-beta1 on the lens and cornea, we constructed transgenic mice harboring the strong, lens-specific chicken betaB1-crystallin promoter driving an activated porcine TGF-beta1 gene. In contrast to the earlier study, the transgenic mice had microphthalmic eyes with closed eyelids. Already at embryonic day (E) 13.5, the future cornea of the transgenic mice was threefold thicker than that of wild-type littermates due to increased proliferation of corneal stromal mesenchyme cells. Staining of fibronectin and thrombospondin-1 was increased in periocular mesenchyme. At E17.5, the thickened transgenic corneal stroma was vascularized and densely populated by abundant star-shaped, neural cell adhesion molecule-positive cells of mesenchymal appearance surrounded by irregular swirls of collagen and extracellular matrix. The corneal endothelium, anterior chamber, and stroma of iris/ciliary body did not develop, and the transgenic cornea was opaque. Fibronectin, perlecan, and thrombospondin-1 were elevated, whereas type VI collagen decreased in the transgenic corneal stroma. Stromal mesenchyme cells expressed alpha-smooth muscle actin as did lens epithelial cells and cells of the retinal pigmented epithelium. By E17.5, lens fiber cells underwent apoptotic cell death that was followed by apoptosis of the entire anterior lens epithelium between E18.5 and birth. Posteriorly, the vitreous humor was essentially absent; however, the retina appeared relatively normal. Thus, excess TGF-beta1, a mitogen for embryonic corneal mesenchyme, severely disrupts corneal and lens differentiation. Our findings profoundly contrast with the mild eye phenotype observed with presumably lower levels of ectopic TGF-beta and illustrate the complexity of TGF-beta utilization and the importance of dose when assessing the effects of this growth factor.
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PMID:Disruption of anterior segment development by TGF-beta1 overexpression in the eyes of transgenic mice. 1224 11


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