Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

We investigated a possible role for fibronectin (Fn) in natural killer (NK) cell activity against K562 tumor cells. Plastic plates that had been incubated with Fn at 60 micrograms/ml bound 49.6% +/- 12.8% (mean +/- SEM) of K562 cells; plates coated with three other proteins bound essentially no tumor cells (P less than 0.01). In similar experiments, 12.6% +/- 4.7% of nonadherent lymphocytes bound to plates that had been coated with 60 micrograms/ml Fn; plates coated with other proteins bound less than or equal to 10% of these cells. Lymphocytes that bound to Fn-coated plates appeared to be slightly enriched for NK cells as assessed by morphology and by cytotoxic activity. Despite these findings, neither NK cytotoxic activity nor binding to K562 targets was affected by the addition of any of three anti-Fn antibody preparations, nor by the addition of exogenous Fn at concentrations found in plasma (300 micrograms/ml). Although Fn appears to bind both to K562 targets and to lymphocyte preparations that contain NK cells, it does not appear to have a functional role in mediating NK cell activity against K562 tumor cells.
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PMID:Fibronectin and cellular cytotoxicity: evidence against a role for fibronectin in natural killer activity. 359 39

Indirect immunofluorescent staining with anti-tubulin antibodies, SEM and TEM were applied to study microtubule (MT) assembly in clones isolated from Friend leukemia cells (FLC, 745 A strain) on the basis of their sensitivity to exogenous fibronectin (FN). Kinetics of cell spreading and elongation were studied using computerized image analysis and SEM. In contrast to 745 A cells, FN-sensitive clones (referred to as FF clones) showed elaborate MT networks when observed by immunofluorescent staining as well as by TEM. A good correlation was found between the degree of spreading and elongation of FF cells and the degree and cellular distribution of their MT. The highest concentration of MT networks oriented parallel to the main cellular axis was observed in very elongated FF cells. The majority of MT in interphase FF cells radiated from the centrosomes; some MT apparently originated from the nuclear membranes. TEM showed the existence of morphological differences between centrosomes of 745 A and FF cells. The characteristic ultrastructure of the centrosomes of FF cells was maintained in trypsinized cells, even if such FF cells lost MT's and acquired a spherical morphology. FF cells, treated with a wide spectrum of MT-disrupting agents, promptly acquired a rounded morphology with rapid dissolution of polymerized tubulin. Removal of MT-disrupting agents from the culture medium rapidly restored a flattened morphology with concurrent regeneration of MT's. During recovery from MT-disrupting agents, FF cells showed increased numbers of centrosomes per cell. We conclude that MT networks cooperate in the attachment, spreading and elongation of FF cells isolated from FLC. Moreover, we hypothesize the existence in FF cells of a variant form of centrosomes as compared with those of 745 A cells.
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PMID:Induction and maintenance of flattened morphology in highly adhesive Friend leukemia clones depends on the time- and space-specific assembly of microtubular networks. 390 71

Several studies have focused on retinal pigment epithelial (RPE) cell proliferation as an important event in proliferative vitreoretinopathy (PVR). Little attention has been given to the question of how RPE cells gain access to the vitreous cavity where proliferation occurs. We have recently demonstrated that the serum components fibronectin and platelet-derived growth factor stimulate and direct RPE migration in vitro. In this study, we used this same in vitro technique to examine vitreous aspirates from 13 eyes with PVR, five eyes with macular puckers, and three eyes with uncomplicated retinal detachments for their ability to stimulate RPE migration. We found that aspirates from eyes with PVR stimulated RPE migration to a much greater extent than aspirates from eyes with macular pucker and uncomplicated retinal detachments. The ability to stimulate RPE cell migration correlated with high levels (mean +/- SEM, 178 +/- 67 mg/L) of immunoreactive fibronectin.
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PMID:Vitreous aspirates from patients with proliferative vitreoretinopathy stimulate retinal pigment epithelial cell migration. 403 35

In this report we characterize the response of the plasma protein fibronectin to hemorrhagic shock and starvation, conditions associated with decreased function of mononuclear phagocyte system (MPS). Rats were starved for 3 days, then half of the animals were subjected to fixed-volume hemorrhagic shock by removing an estimated 35% of their blood volumes for 20 min. After volume replacement, animals were injected iv with [14C]valine. At time points up to 10 hr after hemorrhage, plasma fibronectin concentrations and fibronectin synthesis were quantitated. In additional rats treated identically, fibronectin clearance was assessed by measuring the disappearance of 125I-fibronectin from the plasma. When compared to control animals, either starvation or hemorrhagic shock produced similar perturbations in plasma fibronectin metabolism; fibronectin concentrations were reduced from 241.3 +/- 34.6 micrograms/ml (mean +/- SEM) (controls) to 123 +/- 32.6 micrograms/ml (starvation) or 150.0 +/- 13.0 micrograms/ml (hemorrhage). Plasma [14C]fibronectin specific radioactivities, indicative of fibronectin synthesis, were also significantly reduced. Hemorrhagic shock in rats that previously had been starved did not depress fibronectin concentrations or synthesis to a greater extent than starvation alone. The rates of 125I-fibronectin clearance were increased in starvation and hemorrhagic shock (t1/2 = 233.0 +/- 13.0 min, controls; 174.6 +/- 10.7 min, starvation; 167.4 +/- 13.6 min, hemorrhage). In contrast to changes observed in fibronectin metabolism, total plasma protein concentrations were not significantly altered in any experimental groups. Furthermore, total plasma protein synthesis increased in rats subjected to either starvation or hemorrhagic shock, but decreased in starved rats that were subsequently shocked.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma fibronectin metabolism during hemorrhagic shock and starvation. 405 5

