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At least 1,009 records · Page 56Linked to original sources
PubMed2005

12/15-lipoxygenase regulates intercellular adhesion molecule-1 expression and monocyte adhesion to endothelium through activation of RhoA and nuclear factor-kappaB.

BACKGROUND: 12/15-lipoxygenase (12/15-LO) activity leads to the production of the proinflammatory eicosanoids 12-S-hydroxyeicosatetraenoic acid (12SHETE) and 13-S-hydroxyoctadecadienoic acid. We have previously shown a 3.5-fold increase in endothelial intercellular adhesion molecule (ICAM)-1 expression in mice overexpressing the 12/15-LO gene. We examined whether 12/15-LO activity regulated endothelial ICAM-1 expression. METHODS AND RESULTS: Freshly isolated aortic endothelial cells (EC) from 12/15-LO transgenic mice had significantly greater nuclear factor-kappaB (NF-kappaB) activation and ICAM mRNA expression compared with C57BL/6J control. 12/15-LO transgenic EC showed elevated RhoA activity, and inhibition of RhoA using either C3 toxin or the Rho-kinase inhibitor Y-27632 blocked NF-kappaB activation, ICAM-1 induction, and monocyte adhesion. Furthermore, we show that 12SHETE activates protein kinase Calpha, which forms a complex with active RhoA and is required for NF-kappaB-dependent ICAM expression in response to 12SHETE. CONCLUSIONS: The 12/15-LO pathway stimulates ICAM-1 expression through the RhoA/protein kinase Calpha-dependent activation of NF-kappaB. These findings identify a major signaling pathway in EC through which 12/15-LO contributes to vascular inflammation and atherosclerosis.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1998

Serum levels of soluble intercellular adhesion molecule-1 and soluble vascular cell adhesion molecule-1 in asymptomatic carriers of hepatitis C virus.

High levels of serum-soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) have been noted in patients with chronic hepatitis C. This study aimed to measure serum levels of sICAM-1 and sVCAM-1 in asymptomatic hepatitis C virus carriers and clarify the clinical significance of measuring soluble forms. Serum levels of sICAM-1 were significantly higher than in healthy controls but serum sVCAM-1 levels did not differ statistically from those in healthy controls. Liver biopsy obtained from 12 asymptomatic hepatitis C virus carriers showed evidence of hepatitis. Estimating sICAM-1 and sVCAM-1 in asymptomatic carriers may be helpful, especially in cases in which liver biopsy is not possible.

Adult↗
PubMed2006

Alpha-tocopherol supplementation does not affect monocyte endothelial adhesion or C-reactive protein levels but reduces soluble vascular adhesion molecule-1 in the plasma of healthy subjects.

Vascular monocyte retention in the subintima is pivotal to the development of cardiovascular disease and is facilitated by up-regulation of adhesion molecules on monocytes/endothelial cells during oxidative stress. Epidemiological studies have shown that cardiovascular disease risk is inversely proportional to plasma levels of the dietary micronutrients, vitamin C and vitamin E (alpha-tocopherol). We have tested the hypothesis that alpha-tocopherol supplementation may alter endothelial/monocyte function and interaction in subjects with normal ascorbate levels (> 50 microM), as ascorbate has been shown to regenerate tocopherol from its oxidised tocopheroxyl radical form in vitro. Healthy male subjects received alpha-tocopherol supplements (400 IU RRR-alpha-tocopherol/day for 6 weeks) in a placebo-controlled, double-blind intervention study. There were no significant differences in monocyte CD11b expression, monocyte adhesion to endothelial cells, plasma C-reactive protein or sICAM-1 concentrations post-supplementation. There was no evidence for nuclear translocation of NF-kappaB in isolated resting monocytes, nor any effect of alpha-tocopherol supplementation. However, post-supplementation, sVCAM-1 levels were decreased in all subjects and sE-selectin levels were increased in the vitamin C-replete group only; a weak positive correlation was observed between sE-selectin and alpha-tocopherol concentration. In conclusion, alpha-tocopherol supplementation had little effect on cardiovascular disease risk factors in healthy subjects and the effects of tocopherol were not consistently affected by plasma vitamin C concentration.

Adult↗
PubMed1995

Behavior of soluble intercellular adhesion molecule-1 and endothelial-leukocyte adhesion molecule-1 concentrations in patients with Graves' disease with or without ophthalmopathy and in patients with toxic adenoma.

