SEARCH · PubMed Health

Results for “Cell Adhesion Molecules”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources

PubMed2003

The cell adhesion molecules N-cadherin and neural cell adhesion molecule regulate human growth hormone: a novel mechanism for regulating pituitary hormone secretion.

Pituitary GH secretion is regulated by hypothalamic hormones and peripheral factors. Cell-cell contact may also have an important role in regulating pituitary hormone expression and secretion. The role of pituicyte cell-cell contact mediated by N-cadherin and neural cell adhesion molecule (N-CAM) was studied in the regulation of GH secretion. RT-PCR showed N-cadherin mRNA expression in eight of 12 of GH-secreting adenomas compared with one of seven of prolactin-cell adenomas. N-cadherin and N-CAM were similarly expressed in adenomas and in adult and fetal normal pituitary tissues. The effects of CAM homophilic binding on GH secretion from dispersed human fetal pituitary cultures were studied by manipulating CAM mediated cell-cell contact using either soluble N-cadherin-Fc or pituitary cells cocultured with NIH-3T3 cells stably expressing CAMs. CAM stimulation increased GH secretion from pituitary fetal cultures by 40-60% (P < 0.05) and also from cultured GH adenoma cells by 40-75% (P < 0.05). Disrupting N-cadherin homophilic binding by anti-N-cadherin antibody decreased fetal, but not tumorous GH secretion by 40% (P < 0.05). This study indicates that pituitary cell-cell contact mediated by homophilic interactions between adhesion molecules regulates human GH secretion.

3T3 Cells↗

PubMed1996

Neovascular expression of E-selectin, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 in human atherosclerosis and their relation to intimal leukocyte content.

BACKGROUND: Leukocyte recruitment is an early event in atherogenesis, and the leukocyte adhesion molecules E-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) recently have been detected in human atherosclerosis. However, no previous study has evaluated either the distribution of these three molecules at different sites within the arterial intima or their relation to plaque leukocyte content. METHODS AND RESULTS: Immunohistochemistry was performed on 99 coronary artery segments (34 controls and 65 with atherosclerotic plaque) to identify E-selectin, ICAM-1, VCAM-1, macrophages, smooth muscle cells, and T lymphocytes. For each segment, the presence or absence of adhesion molecule was determined at the arterial lumen, on intimal neovasculature, and on intimal nonendothelial cells. Each segment was scored for intimal macrophage and T-lymphocyte densities on a semiquantitative scale of 0 to 3. In atherosclerotic plaques, the prevalences of E-selectin, ICAM-1, and VCAM-1 on plaque neovasculature were twofold higher than their prevalences on arterial luminal endothelium. E-selectin was the only adhesion molecule for which expression on arterial luminal endothelial cells was more prevalent in plaques than in control segments. Increased plaque intimal macrophage density was associated with expression of VCAM-1 on neovasculature (P < .01) and on nonendothelial cells (P < .01). Increased plaque intimal T-lymphocyte density was associated with the presence of both ICAM-1 and VCAM-1 on neovasculature (both P < .01) and on nonendothelial cells (both P < .01). CONCLUSIONS: In atherosclerotic plaques, the expression of all three leukocyte adhesion molecules was more prevalent on intimal neovasculature than on arterial luminal endothelium. Further, the presence on neovasculature and nonendothelial cells of VCAM-1 and ICAM-1 was strongly associated with increased intimal leukocyte accumulation. These findings suggest that leukocyte recruitment through and/or activation of intimal neovasculature may play important roles in the pathogenesis of human atherosclerosis.

Adult↗

PubMed2000

Intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 are increased in the plasma of children with sepsis-induced multiple organ failure.

