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At least 1,207 records · Page 67Linked to original sources
PubMed1995

Synthesis of stromal glycosaminoglycans in response to injury.

Our goal is to examine the synthesis and deposition of corneal glycosaminoglycans (GAGs) in response to a wound created by the insertion of porous discs into stromal interlamellar pockets. The disc and the surrounding stromal tissue were assayed and compared to contralateral control stroma and to sham operated corneas at 14, 42, and 84 days. The tissue and/or discs were removed and labeled with 35S-sulfate for 18 h; GAGs were extracted with 4 M guanidine-HCl. Extracts were chromatographed on Q-Sepharose columns, bound proteoglycans were eluted with a linear salt gradient, and radioactive fractions were analyzed. Total GAG content was determined colorimetrically, using dimethylmethylene blue. Specific GAGs were determined using enzymatic digestion with selective polysaccharide lyases and protein cores were examined using SDS-PAGE. The nonbound fractions from the chromatography were assayed for TGF-beta using Western blot analysis and for hyaluronic acid using an 125I-radiometric assay. Specific GAGs were localized 42 days after the disc had been implanted in the stroma. The placement of the discs into the stroma resulted in a decrease in the total amount of GAG. However, the ratio of dermatan-chondroitin sulfate and heparan sulfate to keratan sulfate increased in the surrounding tissue and disc. Hyaluronic acid was elevated at day 14 in the surrounding tissue, and not until day 84 in the disc. Western blot analysis of surrounding tissue extracts revealed forms of TGF-beta that migrated with an apparent molecular mass of 63 and 43 kDa. The results indicate that the insertion of discs into interlamellar pockets causes changes in the sulfation and proportion of the glycosaminoglycans in the surrounding tissue and the disc. These changes are coincident with the appearance of TGF-beta. After 84 days, the population of glycosaminoglycans in the disc begins to resemble the surrounding stroma. This model will allow us to examine further the synthesis and deposition of proteins following an extensive wound in which cells must migrate to the wound site and then undergo extensive remodeling.

Animals↗
PubMed2000

Memory of past exposure to the chemokine IL-8 inhibits the contraction of fibroblast-populated collagen lattices.

The inflammatory cytokine makeup of healing wounds helps delineate the phases of the repair process. As an example, during the lag phase (inflammatory phase) of repair, elevated levels of IL-8, a chemokine, participate in the activation and chemotaxis of neutrophils. During the normal proliferative and remodeling phases of repair, IL-8 levels are minimal. Healing burn wounds often have small, open, slow-to-heal areas, which have been shown to contain elevated levels of IL-8. Does a limited exposure of IL-8 to fibroblasts in vitro at the concentrations measured in these unhealed sites cause altered cell behavior? To study this possibility the fibroblast-populated collagen lattice (FPCL) model, an in vitro model of wound contraction, was used to investigate fibroblast response to IL-8. As previously reported, the chronic exposure of fibroblasts to IL-8 at 30 ng/ml within FPCLs significantly inhibited FPCL contraction. Fibroblasts in monolayer culture were incubated with IL-8 for 3 days. In the absence of IL-8, FPCLs were manufactured with these preexposed cells and it was found that FPCL contraction was inhibited. Fibroblasts retained their reduced capacity of reorganizing collagen fibrils when previously exposed to IL-8. Treating fibroblasts in monolayer with IL-8 for only 1 h prior to their incorporation into collagen lattices caused inhibition of FPCL contraction. The speculation is that in vivo open areas in reepithelialized healed burns are the consequence of the local population of fibroblasts having been exposed to elevated levels of IL-8. Such an earlier exposure triggers a memory in this population of fibroblasts that alters their capacity to lay down an extracellular matrix that optimizes the migration of epidermal cells.

Cells, Cultured↗
PubMed1996

Proliferation and motility responses of primary and recurrent gliomas related to changes in epidermal growth factor receptor expression.