Expression of intercellular adhesion molecule-1 (ICAM-1) and endothelial-leukocyte adhesion molecule-1 (ELAM-1) on endothelium can be considered a critical early step for leukocyte migration from blood to tissues during inflammatory processes. Increased circulating soluble ICAM-1 (sICAM-1) levels have been found in sera from patients with Graves' disease (GD) with or without ophthalmopathy. Serum soluble ELAM-1 (sELAM-1) levels have not been measured in these patients. The aim of this study was to clarify the behavior of sICAM-1 and sELAM-1 levels in patients with hyperthyroidism due to GD with or with or without ophthalmopathy and in hyperthyroid patients with toxic thyroid adenoma. We studied sICAM-1 and sELAM-1 levels in 130 subjects (age 23-54 yr), grouped as follows: group 1, 30 untreated hyperthyroid GD patients (21 females and 9 males) with active ophthalmopathy; group 2, 26 euthyroid GD patients (16 females and 10 males) with active ophthalmopathy; group 3, 33 hyperthyroid GD patients (22 females and 11 males) without ophthalmopathy; group 4, 11 untreated hyperthyroid patients (7 females and 4 males) with single toxic adenoma; and a control group of 30 healthy subjects (21 females and 9 males). sICAM-1 and sELAM-1 concentrations were measured by a sandwich enzyme linked immunosorbent assay (ELISA) method. Groups 1, 2, and 3 (P < 0.001 for all 3 groups) but not group 4 showed increased sICAM-1 levels compared with the control group. However, groups 1 and 2 (P < 0.001 for both) showed higher values of sICAM-1 than group 3, and group 1 showed higher sICAM-1 levels than group 2 (P < 0.002). Groups 1 and 2 (P < 0.001 for both) but not groups 3 and 4 showed sELAM-1 levels significantly higher than the control group and positively correlated to the severity score of Graves' ophthalmopathy (GO) (P < 0.002 for group 1 and < 0.01 for group 2). Our results confirm that increased sICAM levels in GD patients with or without ophthalmopathy (with higher levels in patients with GO) but not in hyperthyroid nonautoimmune patients may be the consequence of orbital and thyroid inflammation, and they also suggest that sICAM concentrations could reflect the degree of inflammatory activity. Increased sELAM-1 concentrations only, in patients with ophthalmopathy with or without hyperthyroidism significantly correlated to severity score of GO, suggest the measurement of sELAM-1 levels as a specific marker of endothelium activation in GO.

Adenoma↗
PubMed2002

Cell-to-Cell adhesion via intercellular adhesion molecule-1 and leukocyte function-associated antigen-1 pathway is involved in 1alpha,25(OH)2D3, PTH and IL-1alpha-induced osteoclast differentiation and bone resorption.

Cell-to-cell interaction is required for the differentiation of osteoclast precursors as well as for osteoclast function. The present study was undertaken to determine whether 1,25 dihydroxyvitamin D3 (1,25D), PTH, IL-1alpha and PGE2 depend on cell-to-cell interactions through the intercellular adhesion molecule (ICAM)-1/leukocyte function-associated antigen (LFA)-1 pathway in osteoclast formation and bone resorption. We found that mouse osteoblasts expressed ICAM-1 and that the expression was increased by treatment with PTH, IL-1alpha or 1,25D, but not by PGE2. In resorption assays measuring either 45Ca release from bone organ cultures or pit formation in bone cell cultures, 1,25D-, PTH- and IL-1alpha-stimulated resorption was inhibited by anti-ICAM-1 monoclonal antibody (mAb) and/or anti-LFA-1 mAb, while basal and PGE2-stimulated bone resorbing activities were not affected by these mAbs. Furthermore, in a mouse bone marrow culture system, stimulation of osteoclast-like (OCL) cell formation by 1,25D (10 nM), PTH (10 ng/ml) or IL-1alpha (10 ng/ml) was inhibited by the addition of anti-ICAM-1 mAb and/or anti-LFA-1 mAb. In a coculture system of murine spleen cells and osteoblasts, the ICAM-1/LFA-1 interaction was also involved in 1,25D-, PTH- and IL-1alpha-stimulated TRAP-positive MNC formation. However, anti-ICAM-1 mAb and anti-LFA-1 mAb did not alter either 1,25D- or PTH-stimulated receptor activator of NF-kappaB ligand (RANKL) mRNA transcription in bone marrow cultures. Taken together, we here propose that ICAM-1-mediated cell-to-cell adhesion of osteoblasts and osteoclast precursors is involved in RANKL-dependent osteoclast maturation stimulated by 1,25D, PTH, and IL-1alpha.