OBJECTIVES: To determine concentrations of circulating adhesion molecules endothelial (E)-selectin, intercellular adhesion molecule (ICAM)-1, and vascular cell adhesion molecule (VCAM)-1 in children with sepsis-induced multiple organ failure (MOF), and to determine associations among increased concentrations of these circulating adhesion molecules and important outcome measures. DESIGN: Prospective study. SETTING: University pediatric intensive care unit. PATIENTS: A total of 77 consecutive children with sepsis and 14 acutely ill children without sepsis. INTERVENTIONS: Plasma E-selectin, ICAM-1, and VCAM-1 concentrations and organ failure index (indicating number of failed organ systems) were determined in 77 children on days 1 and 3 of sepsis, and in 14 control children on pediatric intensive care unit day 1. Multivariate logistic regression analysis was used to determine associations between adhesion molecule concentrations and clinically relevant outcome measures. MEASUREMENTS AND RESULTS: Plasma concentrations of E-selectin, ICAM-1, and VCAM-1 were increased in children with sepsis vs. control on day 1 (p < .05). Plasma VCAM-1 (but not ICAM-1 or E-selectin) was increased in children with more than three organ failures vs. children with less than three organ failures (p < .05). Plasma ICAM-1 and VCAM-1 (but not E-selectin) concentrations independently predicted number of organs failed and development of more than three organ failures. Plasma ICAM-1 and VCAM-1 also predicted mortality and development of sequential (pulmonary/hepatic/renal) MOF (p < .05). CONCLUSIONS: The pronounced and persistent increase in plasma VCAM-1 and ICAM-1 that occurs in children with sepsis and persistent MOF may indicate a phenotypic change in endothelium toward a more proinflammatory state. Alternatively, the source for these adhesion molecules may be activated leukocytes and other cell types. Future studies are required to determine the role of ICAM-1 and VCAM-1 in the pathogenesis of sepsis-induced MOF.

Adolescent↗

PubMed2006

Levels of intracellular adhesion molecule-1 and vascular cell adhesion molecule-1 in children with Henoch-Schönlein purpura.

BACKGROUND AND PURPOSE: Henoch-Schönlein purpura (HSP) is a small vessel vasculitis. Soluble adhesion molecules play a very important role in the immuno-inflammatory reaction of damaged vascular tissues. This study investigated the prognostic and diagnostic potential of soluble intracellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1) in HSP. METHODS: Serum levels of sICAM-1 and sVCAM-1 were studied in 26 children with HSP. Paired blood samples (during acute and convalescent stages) were collected from 17 of the children and assayed by enzyme-linked immunosorbent assay. Correlations with clinical manifestations were examined. Seventeen healthy children served as controls. RESULTS: Both sICAM-1 and sVCAM-1 were significantly elevated at the acute stage compared with the remission stage of HSP patients versus controls (p=0.006 and p=0.0173, respectively). CONCLUSIONS: Although the levels of sICAM-1 and sVCAM-1 were not correlated with the severity of clinical manifestations in HSP, these soluble adhesion molecules may serve as diagnostic markers.

Adolescent↗

PubMed2004

Disturbed homeostasis of lung intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 during sepsis.

Cecal ligation and puncture (CLP)-induced sepsis in mice was associated with perturbations in vascular adhesion molecules. In CLP mice, lung vascular binding of (125)I-monoclonal antibodies to intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 revealed sharp increases in binding of anti-ICAM-1 and significantly reduced binding of anti-VCAM-1. In whole lung homogenates, intense ICAM-1 up-regulation was found (both in mRNA and in protein levels) during sepsis, whereas very little increase in VCAM-1 could be measured although some increased mRNA was found. During CLP soluble VCAM-1 (sVCAM-1) and soluble ICAM-1 (sICAM-1) appeared in the serum. When mouse dermal microvascular endothelial cells (MDMECs) were incubated with serum from CLP mice, constitutive endothelial VCAM-1 fell in association with the appearance of sVCAM-1 in the supernatant fluids. Under the same conditions, ICAM-1 cell content increased in MDMECs. When MDMECs were evaluated for leukocyte adhesion, exposure to CLP serum caused increased adhesion of neutrophils and decreased adhesion of macrophages and T cells. The progressive build-up in lung myeloperoxidase after CLP was ICAM-1-dependent and independent of VLA-4 and VCAM-1. These data suggest that sepsis disturbs endothelial homeostasis, greatly favoring neutrophil adhesion in the lung microvasculature, thereby putting the lung at increased risk of injury.

Animals↗

PubMed2004

Effects of different hyaluronic acid products on synovial fluid levels of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in knee osteoarthritis.

The aim of this study was to evaluate the effects of different hyaluronic acid (HA) forms on synovial fluid levels of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) during the treatment of patients with knee osteoarthritis (OA). Forty patients were randomly assigned to 2 groups that were treated with native sodium hyaluronate (group I) or cross-linked hylan G-F 20 (group II). Clinical evaluations and synovial fluid aspirations were performed before the 1st injection (baseline), the 2nd injection (week 1), the 3rd injection (week 2), and at 1 week after the 3rd injection (week 3). Synovial fluid levels of both ICAM-1 and VCAM-1 were significantly reduced at weeks 1 to 3, compared to the baseline values. The Western Ontario and McMaster Universities Osteoarthritis (WOMAC) Index was used for clinical evaluations; the WOMAC pain score and physical function score were progressively improved at weeks 1 to 3 in both groups; the WOMAC stiffness score was significantly improved at week 3 in both groups. No significant differences were noted between the 2 treatment groups in respect to ICAM-1 levels, VCAM-1 levels, WOMAC pain score, stiffness score, or physical function score at any time. The decreased ICAM-1 and VCAM-1 levels after intra-articular HA injection may help to explain the anti-inflammatory effects of HA therapy in knee OA.