Astrocytic neoplasms show a high incidence of elevated or mutated epidermal growth factor receptor (EGFR) expression. Although proliferative effects from EGFR activation are well described, the role that changes in this receptor play in glioma growth and migration remain poorly addressed. This report characterizes changes in the levels of EGFR expression in three glial tumors at initial presentation (resection) and at the time of recurrence. By quantitative flow cytometry the mean level of EGFR expression increased, decreased, or remained the same in different recurrent astrocytomas relative to their primary tumor cells. Immunocytochemistry for EGFR on monolayer cells corroborated the level of expression in the recurrent tumors relative to their matched primary specimen. Immunoprecipitation indicated that 170 kd EGFR was expressed in each of the tumors, and showed normal down regulation following treatment with EGF. Proliferation response to EGF was seen in only 1/6 instances, but was concentration-dependent when observed. Stimulated migration of the cells was frequently seen and was also concentration-dependent on EGF; the magnitude of response was related to the relative level of 170 kd EGFR expression in the cells. EGFR immunostaining of tissue sections from the tumors confirmed the levels of EGFR expressed in primary and recurrent astrocytomas as was seen in the cultured cells. These results indicate that the relative levels of EGFR in early passage cell cultures from glioma specimens concurs with the measured tissue levels of expression. Human glioma cells are more responsive to migration induction than proliferation induction by EGF.

Cell Division↗
PubMed2006

A crucial function of PDGF in TGF-beta-mediated cancer progression of hepatocytes.

Polarized hepatocytes expressing hyperactive Ha-Ras adopt an invasive and metastatic phenotype in cooperation with transforming growth factor (TGF)-beta. This dramatic increase in malignancy is displayed by an epithelial to mesenchymal transition (EMT), which mimics the TGF-beta-mediated progression of human hepatocellular carcinomas. In culture, hepatocellular EMT occurs highly synchronously, facilitating the analysis of molecular events underlying the various stages of this process. Here, we show that in response to TGF-beta, phosphorylated Smads rapidly translocated into the nucleus and activated transcription of target genes such as E-cadherin repressors of the Snail superfamily, causing loss of cell adhesion. Within the TGF-beta superfamily of cytokines, TGF-beta1, -beta2 and -beta3 were specific for the induction of hepatocellular EMT. Expression profiling of EMT kinetics revealed 78 up- and 235 downregulated genes, which preferentially modulate metabolic activities, extracellular matrix composition, transcriptional activities and cell survival. Independent of the genetic background, platelet-derived growth factor (PDGF)-A ligand and both PDGF receptor subunits were highly elevated, together with autocrine secretion of bioactive PDGF. Interference with PDGF signalling by employing hepatocytes expressing the dominant-negative PDGF-alpha receptor revealed decreased TGF-beta-induced migration in vitro and efficient suppression of tumour growth in vivo. In conclusion, these results provide evidence for a crucial role of PDGF in TGF-beta-mediated tumour progression of hepatocytes and suggest PDGF as a target for therapeutic intervention in liver cancer.

Animals↗
PubMed2000

Drug-induced suppression of phosphorylase kinase activity correlates with resolution of psoriasis as assessed by clinical, histological and immunohistochemical parameters.

BACKGROUND: Phosphorylase kinase (PhK), also known as adenosine triphosphate (ATP)-phosphorylase b phosphotransferase, integrates multiple calcium/calmodulin-dependent signalling pathways, including those involved in cell migration and cell proliferation, while coupling these pathways to glycogenolysis and ATP-dependent phosphorylation, thus ensuring continuing energy supply for these activities. OBJECTIVES: Our laboratory recently reported correlation of elevated PhK activity with psoriatic activity. This study further evaluates the significance of drug-induced suppression of PhK activity on psoriatic activity. PATIENTS AND METHODS: PhK activity was assayed in four groups, each with 10 patients: (i) active untreated psoriasis; (ii) resolving psoriasis treated by calcipotriol (Dovonex(R), Bristol Myers Squibb, Princeton, NJ, U.S.A. ), a vitamin D3 analogue and an indirect inhibitor of PhK; (iii) curcumin (diferuloylmethane), a selective PhK inhibitor; and (iv) 10 normal non-psoriatic subjects. RESULTS: PhK activity in units mg-1 protein was highest in active untreated psoriasis (1204 +/- 804.3; mean +/- SD), lower in the calcipotriol-treated group (550.7 +/- 192. 9), lower in curcumin-treated group (207.2 +/- 97.6), and lowest in normal skin (105.4 +/- 44.6). One-way analysis of variance performed on log-transformed PhK activity measure showed significant differences among the four groups, F3,36 = 48.79, P < 0.0001. Decreased PhK activity in curcumin-and calcipotriol-treated psoriasis was associated with corresponding decreases in keratinocyte transferrin receptor (TRR) expression, severity of parakeratosis and density of epidermal CD8+ T cells. CONCLUSIONS: Our results demonstrate that drug-induced suppression of PhK activity is associated with resolution of psoriatic activity as assessed by clinical, histological and immunohistochemical criteria, and support the hypothesis that effective antipsoriatic activity may be achieved through modulation of PhK activity.