Animals↗
PubMed1999

Soluble intercellular adhesion molecule, vascular cell adhesion molecule, and impaired microvascular reactivity are early markers of vasculopathy in type 2 diabetic individuals without microalbuminuria.

OBJECTIVE: Using von Willebrand Factor (vWF) as a marker of endothelial function, previous studies have shown that the development of microalbuminuria is associated with the onset of endothelial dysfunction in individuals with type 2 diabetes. We tested the hypothesis that endothelial dysfunction is already evident in normoalbuminuric individuals with type 2 diabetes. RESEARCH DESIGN AND METHODS: We used laser Doppler imaging scanning to measure vasodilation in the forearm skin in response to iontophoresis of 1% acetylcholine (endothelium-dependent) and 1% sodium nitroprusside (endothelium-independent). Multiple indicators of endothelial function--soluble intercellular adhesion molecule (sICAM), soluble vascular cell adhesion molecule (sVCAM), vWF, and microvascular reactivity--were measured in 20 healthy control subjects, 45 normoalbuminuric (urinary albumin/creatinine ratio < 30 micrograms/mg) individuals with type 2 diabetes, and 14 microalbuminuric (urinary albumin/creatinine ratio between 30 and 300 micrograms/mg) individuals with type 2 diabetes. RESULTS: Serum sICAM and sVCAM levels were elevated in the normoalbuminuric (305 +/- 120, 851 +/- 284 ng/ml) and microalbuminuric (300 +/- 89, 845 +/- 252 ng/ml) individuals with diabetes when compared with the healthy control subjects (213 +/- 58, 661 +/- 176 ng/ml) (P < 0.01). Furthermore, the microvascular endothelium-dependent and -independent vasodilation was reduced in the normoalbuminuric (76 +/- 44, 70 +/- 33) (percent increase in perfusion over baseline) and microalbuminuric (74 +/- 41, 73 +/- 28) individuals with diabetes compared with healthy control subjects (126 +/- 67, 120 +/- 47) (P < 0.05). In contrast, plasma vWF was elevated only in the microalbuminuric individuals with diabetes (129 +/- 35%) compared with the normoalbuminuric individuals with diabetes (110 +/- 34) and healthy control subjects (111.3 +/- 39) (P < 0.05). On stepwise multivariate analysis, fasting blood glucose was the most important contributing factor to the variation in microvascular reactivity and sVCAM, whereas insulin resistance (by homeostasis model assessment) was the most important contributing factor to the variation in sICAM. Addition of all clinical and biochemical measures explained only 15-22% of the variation in sICAM, sVCAM, and microvascular reactivity. CONCLUSIONS: Multiple markers of endothelial dysfunction were evident in normoalbuminuric individuals with type 2 diabetes. The pathogenic process of vasculopathy in type 2 diabetes occurs early and may be operative before the development of microalbuminuria.

Adult↗
PubMed1999

Serum levels of thrombomodulin, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin in the acute phase of Plasmodium vivax malaria.

Elevated plasma or serum levels of thrombomodulin (TM), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin have been reported in several diseases. However, plasma or serum levels of TM, ICAM-1, VCAM-1, and E-selectin have not been investigated in the acute phase of Plasmodium vivax malaria. Serum TM, ICAM-1, VCAM-1, E-selectin, and creatinine levels were determined in six Japanese patients in the acute phase of vivax malaria and in seven healthy Japanese controls. Parasitemias of the peripheral blood were < 0.1% in five patients and 0.8% in one patient. The patients' mean +/- SD serum levels of TM, ICAM-1, VCAM-1, and E-selectin were 5.7 +/- 1.3 Fujirebio units/ml, 709 +/- 397 ng/ml, 2,112 +/- 782 ng/ml, and 99 +/- 28 ng/ml, respectively, and all were significantly greater than those in the controls (TM; P < 0.005, ICAM-1; P < 0.025, VCAM-1; P < 0.005, E-selectin; P < 0.025). However, no significant difference was identified between patients and controls for serum creatinine values. The serum levels of TM and VCAM-1 were not related to parasitemia. The elevation of serum TM levels suggests that endothelial cell damage occurs in the acute phase of vivax malaria.