Aged↗

PubMed1996

Alterations in soluble intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in hemodialysis patients.

Hemodialysis (HD) patients can develop acute reactions during treatment as well as increased long-term susceptibility to infections and malignancies. Abnormalities in leukocyte adhesion may contribute to these processes. Recently, serum levels of soluble adhesion molecules have been detected in circulating blood of normal subjects and in patients with chronic renal failure. We studied the effects of a single dialysis session with new cuprophane membrane on the soluble (s) form of intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), two adhesion molecules with a variety of immunologic roles. Significant elevations in both sICAM-1 (523 +/- 61 v 304 +/- 45 [SEM] ng/mL, P < 0.05) and sVCAM-1 (2,055 +/- 270 v 1,189 +/- 149 ng/mL, P < 0.05) were observed in HD patients at baseline compared with controls. Both sICAM-1 and sVCAM-1 levels decreased after a 3-hour HD session (P < 0.001). Early in HD, sICAM-1 levels, though lower than predialysis, were elevated in the exit line of the dialyzer compared with entrance (339 +/- 64 v 259 +/- 53 ng/mL, P < 0.001), whereas sVCAM-1 was decreased on the exit line compared with entrance (639 +/- 90 v 932 +/- 92 ng/mL, P < 0.001). Because ICAM-1 and VCAM-1 are important for many leukocyte functions, alterations in serum levels of sICAM-1 and sVCAM-1 may play a role in the immunologic consequences of uremia and HD treatment.

Case-Control Studies↗

PubMed2004

Detection of soluble intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in both cerebrospinal fluid and serum of patients after aneurysmal subarachnoid hemorrhage.

OBJECT: The aim of this study was to explore whether levels of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are elevated in the cerebrospinal fluid (CSF) and serum of patients after aneurysmal subarachnoid hemorrhage (SAH). METHODS: This prospective clinical study focused on 21 patients who had recently suffered an SAH due to aneurysmal rupture and 15 control patients with hydrocephalus who had no other central nervous system disease. Cerebrospinal fluid and serum samples obtained within the first 3 days and on the 5th and 7th days of SAH were assayed for ICAM-1 and VCAM-1 by using quantitative enzyme-linked immunosorbent assays. Levels of soluble forms of ICAM-1 (p = 0.00001) and VCAM-1 (p = 0.009) in the patients' CSF and those of ICAM-1 (p = 0.00001) and VCAM-1 (p = 0.00001) in their serum were found to be elevated after SAH compared with levels in the CSF and serum of control patients with hydrocephalus. In addition, when the authors compared the increased levels of adhesion molecules in the CSF and serum of patients after SAH, the only statistically insignificant difference that they found was between the levels of VCAM-1 in serum obtained on Days 5 and 7 after SAH (p = 0.27). CONCLUSIONS: Adhesion molecules are a group of macromolecules that may participate in the inflammatory process, a common pathway leading to vasospasm after SAH. Leukocyte adherence to the vascular endothelium, which is induced by adhesion molecules, has been believed to be the initial signal of the development of vasospasm. The authors have demonstrated the synchronized elevation of two adhesion molecules in both CSF and serum following aneurysmal SAH. Blocking of ICAM-1 as well as VCAM-1 by monoclonal antibodies post-SAH may provide a beneficial effect on vasospasm.

Adult↗

PubMed1991

Endothelial and epithelial cell adhesion molecules.

This review will discuss a number of specific cell adhesion molecules present on the surface of endothelial and epithelial cells in the lung. Molecules such as integrins, proteoglycans, and the hyaluronic acid receptor, CD44, are found on the abluminal or basement membrane side of the cell and function as cell-substratum receptors. Cadherins, integrins, and platelet-endothelial cell adhesion molecule-1 (PECAM-1) are present at the cell-cell borders of adjacent endothelial and/or epithelial cells and function to initiate or maintain cell-cell adhesion. Finally, a number of inducible cell adhesion molecules such as endothelial-leukocyte adhesion molecule-1 (ELAM-1), granule-associated membrane protein 140 (GMP140), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) are expressed on the luminal surfaces of these cells during inflammation and function as cell-cell adhesion molecules important in white blood cell, platelet, or tumor cell adhesion. These adhesion molecules likely play important roles in maintaining the normal structure and function of the lung, as well as participating in pulmonary processes such as inflammation, wound healing, and the development and spread of malignant disease.