Blood mononuclear cells from patients with rheumatoid arthritis produce the lymphokine, leukocyte inhibitory factor (LIF) in response to collagens in vitro, and blood monocytes release prostaglandins (PGE2) and a factor, mononuclear cell factor (MCF) which stimulates collagenase and PGE2 production by cultured synovial cells. We therefore examined the effect of collagens on the production of PGE2 and MCF. Blood mononuclear cells from 6 patients with rheumatoid arthritis and 6 normal subjects were cultured in native human types I, II, or III collagen-coated tubes, or with streptokinase-streptodornase (SK-SD), and the supernatant media derived from these cultures analyzed for the presence of MCF, PGE2, and LIF. Types II and III collagens, as well as SK-SD, markedly stimulated MCF production by the cells from all 12 subjects (MCF activity, expressed as a mean stimulation index (SI) +/- SEM, was 43 +/- 12 for type II, 33 +/- 7 for type III, and 37 +/- 23 for SK-SD). Type I collagen was less stimulatory (mean SI 10 +/- 7). Cells from the patients with rheumatoid arthritis, but not the normal subjects, produced LIF in response to types II or III collagens but not to type I collagen. PGE2 production by blood mononuclear cells paralleled that of MCF, although abrogation of PGE2 release with indomethacin did not reduce MCF production. alpha chains purified from denatured collagens also stimulated MCF production. Using cells from patients with rheumatoid arthritis, type II collagen stimulated production of all three factors in the presence of polymyxin B or fibronectin-depleted serum, suggesting, respectively, that neither endotoxin nor fibronectin were responsible for their generation. Monocytes, purified from normal blood by an adherence technique, but not lymphocytes depleted of monocytes, released MCF and PGE2 when cultured with type II collagen. These results demonstrate that collagens can act as ligands to stimulate monocytes, as well as antigens to stimulate sensitized lymphocytes, to produce soluble factors that may contribute to the destruction of connective tissue.
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PMID:Collagens act as ligands to stimulate human monocytes to produce mononuclear cell factor (MCF) and prostaglandins (PGE2). 630 48

We have measured plasma von Willebrand factor (VWF) as the factor VIII-related antigen, plasma fibronectin, and two of the serum somatomedins, insulin-like growth factor I (IGF I) and IGF II, in 51 diabetic patients and 25 nondiabetic control subjects. VWF was significantly higher in the diabetic group than in the controls (173 +/- 9% SEM versus 101 +/- 9%, P less than 0.001), as has been reported by others. However, within the diabetic group there was no significant difference in VWF between those patients without retinopathy, those with background or proliferative retinopathy, or those with macular edema. There was also no difference in VWF between the diabetic subjects with and those without proteinuria. These results rule against a previously advanced hypothesis that the increase in VWF in patients with diabetes is secondary to microangiopathy. No significant difference was observed in fibronectin, IGF I, or IGF II between the diabetic and control groups, between the diabetic group without retinopathy and the retinopathic subgroups, and between the diabetic subjects with and without proteinuria. In the diabetic patients, there was no correlation between diabetic control as assessed by glycosylated hemoglobin and glycosylated serum protein, and the plasma levels of VWF, fibronectin, IGF I, or IGF II. The results of this study strongly suggest that neither plasma VWF, fibronectin, IGF I, nor IGF II plays an important primary role in the pathogenesis of diabetic microvascular disease, although one or more of these factors might play a permissive role.
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PMID:Von Willebrand factor (VIII R:Ag), fibronectin, and insulin-like growth factors I and II in diabetic retinopathy and nephropathy. 636 66

The relative contributions of glomerular epithelial cells, macrophages, and other cell types to the formation of cellular crescents characteristic of human rapidly progressive glomerulonephritis remain controversial. To identify and quantitate the cell types present during different stages of glomerular crescent formation, immunoperoxidase labelling of cryostat sections from renal biopsies with cellular (n = 9) or sclerosed (n = 3) crescents was performed using monoclonal antibodies to cell-specific antigens of leucocytes, epithelial cells, and other glomerular cell types. Fresh cellular crescents consisted of macrophages (34.5 +/- 7.0%; mean +/- SEM) plus lesser proportions of polymorphs (12.8 +/- 4.7%) and epithelial cells (10.4 +/- 1.5%). Sclerosed crescents contained fewer macrophages (5.1 +/- 1.0%), but similar proportions of polymorphs (11.1 +/- 2.9%) and epithelial cells (11.5 +/- 2.1%). Lymphocytes were not detected within crescents. Many of the remaining unlabelled cells morphologically resembled fibroblasts and expressed surface fibronectin, though fibroblast-specific cell markers were not available. These results show that macrophages and not epithelial cells constitute the major cell type within cellular crescents. Therapeutic manoeuvres directed against macrophages may, therefore, be of clinical value in the management of human crescentic rapidly progressive glomerulonephritis.
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PMID:Cellular composition of crescents in human rapidly progressive glomerulonephritis identified using monoclonal antibodies. 637 97

