Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasmin can degrade fibronectin and laminin, two important components of the extracellular matrix facilitating cell sliding and healing following a wound. In this study we investigated the relationship between the tear fluid level of plasmin and plasminogen activator and the healing of a corneal wound. Anterior keratectomy (AKE) was performed for seven rabbits (11 eyes). Eight eyes were rewounded after re-epithelialization. Tear fluid samples were collected with capillaries before wounding and during wound healing. Plasmin and plasminogen activator (PA) activities were determined using radial caseinolysis procedures. After AKE the plasmin concentrations increased rapidly, from a mean (+/- SEM) of 3.9 +/- 0.9 micrograms/ml to a mean of 37.9 +/- 7.8 micrograms/ml (p less than 0.01), and decreased during wound healing. Rewounding also resulted in an increase in plasmin concentration in the tear fluid (from a mean of 2.9 +/- 0.6 micrograms/ml to a mean of 5.0 +/- 1.1 micrograms/ml; p greater than 0.05). The PA activity showed an inverse trend as it decreased after AKE from a mean of 2.0 +/- 0.6 IU/ml to a mean of 0.3 +/- 0.1 IU/ml (p less than 0.001). During wound healing and re-epithelialization, the PA activity increased again, to 2.1 +/- 0.3 IU/ml (p less than 0.001). Abrasion of the newly grown epithelium in eight eyes caused a second elevation of PA activity which was not significant. This study demonstrates a close association between the healing of corneal wounds and changes in the plasmin and PA activities in tear fluid. Determination of the activity of these enzymes may therefore be useful for monitoring corneal wound healing.
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PMID:Plasmin and plasminogen activator activities in tear fluid during corneal wound healing after anterior keratectomy. 253 68

Some endothelial-injury syndromes, including atherosclerosis, may involve herpes simplex virus (HSV) infection. Examining the mechanism of injury, we found adherence of unstimulated granulocytes to HSV infected endothelium to be twice that to uninfected endothelium (34.8 +/- 1.1 versus 18.8 +/- 0.5%; mean +/- SEM; p less than 0.001) which further increased in the presence of anti-HSV antibodies. Enhanced adhesion was accompanied by excessive granulocyte-mediated lysis of 51Cr-labeled, HSV-infected endothelium (16.4 +/- 0.9%, HSV-infected versus 0.9 +/- 4.5% for uninfected endothelium; p less than 0.01). HSV infection also increased granulocyte-mediated endothelial cell detachment from its substratum (14.7 +/- 1.7% versus 3.3 +/- 0.3% for uninfected endothelium; p less than 0.001), which further increased (p less than 0.01) in the presence of immune complexes (IgG-sensitized erythrocytes). This suggests that neo-Fc receptors of infected endothelium bind IgG-coated particles, which, in turn, attract and stimulate granulocytes. In support, granulocyte-mediated detachment was not enhanced by immune complexes if endothelium was infected with a mutant HSV strain (E3/3) that does not produce glycoprotein E, the viral glycoprotein having Fc-receptor activity. Exaggerated endothelial detachment correlated with poor binding of infected endothelial cells to the substratum matrix protein, fibronectin. Resuspended, virus-infected endothelial cells bound significantly less well to tissue-culture wells coated with both low (p less than 0.001) and high (p less than 0.05) concentrations of fibronectin as compared with uninfected endothelial cells, a dichotomy further worsened in the presence of granulocyte-released elastase. We conclude that HSV-infected human endothelium is vulnerable to granulocyte-mediated injury by opposing alterations in its adhesive properties: its increased binding of granulocytes and its weakened tethering to matrix fibronectin, particularly when exposed to secreted granulocyte proteases, such as elastase.
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PMID:Granulocyte-mediated injury to herpes simplex virus-infected human endothelium. 253 63

Changes of (Na+-K+)-ATPase activity, cAMP and fibronectin (FN) content and cell surface microvilli were studied cytochemically, immunocytochemically and scanning electron microscopically on human stomach Glandular carcinoma (SGC-7901) cells treated with NaBT(2.5 mM). It was found that NaBT not only inhibited cell growth but also remarkably decreased the activity of cell surface (Na+-K+)-ATPase of SGC-7901 cells. Note worthy was that, in comparison with the untreated tumor cells, the increase of the intensity of intracellular cAMP and FN immunofluorescence in NaBT-treated tumor cells was striking. Moreover, in contrast to untreated tumor cells, the cell surface of NaBT-treated tumor cells showed more smooth and fewer microvilli under SEM. That NaBT may induce differentiation of SGC-7901 cells through inhibition of (Na+-K+)-ATPase activity and modulation of cellular cAMP and FN content was discussed.
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PMID:[The biological effect of sodium butyrate (NaBT) on SGC-7901 cells]. 255 15