Animals↗

PubMed2005

The influence of garlic (Allium sativum) extract on interleukin 1alpha-induced expression of endothelial intercellular adhesion molecule-1 and vascular cell adhesion molecule-1.

Inflammation plays an important role in both the initiation of atherosclerosis and development of atherothrombotic events. The adherence of leukocytes/monocytes to the endothelium is an early event in atherogenesis. Phytotherapeutica as garlic and garlic extracts were shown to have beneficial modulating effects in patients with atherosclerotic disease. The aim of this study was to evaluate in vitro the influence of water-soluble garlic (Allium sativum) extract on the cytokine-induced expression of endothelial leukocyte adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1, CD54) and vascular cell adhesion molecule-1 (VCAM-1, CD106). Cytokine-induced expression of cellular adhesion molecules was measured on primary human coronary artery endothelial cell (HCAEC) cultures. HCAEC were cultured in microvascular endothelial cell growth medium and preincubated with garlic extract at various concentrations (0.25-4.0 mg/ml), after which human interleukin-1alpha (IL-1alpha, 10 ng/ml) was added for 1 day. Fluorescein isothiocyanate (FITC)-labeled anti-ICAM-1 and FITC-labeled anti-VCAM-1 were used to analyze the IL-1alpha-induced expression of ICAM-1 and VCAM-1 by flow cytometry. Incubation of HCAEC with garlic extract significantly decreased ICAM-1 and VCAM-1 expression induced by IL-1alpha. In addition, we examined the effects of garlic extract on the adhesion of monocytes to endothelial cells, using the monocytic U937 cell line. The presence of garlic extract significantly inhibited the adhesion of monocytes to IL-1alpha-stimulated endothelial cells. These results indicate that garlic extract modulates the expression of ICAM-1 and VCAM-1, thus potentially contributing to the beneficial effects traditionally attributed to garlic.

Cell Adhesion↗

PubMed2002

Expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in human crescentic glomerulonephritis.

AIMS: In glomerulonephritis, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) may play important roles in the formation of crescents. These studies are designed to evaluate the expression patterns of ICAM-1 and VCAM-1 in human crescentic glomerulonephritis and to determine the cellular origin of adhesion molecules in the crescentic lesions. METHODS AND RESULTS: We examined the expression of ICAM-1 and VCAM-1 proteins in renal biopsies with cellular (n=7), fibrocellular (n=9) or fibrous (n=4) crescentic glomerulonephritis, and six controls by immunohistochemistry. mRNA expression of ICAM-1 and VCAM-1 was further evaluated by RNA in-situ hybridization. Cytokeratin or CD68 immunohistochemistry was performed on the same sections, where in-situ hybridization had been carried out. In cellular crescents, ICAM-1 and VCAM-1 proteins were over-expressed to a similar extent. Of the three types of crescents, the extent of ICAM-1 immunopositivity was the greatest in the cellular crescents and decreased towards the fibrous crescents (P < 0.05). Yet the extent of VCAM-1 immunoreactivity was not different between the types. Fibrous crescents still contained some epithelial cells and showed only VCAM-1 expression. In the glomeruli with cellular or fibrocellular crescents, the extent of ICAM-1 immunopositivity in the glomerular tufts was significantly larger than that of VCAM-1 (P < 0.05). In an in-situ hybridization study, the mRNA expression patterns of ICAM-1 and VCAM-1 paralleled their protein expressions. A double-labelling study showed that the signal for ICAM-1 and VCAM-1 mRNAs was mainly present in cytokeratin-positive and CD68-negative cells in the crescentic lesions. CONCLUSIONS: These results suggest that glomerular parietal epithelial cells in cellular crescents up-regulate both ICAM-1 and VCAM-1, and that some epithelial cells retained in fibrous crescents persistently over-express VCAM-1, but not ICAM-1. They also suggest that ICAM-1 is involved in early leucocyte recruitment into glomeruli in crescentic glomerulonephritis.

Endothelium, Vascular↗

PubMed1984

Two different cell adhesion molecules--cell-CAM 105 and a calcium-dependent protein--occur on the surface of rat hepatocytes.