Adult↗
PubMed1984

Increased chromium uptake in polymorphonuclear leukocytes from burned patients.

Following thermal injury neutrophil function is severely impaired and thought to be hypometabolic; however, the host is considered to be hypermetabolic. To further investigate the metabolism and the function of neutrophils following thermal injury, neutrophil migration and chromium uptake were studied using radio-labelled neutrophils. Random and directed migration were found to be significantly reduced compared to control values. Neutrophil lysozyme content was also reduced in these burn cells while serum lysozyme from the same patients was significantly elevated over control values. These data suggest lysozyme is released by the neutrophil into the circulatory system. The influx of chromium in cells from burned patients was much greater than the influx in normal cells used in studies for chemotaxis. Influx of chromium over time and over varying concentrations of chromium was linear (r2 = 0.90) in cells from burned patients and normals. Cells from burned patients, however, took up more chromium than normals. Influx velocity of chromium was also determined and found to be greater in burn cells than normal cells. Since it has been shown that chromium influx is an energy-dependent reaction it is suggested that cellular energy stores are being depleted by the influx of chromium. Whether this is a response to an intracellular deficit or uncoupling of metabolic pathways is not known at this time.

Adult↗
PubMed2002

Management of glaucoma after retinal detachment surgery.

Secondary glaucoma may complicate retinal detachment surgery. Intraocular pressure (IOP) elevation has been described after scleral buckling procedures and vitrectomy with intravitreal injection of gas or silicone oil. Angle-closure glaucoma after scleral buckling develops because of congestion and anterior rotation of the ciliary body. Medical therapy and laser iridoplasty are usually successful in controlling IOP, but the presence of conjunctival scarring and recession and retinal hardware after scleral buckling procedures can make surgical management challenging. Intravitreal injection of expansile gases like sulfur hexafluoride (SF6) and perfluoropropene (C3F8) may produce secondary angle-closure glaucoma with or without pupillary block. Aspiration of a portion of the intraocular gas may be needed, especially if IOP is elevated to a level that may compromise ocular perfusion. Glaucoma also can develop after intravitreal injection of silicone oil secondary to pupillary block, inflammation, synechial angle closure, rubeosis iridis, or migration of emulsified or nonemulsified silicone oil into the anterior chamber. A prophylactic inferior iridectomy at the time of surgery serves to prevent pupillary block. Patients with medically uncontrolled glaucoma after silicone oil injection may require oil removal with or without concurrent glaucoma surgery.

Fluorocarbons↗
PubMed2004

Characterization of lymphocyte subpopulations and cytokine profiles in peripheral blood of nickel-sensitive individuals with systemic contact dermatitis after oral nickel exposure.