Plasma fibronectin and serum thyroid parameters were determined in 6 hyperglycemic nonketoacidotic patients (HNK) and 12 subjects with diabetic ketoacidosis (DKA). The DKA patients showed a marked increase in both plasma fibronectin and serum T3 over 5 days of insulin treatment [175.2 +/- 18.1% (+/- SEM) and 208.7 +/- 17.6% of initial values respectively], while these parameters did not change in the HNK patients despite equivalent control of diabetes. Serum rT3 levels declined, as expected, to 65.8 +/- 10.9% of the initial values in the DKA patients, but did not change in the HNK patients. There was a significant positive correlation between changes in plasma fibronectin and serum T3 values in the DKA patients (r = 0.5; P less than 0.005). Other reports have shown a decrease in plasma fibronectin concentrations in fasted patients, a well known low T3 state; therefore, the association between changes in plasma fibronectin and serum T3 values may be a widely observed phenomenon. The parallel changes in fibronectin and T3 may reflect alterations in the metabolic state of these patients. The precise nature of the relationship between changes in fibronectin and T3 concentrations requires additional investigations.
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PMID:Rapid increase in both plasma fibronectin and serum triiodothyromine associated with treatment of diabetic ketoacidosis. 640 48

Fibronectin has been localized to basement membranes and cell surfaces with the light microscope by fluorescent staining of thick sections, and with the TEM by immunoperoxidase reaction. However, these methods are limited because it is difficult to appreciate the patterned distribution of fibronectin from sectioned material. We have developed a probe for fibronectin that facilitates its identification with the SEM. Our probe consists of two parts; the first component is a derivatized methacrylate microsphere 90 nm in diameter, linked to purified sheep anti-rabbit IgG. The second component is anti-fibronectin IgG raised in rabbits. Stage-3 to -12 chick embryos were fixed and the ectoderm covering the cranial mesoderm was removed. Embryos were treated with testicular hyaluronidase, exposed to rabbit anti-fibronectin IgG and finally to sheep anti-rabbit IgG conjugated microspheres. As expected, the basal lamina of surface and neural ectoderm as well as the remaining fibrous ECM were heavily decorated with microspheres, whereas control embryos treated with preimmune serum were beadless. Fibronectin was localized on the cell soma and processes of primary mesenchyme as early as stage 3. In addition, it was possible to decorate to various extents, populations of prosencephalic, mesencephalic, and rhombencephalic cranial neural crest cells. Our studies suggest that fibronectin is present in the cranium of chick embryos at earlier times than heretofore realized, and that fibronectin accumulates in a cranial to caudal gradient that reflects the sequential differentiation of the embryonic axis.
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PMID:SEM localization of cell-surface-associated fibronectin in the cranium of chick embryos utilizing immunolatex microspheres. 674 25

Addition of 12-tetradecanoylphorbol 13-acetate (TPA) to cultures of intact Swiss mouse 3T3 fibroblasts induced a dose-dependent increase in ornithine decarboxylase (OrnDCase) activity. Over the same concentration range, 10(-9) to 10(-6) M, TPA induced the release of radioactively labeled fibronectin (FN) from the cells into the culture medium. Retinoic acid, a derivative of vitamin A, inhibited in a dose-dependent manner both the increase in OrnDCase activity and the release of FN induced by TPA. To examine the effects of TPA and retinoic acid in enucleated cells, the cells were treated with 7.5 micrograms of cytochalasin B per ml of medium during centrifugation at 10,000 X g for 35 min at 37 degrees C. In a series of five experiments, the treated cells were 94.7 +/- 4.8% (+/- SEM) enucleated as measured by [3H]thymidine incorporation and verified by Giesma staining for nuclei. In the enucleated cells, TPA did not induce increased OrnDCase activity but did induce FN release in a dose-dependent fashion over the same concentration range effective for FN release from intact cells. Moreover, addition of retinoic acid to the enucleated cells inhibited the phorbol ester-induced release of FN in a dose-dependent manner. A series of phorbol ester derivatives showed the same order of activity in causing FN release from the enucleated cells as reported for inducing OrnDcase activity in intact cells or in promoting mouse skin tumors in vivo. Similarly, several retinoids were tested for their ability to inhibit the phorbol ester-induced release of FN from enucleated cells. The efficacy of the retinoids in preventing FN release paralleled their activity in inhibiting phorbol ester-induced OrnDCase activity and skin tumor promotion, as reported in the literature. We conclude that at least one aspect of tumor promotion induced by phorbol esters--the loss of FN--does not require the cell nucleus, and further, that retinoids can inhibit this aspect of tumor promotion without nuclear involvement.
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PMID:Retinoids and phorbol esters alter release of fibronectin from enucleated cells. 695 35


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