Acute Disease↗
PubMed2000

[Inhibitory effects of ligustrazine on the expression of intercellular cell adhesion molecule-1, vascular cell adhesion molecule-1 in human umbilical vein endothelial cells induced by preeclamptic plasma].

OBJECTIVE: To determine whether plasma from preeclamptic women induces expression of intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) on cultured endothelial cells, and the effects of ligustrazine (LTZ) on the expression of ICAM-1, VCAM-1. METHODS: Human umbilical vein endothelial cells (HUVEC) were isolated by collagenase mixed with trypsin. LTZ was added to HUVEC monolayers grown to confluency on 96-well microplates for 30 minutes. Then HUVEC were incubated with medium containing 20% plasma (volume/volume) either from women with preeclampsia or normotensive pregnancy or nonpregnant women. ICAM-1, VCAM-1 expression was determined after 16 hours of exposure by an enzyme-linked immunosorbent assay (ELISA) technique performed on the cell monolayer. RESULTS: There was a statistically significant increase in ICAM-1, VCAM-1 expression in the endothelial cells exposed to preeclamptic and nonpregnant plasma compared with those exposed to normotensive plasma. Pretreatment with LTZ could reduce the expression of ICAM-1 exposed to preeclamptic plasma, and reduce the expression of VCAM-1 exposed to any of the three sources of plasma. CONCLUSIONS: Preeclamptic plasma induces ICAM-1 and VCAM-1 expression in HUVEC in vitro. Ligustrazine may inhibit the upregulation effects of ICAM-1 and VCAM-1 expression induced by preeclamptic plasma.

Adult↗
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↗
PubMed1992

Functional expression of a full-length cDNA coding for rat neural cell adhesion molecule L1 mediates homophilic intercellular adhesion and migration of cerebellar neurons.

Neural cell adhesion molecule L1 is postulated to be involved in cell-cell interaction, neurite elongation, fasciculation of axons, cell migration, and myelination. To determine the function of L1 directly, we have transfected rat L1 cDNA into mouse fibroblast L cells. Stable transformants expressing L1 showed uniform surface expression of the molecule without phenotypic changes. Dispersed L1-expressing transfectants aggregated with faster kinetics than control cells in a homophilic manner. Divalent cations were not required for this cell aggregation. L1-transfected cells markedly enhanced neuronal cell adhesion and migration in co-culture with rat cerebellar neurons. These results indicate that L1 is involved in a determinant step of neural development through molecular interactions.

Animals↗
PubMed2006

Expression and adhesive activity of SC1, an Ig superfamily cell adhesion molecule, in sporadic nephroblastomas of chicken.

SC1, an immunoglobulin superfamily cell adhesion molecule, is transiently expressed during avian embryogenesis by a variety of cell types. This molecule has a homophilic binding activity with SC1 itself and promotes neurite projection from embryonic neurons. However, the potential role of this molecule in pathologic tissue specimens from chickens has yet to be elucidated. In this study, we examined the expression and functional role of SC1 in the sporadic nephroblastomas of chickens. Western blot analysis showed SC1 to be recognized as approximately 100 kDa and enriched in embryonic metanephros with a lower level in the adult kidney, while it was overexpressed in nephroblastomas. Immunohistochemically, SC1 was abundantly found in the tubular epithelia and blastemal cells of embryonic metanephros. In contrast, it had almost completely disappeared in the adult kidney; parts of the distal convoluted and intermediated tubules, collecting ducts, and Bowman's capsule slightly expressed SC1. In all 32 cases of nephroblastoma, SC1 was overexpressed in most characteristic components in tumors such as neoplastic epithelia with various types of differentiation, blastemal cell condensations, and glomeruloid bodies. Primary culture cells from a nephroblastoma expressed SC1 on the cell surface, whereas cells from the adult kidney showed only weak expression. A cell aggregation assay revealed that the dissociated cells from a nephroblastoma have strong aggregation activity, which was inhibited by anti-SC1 antibody. In contrast, the self-aggregation of adult chicken kidney cells was weaker than that of the tumor and not inhibited by the antibody. These findings suggest that the expression of SC1 might play a potential role in both the structural formation of nephroblastomas, based on its adhesive activity, and normal renal development.