Several studies have shown that oral nickel exposure can elicit systemic contact dermatitis (SCD) in nickel-sensitive individuals. The current study describes some of the immunological mechanisms underlying such nickel-allergic reactions elicited by oral exposure to nickel. Following oral exposure to graded concentrations of nickel or placebo, blood samples were taken from nickel-sensitive individuals and from non-nickel-sensitive controls. T-cell subtypes (CD3+, CD4+, CD8+ and CD45RO+), expression of skin-homing receptor, cutaneous lymphocyte-associated antigen (CLA) and cytokine profiles [interleukin (IL)-2, IL-4, IL-5, IL-6, IL-10, interferon-gamma and tumour necrosis factor-alpha] were investigated. A definite dose-response reaction pattern to oral nickel exposure was observed among nickel-sensitive individuals. Nickel-sensitive individuals whose dermatitis flared after oral challenge with nickel showed significant decreases in fractions of CD3+ CD45RO+ CLA+ and CD8+ CD45RO+ CLA+ blood lymphocytes, suggesting migration of CD8+ 'memory' CLA+ T lymphocytes from the blood to peripheral tissues. Only those nickel-sensitive individuals who clinically reacted to oral challenge with nickel (4 mg) had elevated levels of IL-5 in the serum, indicating an activation of type 2 T lymphocytes in the peripheral blood. In conclusion, the study indicates that CD8+ CD45RO+ CLA+ T lymphocytes and T lymphocytes with a type 2 cytokine profile are involved in SCD elicited by nickel.

Administration, Oral↗
PubMed1995

Hydroxylation of collagen type I: evidence that both lysyl and prolyl residues are overhydroxylated in osteogenesis imperfecta.

The composition of the collagens secreted into the media of fibroblast cultures of 39 patients with osteogenesis imperfecta (OI) was the same in controls and OI cultures. An abnormal migration pattern of collagens upon SDS-PAGE was evident in one third of the cultures investigated. Lysyl and prolyl hydroxylation of HPLC-purified alpha 1(I) chains was elevated in about 60% of cultures. The degree of hydroxylation was highest in the lethal forms. The extent of lysyl and prolyl hydroxylation showed a strong correlation (r = 0.74, P < 0.001). While high levels of hydroxylation are frequently observed in OI patients, a direct correlation between lysyl or prolyl hydroxylation and fracture rate or growth retardation could not be established.

Adolescent↗
PubMed2006

Altered localization of CXCL13 expressing cells in mice deficient in Pactolus following an inflammatory stimulus.

The mouse Pactolus gene is an evolutionary paralogue to the CD18/beta2 integrin subunit and is preferentially expressed by neutrophils. When first identified, it was assumed Pactolus would function as an adhesion receptor similar to other beta integrin subunits. The analysis of mice genetically deficient in Pactolus, however, did not define any lesion in neutrophil migration, adhesion or phagocytosis. Therefore a wider analysis of the Pactolus deficiency was initiated using transcriptional profiling during an inflammatory insult. This screen identified a single transcript, CXCL13, that was elevated in cells from a peritoneal lavage of the wild type animal compared to the Pactolus-deficient animal. Our analyses confirmed resident macrophages as being responsible for the chemokine using intracellular CXCL13 staining and additional cell markers to phenotypically characterize such cells. The resident CXCL13-expressing cells (which do not express Pactolus) are functionally distinct from the macrophages recruited into the peritoneal cavity following the inflammatory stimulation since the recruited macrophages do not express detectable levels of the chemokine. The numbers and expression patterns of these resident CXCL13-expressing cells do not vary in naïve animals of wild type or Pactolus-deficient origin. Additionally, Pactolus-deficient neutrophils do not preferentially kill (compared to wild type) CXC13-expressing macrophages. These data suggest that during an inflammatory response, Pactolus may help retain CXCL13-expressing cells within the peritoneal environment.

Animals↗
PubMed2001

Antimitogenic actions of organic nitrates are potentiated by sildenafil and mediated via activation of protein kinase A.