We have recently identified a 105000 D plasma membrane glycoprotein, denoted cell-CAM 105 (CAM, cell adhesion molecule), that is involved in intercellular adhesion of reaggregating rat hepatocytes (Ocklind & Obrink, J biol chem 257 (1982) 6788 [11]). In this communication we identify another cell surface protein that is also involved in hepatocyte cell-cell adhesion. This protein has an apparent molecular weight (MW) of 70000 and can be released from the surface membrane by chelation of calcium with EGTA. Results are presented indicating that it is identical with a previously discovered protein, CDP-1 (CDP, calcium-dependent protein) (Obrink, Lindström & Svennung, FEBS lett 70 (1976) 28 [28]). Antisera produced against either cell-CAM 105 or CDP-1 inhibit hepatocyte aggregation, but not attachment to collagen. Cell-CAM 105 and CDP-1 are present on the cell surface as separate components, as judged by the fact that both EGTA treatment and trypsin treatment of hepatocytes selectively make the cells insensitive to blocking of aggregation by antibodies against CDP-1 but not by antibodies against cell-CAM 105. However, although much less efficiently, the antibodies against CDP-1 can recognize a 105000 D protein which is also bound by the antibodies against cell-CAM 105, and under certain conditions the antibodies against cell-CAM 105 seem to recognize a 70000 D protein. CDP-1 may thus be derived from cell-CAM 105, or the two proteins might have a common precursor.

Adenosine Triphosphatases↗

PubMed2001

Modulation of soluble phases of endothelial/leukocyte adhesion molecule 1, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1 with interleukin-1beta after experimental endotoxic challenge.

OBJECTIVE: To evaluate the effect of treatment with interleukin 1beta (IL-1beta) on the concentrations of soluble adhesion molecules after an endotoxic challenge. DESIGN: Randomized, controlled study. SETTING: Experimental Unit, Virgen de las Nieves University Hospital. SUBJECTS: Seventy-two female CBA/H mice of 20 to 21 g, supplied by the animal center of the Experimental Unit. INTERVENTION: The mice were randomized into three groups of 24. Group 1 (sham) received two intraperitoneal (ip) doses of 0.1 mL of phosphate-buffered saline; group 2 (lipopolysaccharide) was injected with 125 mg/kg lipopolysaccharide (Escherichia coli) (i.p.) 24 hrs after 0.1 mL of phosphate-buffered saline; group 3 was pretreated with 80 ng (i.p.) of IL-1beta per mouse 24 hrs before the endotoxic challenge. MEASUREMENTS AND MAIN RESULTS: At 1, 2, 4, and 24 hrs after the endotoxic challenge, the concentrations of soluble endothelial/leukocyte adhesion molecule 1 (ELAM-1), intercellular adhesion molecule 1 (ICAM-1), and vascular cell adhesion molecule 1 (VCAM-1) were measured in the three groups. There was a significant increase (p <.01) in these concentrations at these times in comparison with the sham group. The use of IL-1beta produced a significant decrease (p <.05) in the three molecules among the treated group versus the group submitted only to the challenge; concentrations of ELAM-1 significantly decreased to below those of the sham group, and those of VCAM-1 reduced to levels that did not significantly differ from those of the sham group. CONCLUSION: Endotoxin administration significantly increases the concentrations of soluble ELAM-1, ICAM-1, and VCAM-1 in mice. Treatment with IL-1beta significantly decreases these concentrations, probably attenuating cell injury and organ dysfunction.

Analysis of Variance↗

PubMed1990

The cell adhesion molecule Cell-CAM 105 is an ecto-ATPase and a member of the immunoglobulin superfamily.

Cell-CAM 105 (C-CAM), a cell adhesion molecule in rat hepatocytes, was digested with trypsin, and peptides were isolated and sequenced by Edman degradation. The sequences of 4 peptides agreed with different regions of rat liver ecto-ATPase. Detailed biochemical analyses confirmed the identity between C-CAM and the ecto-ATPase. C-CAM/ecto-ATPase is a transmembrane protein having 4 immunoglobulin-like domains in the extracellular portion, demonstrating membership of the immunoglobulin superfamily. The ATPase activity suggests that ATP might influence cell adhesion, which would explain the inhibitory effect of exogenously added ATP on adhesion of several cell types.

Adenosine Triphosphatases↗

PubMed1994

Gold sodium thiomalate down-regulates intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression on vascular endothelial cells.