Activated-Leukocyte Cell Adhesion Molecule↗
PubMed1991

A monoclonal antibody to the human leukocyte adhesion molecule intercellular adhesion molecule-2. Cellular distribution and molecular characterization of the antigen.

The DNA of the human leukocyte adhesion molecule intercellular adhesion molecule-2 (ICAM-2) was synthesized by the polymerase chain reaction, and a protein A-ICAM-2 fusion protein was expressed in Escherichia coli. The fusion protein was used as immunogen to obtain mAb to ICAM-2. The 6D5 antibody was selected by its reactivity in immunofluorescence with the endothelial cell line Eahy926. The antibody precipitated a 55,000 m.w. glycoprotein from radioactivity surface labeled cells and also reacted in Western blotting. As measured by immunofluorescence flow cytometry, the antibody reacted with lymphoblastoid B cells of normal origin, some Burkitt lymphoma cell lines, vascular endothelial cells, the endothelial cell line Eahy926, 4 and a subpopulation of Con A-stimulated blood mononuclear cells. The two Ig-like domains of ICAM-2 were separately expressed in E. coli, and the antibody was shown to react with the NH2-terminal domain. The antibody inhibited the CD11/CD18-dependent binding of HL-60 promyelocytic leukemia cells to transfected COS-1 cells.

Antibodies, Monoclonal↗
PubMedDate not supplied

[The molecular factors of the cell adhesion of neural tissues and the Ca2+-independent adhesion system].

The review discusses various technical approaches to identification of plasma membrane and extracellular matrix proteins involved in cell adhesion. Physicochemical characteristics of macromolecular factors of the Ca2(+)-independent adhesion system in neural tissue cells are discussed alongside with the findings on their biosynthesis and expression on the cell surface at different stages of embryogenesis.

Animals↗
PubMed1994

Function of adhesion molecules lymphocyte function-associated antigen-3 and intercellular adhesion molecule-1 on human epidermal Langerhans cells in antigen-specific T cell activation.

In addition to the interaction between the TCR and the MHC/Ag complex on the APC, optimal T cell activation also requires interaction between adhesion molecules on the APC and their ligands on T cells. We determined the presence of adhesion molecules on human epidermal Langerhans cells (LC) and their role in Ag-specific T cell activation. Freshly isolated LC did not display ICAM-1 (CD54), ICAM-2, LFA-1 (CD11a), and LFA-3 (CD58), as detected by double-color FACS analysis, using HLA-DR expression for LC identification. Upon culture, LC clearly expressed ICAM-1 and LFA-3, both already detectable after 1 day, reaching a plateau at day 2. ICAM-2 and LFA-1 were undetectable on cultured LC and attempts to induce this expression by different culture conditions remained unsuccessful. mAb against ICAM-1, LFA-1, LFA-3, and CD2, continuously present during culture, inhibited the T cell proliferative response to Candida albicans presented by cultured LC. Pretreatment of LC and/or T cells with mAb indicated that anti-ICAM-1 and anti-LFA-3 inhibited at the LC level, whereas anti-LFA-1 and anti-CD2 inhibited at the T cell level. The mAb-induced inhibition was dose-dependent, but a total blockade of the response was never achieved. Time-course observations revealed that ICAM-1 and LFA-3 on LC only functioned during the initiation phase of T cell activation. Our study demonstrates that both ICAM-1 and LFA-3 on LC considerably contribute to the generation of a T cell response. The high expression of these accessory molecules enable LC, at least in part, to perform their powerful Ag-presenting function.

Antigen-Presenting Cells↗
PubMed1994

High endothelial venules and cell adhesion molecules in B-cell chronic lymphocytic leukaemia and related low grade B-cell lymphoma/leukaemia: II. Expression of cell adhesion molecules in lymph nodes biopsies.