Migration and proliferation of vascular smooth muscle cells (SMC) in response to platelet-derived growth factor (PDGF) and other mitogens play an important role in restenosis after coronary angioplasty. Elevation of both cAMP and cGMP has been shown to inhibit SMC mitogenesis. The aim of this study was to examine the antimitogenic actions of organic nitrates and sildenafil and to clarify the role of cyclic nucleotide-dependent protein kinases (PKA, PKG) in this action. Organic nitrates [glycerol trinitrate (GTN), isosorbide 5'-mononitrate (ISMN), pentaerythrityl-tetranitrate (PETN)] and the PDE5 inhibitor sildenafil reduced PDGF-induced DNA synthesis, measured by ((3)H]thymidine incorporation. GTN, ISMN, and PETN acted synergistically with sildenafil (1 microM) on inhibition of PDGF-induced DNA synthesis, increase of intracellular cyclic nucleotides, and vasodilator-stimulated phosphoprotein phosphorylation. The highly selective PKA inhibitor PKI abolished these actions of sildenafil and organic nitrates, whereas the PKG inhibitors KT5823 and (Rp)-8-pCPT-cGMPS had no effect. In addition, selective activation of PKG without inhibition of PDE3 by the cGMP analog 8-pCPT-cGMP (100 microM) had no antimitogenic effect. The data suggest that 1) organic nitrates and sildenafil exert antimitogenic actions by activation of PKA via inhibition of PDE3, but not by activation of PKG and 2) that antimitogenic effects of organic nitrates are potentiated by sildenafil at therapeutic plasma levels.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1979

Toxocariasis: serological diagnosis by enzyme immunoassay.

An enzyme-immunoassay was developed to measure the concentration of serum antibody specific for the secretory antigens released by migrating toxocaral larvae. This technique was evaluated by testing sera from healthy UK adults, and from patients with and without toxocariasis. In 922 healthy adults, 2.6% were found to have elevated specific antibody levels. Elevated values were observed twice as frequently in males as in females but showed no significant regression with age between 20 and 65 years. Of 62 patients with non-toxocaral helminthic infections, all had antitoxocaral antibody levels within the range of values observed in healthy controls and had a mean level which was not significantly elevated. All of 13 patients with clinical toxocariasis had enzyme-linked immunosorbent assay (ELISA) antibody levels above the 100th percentiles of both the healthy population and the helminth-infected group and had a significantly high mean value (p less than 0.001) more than 12 times that of the healthy or infected controls. The high degree of sensitivity and specificity of the toxocariasis enzyme-immunoassay indicates that this new test should be useful in reference immunodiagnostic applications and in large-scale seroepidemiological surveys.

Antibodies↗
PubMed2006

Increased angiogenesis at the site of abdominal aortic aneurysm rupture.

Abdominal aortic aneurysm (AAA) rupture is associated with elevated levels of matrix metalloproteinase (MMP). Medial neovascularization is a known characteristic of established AAAs and involves proteolytic degradation of extracellular matrix by MMPs to facilitate endothelial cell proliferation and migration. This study evaluated the extent of neovascularization in abdominal aortic aneurysm rupture. Results indicated upregulation of proangiogenic cytokines and increased medial neovascularization at the aneurysm rupture edge compared with paired aneurysm anterior sac. Further investigations into the role of angiogenesis in aneurysm rupture may open novel therapeutic avenues to prevent aneurysm rupture.

Aortic Aneurysm, Abdominal↗
PubMed2004

Differential requirement for steroidogenic factor-1 gene dosage in adrenal development versus endocrine function.

The importance of steroidogenic factor-1 (SF-1) gene dosage in endocrine function is evidenced by phenotypes associated with the heterozygous state in mice and humans. Here we examined mechanisms underlying SF-1 haploinsufficiency and found a striking reduction (12-fold) in SF-1 heterozygous (+/-) adrenocortical size at embryonic day (E) 12. Loss of one SF-1 allele led to a selective decrease in adrenal precursors within the adrenogonadal primordium at E10.0, without affecting the number of gonadal precursors, as marked by GATA-4. Beginning at E13.5, increased cell proliferation in SF-1 +/- adrenals allows these organs to approach but not attain a normal size. Remarkably, neural crest-derived adrenomedullary precursors migrated normally in SF-1 +/- and null embryos. However, later in development, medullary growth was compromised in both genotypes. Despite the small adrenal size in SF-1heterozygotes, an unexpected elevation in steroidogenic capacity per cell was observed in primary adult adrenocortical SF-1 +/- cells compared with wild-type cells. Elevated cellular steroid output is consistent with the up-regulation of some SF-1 target genes in SF-1 +/- adrenals and may partially be due to an observed increase in nerve growth factor-induced-B. Our findings underscore the need for full SF-1 gene dosage early in adrenal development, but not in the adult adrenal, where compensatory mechanisms restore near normal function.