Plasma concentrations of fibronectin, alpha 2-macroglobulin and orosomucoid were monitored immunochemically in 20 patients before, during and after surgery. At 2 h after the induction of anaesthesia fibronectin concentrations were lowered 31 +/- 6% (SEM) compared to values obtained 1-3 d preoperatively. However, the fibronectin concentration decreased 17 +/- 5% (SEM) compared to preoperative values at the beginning of surgery. Most of the decline was thus not caused by the operative trauma. The perioperative changes in fibronectin concentrations did not differ from those found in alpha 2-macroglobulin and, up to 2 h postoperatively, orosomucoid.
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PMID:Plasma fibronectin in relation to surgical trauma. 257 16

Approximately 1 out of every 10 eyes undergoing surgery for retinal detachment develops excessive intraocular fibrosis that can lead to traction retinal detachment and ultimate blindness. This disease process has been termed proliferative vitreoretinopathy (PVR). The ability to monitor and grade this fibrotic response accurately within the eye as well as the ability to aspirate vitreous cavity fluid bathing the fibrotic tissue makes this an ideal setting in which to investigate the development of fibrosis. Although laboratory studies have recently shown that transforming growth factor-beta (TGF-beta) can enhance fibrosis, little clinical evidence is yet available correlating the level of this or other growth factors with the degree of fibrosis in a clinical setting. We have found that vitreous aspirates from eyes with intraocular fibrosis associated with PVR have more than three times the amount of TGF-beta (1,200 +/- 300 pM [SEM]) found in eyes with uncomplicated retinal detachments without intraocular fibrosis (360 +/- 91 pM [SEM]). Using an in vitro assay, 84-100% of the TGF-beta activity could be blocked with specific antibodies against TGF-beta 2, whereas only 10-21% could be blocked by specific antibodies against TGF-beta 1. TGF-beta 1 was used in an animal model of traction retinal detachment. Since beta 1 and beta 2 have essentially identical biologic effects and only human beta 1 was available in quantities required, beta 1 was chosen for these in vivo studies. The injection of TGF-beta1 plus fibronectin (FN) but not TGF-beta1 alone into the vitreous cavity of rabbits resulted in the increased formation of intraocular fibrosis and traction retinal detachments as compared to control eyes. In previous studies, intravitreal FN levels were also found to be elevated in eyes with intraocular fibrosis.
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PMID:Correlation of fibrosis and transforming growth factor-beta type 2 levels in the eye. 270 27

We studied the phagocytosis of agarose beads by human alveolar macrophages in terms of the morphology, the receptors involved, and the cellular substrates (plastic or fibronectin) used. Beads coated with C3b (58%) and iC3b (42%) by treatment with serum, were ingested during 45 min by CR1 and CR3 on the macrophages. This ingestion was inhibited 80-90% by the presence of polyclonal F(ab')2 anti-C3 fragments. Since the phagocytosis of both C3b- and iC3b-coated beads was about threefold stronger than for C3b-coated beads (trypsinized serum-treated beads), the results indicate that the CR3 is more phagocytic than the CR1. The phagocytosis of initially complement uncoated beads, which are slowly opsonized with macrophage-produced C3b and iC3b in vitro, was also strongly inhibited (70-80%) by the presence of anti-human C3 F(ab')2 fragments. There was an increased phagocytosis (10-17%) of complement precoated beads by macrophages cultured on the fibronectin substrate versus the plastic substrate. The morphology and rapid phagocytosis of the complement precoated beads was demonstrated by SEM. The general impression was that membranous protrusions stretched towards the beads, which became increasingly enclosed by plasma membrane.
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PMID:Phagocytosis of agarose beads by receptors for C3b (CR1) and iC3b (CR3) on human alveolar macrophages cultured on fibronectin in vitro. A scanning electron microscopic study. 294 72

Previous investigations have shown that animals maintained with enteral nutrition are better able to survive an intraperitoneal bacterial challenge than animals receiving parenteral nutrition. The aim of this study was to assess the effects of enteral and parenteral nutrition on reticuloendothelial function. Eighteen enteral-fed male Sprague-Dawley rats had access to a standard hyperalimentation solution via a sipper tube ad libitum. Seventeen parenteral-fed animals received the same solution at an infusion rate determined by the volume ingested by the pair-fed enteral animals. All animals had central venous catheters. After 12 days, reticuloendothelial function was assessed by measuring the clearance rate (K) and the organ distribution of intravenous 51Cr-labeled sheep red blood cells and by plasma fibronectin levels. Nutritional status was assessed by body weight and nitrogen balance. K values in enteral and parenteral animals were similar (0.110 +/- 0.011 and 0.140 +/- 0.012, respectively, mean +/- SEM) as were plasma fibronectin levels (196 +/- 22 and 228 +/- 15 micrograms, respectively). Organ distribution of the 51Cr-labeled sheep red blood cells was the same in both groups. Nitrogen balance and body weights were also similar in both groups. These data demonstrate that in this experimental model enteral nutrition and parenteral nutrition were equally effective at maintaining reticuloendothelial function and nutritional status.
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PMID:Effects of enteral vs parenteral nutrition on reticuloendothelial function. 310 83