The expression of cell adhesion molecules (LECAM-1, LFA-1, VLA-4, ICAM-1 and CD44) of lymph nodes from B-cell chronic lymphocytic leukaemia (B-CLL; mature: 16 cases, immature: 8), lymphocytic lymphoma (LL; M:5, IM:2) and reactive lymph nodes (10) were investigated in frozen tissue sections. In order to assess the B- and T-cell compartments of the lymph nodes some additional markers CD3, CD20, CD45 RO were used, and for follicular dendritic reticulum cells (FDCs) CD35. The expression of the LECAM-1 molecule was correlated to the expression of activation (CD23, CD25) and proliferation (Ki67) markers. Findings, in accordance with the relevant data of the literature, indicate that B-CLL and LL show and identical adhesion profile to the mantle zone of the germinal centres of reactive lymph nodes; namely, they were CD44+/LECAM-1+/VLA-4+. The T-zones of the reactive lymph nodes were characterized by an LFA-1+ and the follicles by an ICAM-1+ pattern, while in B-CLL and LL cases the LFA-1+ and ICAM-1+ were detected without coexpression of these molecules in only a small number of cases. The ratio and location of CD3+ and LFA-1+ cells was very similar in lymph nodes from B-CLL and LL, and from this fact may arise the suspicion that LFA-1+ reported in LL cases derive from the sometimes significant T-cell compartment of the diseased lymph nodes. The LECAM-1 molecule did not show any correlation with the investigated activation/proliferation markers.

Biopsy↗
PubMed1994

Expression of distinct fucosylated oligosaccharides and carbohydrate-mediated adhesion efficiency directed by two different alpha-1,3-fucosyltransferases. Comparison of E- and L-selectin-mediated adhesion.

Among five different human alpha 1 --> 3 fucosyltransferases cloned, fucosyltransferases III (Fuc-TIII) and IV (Fuc-TIV) differ significantly from each other. Fuc-TIII transfers a fucose to both sialylated and nonsialylated N-acetyllactosamine, but Fuc-TIV apparently transfers a fucose only to neutral N-acetyllactosamine. In this study, Chinese hamster ovary (CHO) cells were stably transfected with Fuc-TIII or Fuc-TIV, and the resultant cell lines, CHO-FTIII and CHO-FTIV, were compared for the carbohydrate structures and for their binding to E-selectin or L-selectin. CHO-FTIII and CHO-FTIV cells were labeled metabolically with [3H]galactose, and glycopeptides obtained from these cells were fractionated by serial lectin affinity chromatography. The fractionated glycopeptides were then subjected to various combinations of exoglycosidase treatment or endo-beta-galactosidase digestion. The results obtained can be summarized as follows. CHO-FTIII cells express sialyl Lewisx, Lewisx, and VIM-2 structures, whereas CHO-FTIV cells express only an Lex structure with a small amount of VIM-2 structure. When CHO-FTIII and CHO-FTIV cells were tested for adhesion to E-selectin expressed by tumor necrosis factor-activated endothelial cells and to an E-selectin chimeric protein, only CHO-FTIII cells were found to adhere well to E-selectin. Moreover, both CHO-FTIII and CHO-FTIV cells failed to adhere to an L-selectin chimeric protein. These results clearly indicate that FT-III and FT-IV direct distinctly different fucosylated oligosaccharides. This difference in oligosaccharide structures results in an entirely different efficiency in adhesion to E-selectin. The results also demonstrate that expression of sialyl Lex itself is not sufficient for L-selectin binding.

Animals↗
PubMed1994

12-O-tetradecanoylphorbol-13-acetate- and tumor necrosis factor alpha-mediated induction of intercellular adhesion molecule-1 is inhibited by dexamethasone. Functional analysis of the human intercellular adhesion molecular-1 promoter.

Transcription regulation of the human intercellular adhesion molecule-1 gene by the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA), tumor necrosis factor alpha (TNF alpha), and the glucocorticoid dexamethasone was studied using transient transfections in 293 cells with intercellular adhesion molecule-1 promoter-luciferase constructs (together with a glucocorticoid receptor expression vector). TPA and TNF alpha induced promoter activity, which was repressed by dexamethasone. Four TPA-responsive DNA regions were identified, each containing a potential TPA-responsive enhancer sequence: 1) -677/-340 an AP3-like sequence; 2) -290/278 a TPA-response element (TRE); 3) -227/-175 an NF kappa B-like sequence; 4) -105/-38 an AP2-like sequence. TNF alpha enhanced transcription only through region 3. The TRE in region 2 appeared to be functionally coupled to a distal TATA box at -313 and differed from the consensus TRE with respect to binding characteristics for members of the AP1 family. The newly identified NF kappa B enhancer (TGGAAATTCC) is bound by a TNF alpha-induced nuclear protein and appears to be the key element in rapid transcription induction by TNF alpha (and TPA), while transactivation of this element is repressed by the ligand-bound glucocorticoid receptor. We propose a negative cross-talk between the NF kappa B transcription factor and the glucocorticoid receptor.

Base Sequence↗