Adrenal Glands↗
PubMed1978

Studies on the function of cell membrane. 11th Report: Binding of cytochrome b5 to liver microsomes and plasma membranes isolated from normal and CCl4-treated rats.

Cytochrome b5 was isolated from liver microsomes using a detergent-method. The hemoprotein was found to bind to liver plasma membranes in vitro and was accompanied by an increase in NADH-cytochrome c reductase activity, but not NADH-ferricyanide reductase activity. As in the case of microsomes, the binding to plasma membranes was temperature-dependent and was tight to the extent that the bound cytochrome b5 was little released under high ionic strength. The capacity of plasma membranes for the binding was less than that of microsomes. Administration of CCl4 did not significantly affect the binding of the hemoprotein in both fractions. These results add support to our previous proposal that the elevation of NADH-cytochrome c reductase activity of liver plasma membranes observed early after administration of CCl4 may be caused by the binding of cytochrome b5 which has probably migrated from the endoplasmic reticulum.

Animals↗
PubMed2001

[The role of selected cell adhesion molecules in chronic renal failure patients treated conservatively].

Cell adhesion molecules play a pivotal role in many biological processes. Their membrane-bound forms take part in leukocyte migration in case of inflammation and therefore determine effective immune response. Uremia is a state of immunologic imbalance. By comparison with healthy controls, levels of soluble adhesion molecules are either elevated or lowered in chronic renal failure patients. This fact proves conclusively that activation and inhibition of immunocompetent cells coexist in end stage renal disease, thus showing the complexity of immune disorders in uremia. Taking into account the competitive action between circulating adhesins and their bound counterparts, one can come to the conclusion that soluble forms' dysregulation results in the blockage of membrane-bound adhesion molecules and leads to disordered adhesion. Although the effects of change in circulating adhesins' concentrations seem evident, the reason for this change is still unclear.

Cadherins↗
PubMed1990

p185neu is phosphorylated on tyrosine in human primary breast tumors which overexpress neu/erbB-2.

A series of primary human breast tumors was analysed by immunoblotting with anti-neu antibodies. Overproduction of the neu protein-tyrosine kinase, p185neu, was observed in 23 of 56 malignant tumor samples. 29 of these tumors were also immunoblotted with antiphosphotyrosine antibodies. A single prominent phosphotyrosine-containing protein, which co-migrated with p185neu was identified in 11 of the 29 tumors examined. There was an exact concordance between the tumors with a 185kDa phosphotyrosine-containing protein, and those with elevated p185neu. These results indicate that overexpressed p185neu in primary human breast cancer is phosphorylated on tyrosine, most likely by autophosphorylation, and by inference is enzymatically activated as a protein-tyrosine kinase. Aberrant tyrosine phosphorylation may therefore be important in the development of a substantial fraction of breast cancers.

Antibodies↗
PubMedDate not supplied

Immunotoxic effects of dialkyltins used for stabilization of plastics.

After single administration of di-n-octyltin dichloride (DOTC) 4-61 mg/kg iv, 30-120 mg/kg im, and 120-240 mg/kg p.o.--a reversible, dose-dependent reduction of thymus weight and of the number of thymocytes was observed in mice. Di-n-butyltin dichloride (DBTC) induced similar effects. After iv administration of DBTC the level of total bilirubin in serum of mice was highly increased. DOCT did not elevate the bilirubin content of the serum. The level of bilirubin in serum did not correlate with the thymotoxic effects of DOTC and DBTC in mice. The inhibition of macrophage migration from spleen fragments of guinea pigs, which was measured as a parameter of the cytotoxic activity of DOTC in vitro, appeared at 10(-5)-10(-4) M.

Animals↗