We examined whether antirheumatic drugs alter cytokine- or lipopolysaccharide-induced expression of adhesion molecules on vascular endothelial cells. Human umbilical cord vein endothelial cells were co-cultured with various antirheumatic drugs in the presence of inflammatory cytokines, and adhesion molecule expression was measured by cell enzyme-linked immunosorbent assay and Northern blot analysis. Among these antirheumatic drugs, gold sodium thiomalate significantly inhibited intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression on vascular endothelial cells and suppressed cellular binding between human monocytic cell lines, including U937 and HL-60 cells, and interleukin-1 beta-stimulated vascular endothelial cells. It is speculated that down-regulation of adhesion molecules might be one of the novel mechanisms of action of gold sodium thiomalate.

Adrenal Cortex Hormones↗

PubMed1995

Memory consolidation induces a transient and time-dependent increase in the frequency of neural cell adhesion molecule polysialylated cells in the adult rat hippocampus.

Animals trained in a passive avoidance task exhibit a transient time-dependent increase in hippocampal neural cell adhesion molecule (NCAM) polysialylation at 12-24 h following the initial learning trial. Using immunocytochemical techniques with a monoclonal antibody that specifically recognises NCAM-polysialic acid homopolymers, a distinct population of granule-like cells, at the border of the granule cell layer and the hilus in the dentate gyrus of the adult rat hippocampus, has been demonstrated to exhibit time-dependent change in frequency at 10-12 h following the initial learning of a one-trial, step-through, passive avoidance response. These changes were paradigm specific as they failed to occur in those animals rendered amnesic with scopolamine. These polysialylated dentate neurons are not de novo granule cell precursors as administration of 5-bromo-2'-deoxyuridine every 2 h from the point of learning to the 12-h posttraining time showed no significant difference between trained and passive animals in the small number of heterogeneously distributed, labelled cells. These findings directly identify a morphological substrate of memory, implied by previous correlative and interventive studies on NCAM function.

Animals↗

PubMed1986

Nerve growth factor enhances expression of neuron-glia cell adhesion molecule in PC12 cells.

The neuron-glia cell adhesion molecule (Ng-CAM) has been identified in mammalian brain tissue and PC12 pheochromocytoma cells as Mr 200,000 and Mr 230,000 species, respectively. When PC12 cells were treated with nerve growth factor (NGF), the amount of Ng-CAM at the cell surface was increased approximately threefold, whereas the amount of the neural cell adhesion molecule (N-CAM) remained unchanged. An NGF-inducible large external glycoprotein (NILE) has been previously identified by its enhanced expression in NGF-treated PC12 cells. Ng-CAM and NILE are similar in molecular weight, expression during development, and responsiveness to NGF in PC12 cells, suggesting that the two molecules are related. In addition, antibodies to Ng-CAM and NILE cross-reacted and the molecules had similar peptide maps after limited proteolysis. Moreover, antibodies to Ng-CAM inhibited fasciculation of neurites, a functional property shared with NILE. The results show that cell adhesion molecules can respond selectively to growth factors and suggest that NILE is, in fact, mammalian Ng-CAM.

Animals↗

PubMed2000

Effect of vaccination on expression of intracellular adhesion molecules 1 and vascular cell adhesion molecules 1 in murine schistosomiasis.

This work studied the approach of vaccination by utilizing ultraviolet attenuated S. mansoni cercariae on two surface adhesion molecules expression, intercellular adhesion molecules 1 (ICAM-1) and vascular cell adhesion molecules 1(VCAM-1). ICAM-1 and VCAM-1 expression were studied in livers of 37 CD-1 female mice (2 months aged and about 30 gm waited) which were divided into 3 groups. Analysis of adhesion molecules expression was done by direct immunofluorescence staining and quantitative measurement of positive signals by image analyzer. The main findings were: (1) ICAM-1 and VCAM-1 expression was mainly localized on granuloma cells. (2) The video count areas that expressed ICAM-1 and VCAM-1 were markedly increased in vaccinated than naive animals. The ICAM-1 intensity was (58.7%) in VC while (31.1%) in NC mice group. (3) Similarly the intensity of VCAM-1 expression was (73%) In VC while (54.2%) in NC. (4) The % change in ICAM-I expression relative to naive mice group was (326.9%) and (704.7) in NC and VC mice group respectively. (5) The % change in VCAM-1 expression in vaccinated animals relative to naive animals was (67,700) and (91,175) in NC and VC mice groups respectively.

Animals↗