Hepatocytes were isolated by application of the two-step collagenase perfusion technique to pieces of human liver. Hepatocytes were cultivated in serum-free medium or 10% fetal calf serum medium supplemented with insulin, glucagon and dexamethasone. The cells were kept in culture for up to 16 days and 75% of the medium was regularly changed. Fibronectin in culture medium was detected by means of an ELISA with an assay range of 2.2-560 micrograms/l. The interassay imprecision was 6.3% at 500 micrograms/l and 14.3% at 10 micrograms/l. Significant amounts of fibronectin were detected in all cultures. During culture, fibronectin accumulated in the medium and the quantity secreted by hepatocytes by far exceeded the amounts of fibronectin associated with hepatocytes prior to cultivation. Maximum secretion rate by 10(6) hepatocytes was 167.5 +/- 73.3 ng fibronectin (mean +/- SEM, n = 3) in 24 h. When analysed by means of SDS-PAGE and immunoblotting the fibronectin isolated from hepatocyte culture medium and cell lysate co-migrated with fibronectin obtained from plasma. Our data show, for the first time, that human hepatocytes synthesize and secrete fibronectin, and it is suggested that the human liver is an important source of plasma fibronectin.
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PMID:Human hepatocytes in culture synthesize and secrete fibronectin. 320 Nov 2

Sclerosing or morphea-like variant of basal cell carcinoma (BCC) is characterized by an extensive connective tissue stroma, and histopathology has suggested that the extracellular matrix is largely composed of collagen. In addition, fibronectin deposition has been proposed to modulate tumor growth in BCC. In this study, we examined the expression of genes coding for type I, III, and IV procollagens, as well as for fibronectin, in tissue from 10 patients with sclerosing BCC. For comparison, tissues from 5 patients with nodular BCC and 4 controls were examined. Total RNA was isolated by CsCl density gradient centrifugation, and messenger RNA (mRNA) steady-state levels were determined by slot-blot hybridizations with human sequence specific complementary DNAs (cDNAs). The abundance of type I procollagen mRNA in sclerosing BCC tissue was increased to 233.6 +/- 36.7% of the controls (mean +/- SEM). The corresponding value for type III procollagen mRNA in sclerosing BCC was 281.8 +/- 54.8% of the controls. Consequently, the steady-state ratio of type I/III procollagen mRNAs in sclerosing BCCs (5.0 +/- 1.2; mean +/- SD) was within the control range. Thus, there is a coordinate increase in type I and type III procollagen mRNA levels in sclerosing BCC. In contrast, the values for type I and type III procollagen mRNAs in nodular BCC were not different from the controls. In addition, type IV procollagen and fibronectin mRNA levels were not different from the controls either in sclerosing or nodular BCCs, attesting to the selectivity of the increase in type I and III procollagen mRNA levels in sclerosing BCC. These observations may relate to the excessive deposition of the extracellular matrix stroma surrounding the tumor cells in sclerosing BCC.
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PMID:Selectively enhanced procollagen gene expression in sclerosing (morphea-like) basal cell carcinoma as reflected by elevated pro alpha 1(I) and pro alpha 1(III) procollagen messenger RNA steady-state levels. 336 Nov 39

Numerous investigations have demonstrated that basement membranes (BMs) are composed of type IV collagen, laminin, heparan sulfate proteoglycan, nidogen, and possibly fibronectin. The precise proportion and supramolecular organization of these molecules within BMs is unclear, but is believed to be tissue-specific. In an effort to provide morphological evidence for BM specificity, we studied isolated bovine retinal capillary BMs by high-resolution SEM. Cryofractured specimens demonstrated that surfaces of BM leaflets and pericytic matrix (PCM) within the retinal capillary BM complex are composed of 20- to 100-nm granules and beaded fibrils arranged in patterns which are specific for each cell type. Subendothelial BMs and the subjacent PCM are composed of 20- to 30-nm granules loosely arranged and marked by numerous pits, features that are consistent with their TEM morphology and known susceptibility to proteolytic attack. These BMs also frequently exhibit large openings or fenestrations. These compare favorably with their fragmented image by TEM and probably represent BM discontinuities necessary for direct contact of pericytes and endothelial cells. Muller cell BMs are also composed of granules though they are much larger (40-100 nm) and more densely packed then those of subendothelial BMs. Moreover, they frequently contain interstitial collagen fibrils which could account for the tube-like structural rigidity exhibited by acellular retinal vessel BMs in SEM views. Data in the current study provide morphological evidence for direct contact of pericytes and endothelial cells in vivo and support the view that tissue specificity of BMs may be more exquisite than previously believed, extending even to surface topography of BM leaflets within capillary BM complexes.
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PMID:Topographical specificity in isolated retinal capillary basement membranes: a high-resolution scanning electron microscope analysis. 336 94


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