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PubMed2006

Binding of human serum amyloid P componentto L-selectin.

Serum concentrations of soluble L-selectin by far exceed those of other soluble adhesion molecules, and serum soluble L-selectin concentrations are remarkably stable upon prolonged storage. We present evidence for Ca(2+)-dependent binding interactions between human serum amyloid P (SAP), a proteolysis-resistant pentraxin glycoprotein, and L-selectin, as shown by surface plasmon resonance measurements, protein band shift assays in a native PAGE system, and after SDS-PAGE and membrane transfer. Monoclonal antibodies to L-selectin strongly reduced binding of biotinylated SAP to L-selectin-IgG chimeras immobilized on microtiter plates. As binding was reduced by prior glycopeptidase F treatment of L-selectin but not of SAP, it appears to be based on SAP lectin domain interactions with N-linked L-selectin carbohydrates. In freshly prepared human lymphocytes, SAP incubation induced expression of a beta2 integrin neoepitope associated with high-affinity binding. This was partially blocked by pre-incubation with Fab fragments of two anti-L-selectin antibodies. In flow chamber experiments, SAP inhibited the adherence of human neutrophils to activated endothelium under shear stress. Thus, SAP binds to human L-selectin and affects L-selectin-dependent leukocyte-endothelial interactions.

Antibodies, Monoclonal↗
PubMed2000

Acquisition of P-selectin binding activity by en bloc transfer of sulfo Le(x) trisaccharide to the cell surface: comparison to a sialyl Le(x) tetrasaccharide transferred on the cell surface.

Sialyl Le(x), NeuNAcalpha2 --> 3Galbeta1 --> 4(Fucalpha1 --> 3)GlcNAcbeta --> R, is known to be a ligand for E-selectin in various assays. The sulfated counterpart of sialyl Le(x), sulfo Le(x), (Sulfo --> 3) Galbeta1 --> 4 (Fucalpha1 --> 3) GlcNAcbeta --> R, was also shown to be a ligand for E-selectin in solid-phase assays employing immobilized oligosaccharides. In order to determine whether sulfo Le(x) structure on the cell surface also works as E-selectin or P-selectin ligand, a novel approach for in vitro transfer of oligosaccharides (S. Tsuboi, Y. Isogai, N. Hada, J. K. King, O. Hindsgaul, and M. Fukuda (1996) J. Biol. Chem. 271, 27213-27216) was utilized. A synthetic GDP-fucose harboring sialyl Le(x) or sulfo Le(x) oligosaccharide was enzymatically transferred to Chinese hamster ovary (CHO) cells with a milk fucosyltransferase. The resultant cells, CHO-sialyl Le(x) and CHO-sulfo Le(x) were tested for adhesion to E-selectin. IgG or P-selectin. IgG chimeric protein coated on plates. The results indicate that CHO-sialyl Le(x) adhered efficiently to E-selectin, while adhesion of CHO-sulfo Le(x) was very poor despite the fact that near equal number of the ligands had been attached to the cell surface. In contrast, CHO-sulfo Le(x) adhered efficiently to P-selectin, while CHO-sialyl Le(x) adhered modestly to P-selectin. These results demonstrate that sialyl Le(x) and sulfo Le(x) structures on the cell surface differ substantially in their ability to adhere to E- and P-selectin.

Animals↗
PubMed2001

Species-specific and conserved epitopes on mouse and human E-selectin important for leukocyte adhesion.

Selectins are C-type, cell surface lectins that are key players in leukocyte adhesion to the blood vessel wall endothelium. We describe here epitopes for a series of novel monoclonal antibodies (moAbs), UZ4-UZ7, directed against mouse E-selectin. All four antibodies specifically bind to mouse E-selectin, but not to P- or L-selectin, and all inhibit the adhesion of granulocytes, peripheral blood lymphocytes, and promyelocytic HL-60 cells to cytokine-activated mouse endothelium. Three moAbs, UZ5, UZ7, and UZ6, specifically inhibit mouse E-selectin-mediated adhesion by binding to epitopes in domains CR1 or CR2. moAb UZ4 inhibits leukocyte adhesion to both human and murine endothelium activated with IL-1 or other proinflammatory stimuli. UZ4 is the first described moAb that detects an epitope in the lectin domain which is conserved in both murine and human E-selectin (CXKKKL), but is not present in the other members of the selectin family, P- and L-selectin. Interestingly, UZ5, UZ6, and UZ7 more efficiently interfere with lymphocyte than with granulocyte adhesion to cytokine-activated endothelium, while UZ4 completely blocks adhesion of PMN, lymphocytes, and HL-60 and U937 cell lines. The data suggest that E-selectin-ligand engagement differs between lymphocytes and PMN, and that these differences may be accentuated by the CR1 and CR2 domains in the E-selectin cell adhesion molecule.

Amino Acid Sequence↗
PubMed2001

Induction of E-selectin after partial hepatectomy promotes metastases to liver in mice.

BACKGROUND: The liver is the most frequent site of tumor metastasis. It has been suggested that partial hepatectomy promotes liver metastasis of malignant disease and that expression of E-selectin, a cell adhesion molecule, plays roles in tumor metastasis. However, no reports are available concerning the expression of E-selectin after hepatectomy. METHODS: In the present study, we used BALB/c mice subjected to 30% partial hepatectomy after injection of 1 x 10(4) colon 26 cells to determine the effects of partial hepatectomy on tumor metastasis to liver. E-Selectin expression within the liver after partial hepatectomy was evaluated using reverse transcription polymerase chain reaction and Western blotting. In addition, we injected polyclonal antibody to E-selectin into mice in which partial hepatectomy had augmented liver metastasis. RESULTS: Mice subjected to partial hepatectomy had significantly increased numbers of liver metastases (sham operation, 1.5 +/- 2.0, vs partial hepatectomy, 35.5 +/- 19.3; P < 0.001). Expression of E-selectin mRNA within the liver was markedly increased 4 h after partial hepatectomy, but subsequently decreased at 24 h. E-Selectin protein was detected 8 h after hepatectomy, but subsequently decreased at 24 h as measured by Western blotting. Mice subjected to intraperitoneal injection of neutralizing antibody after operation had significantly decreased numbers of liver metastases (phosphate-buffered saline, 20.6 +/- 9.2, P < 0.05, and normal IgG, 18.0 +/- 8.0, P < 0.05, compared with polyclonal antibody to E-selectin, 5.6 +/- 4.8). CONCLUSION: Induction of E-selectin by partial hepatectomy promotes hematogenous liver metastasis. Our findings can be applied to surgical treatment of liver tumor to reduce the recurrence of liver metastasis after hepatectomy by inhibiting E-selectin-mediated adhesion using reagents to E-selectin.

Animals↗
PubMed2001

Inhibition of P-selectin specific cell adhesion by a low molecular weight, non-carbohydrate compound, KF38789.

OBJECTIVE AND DESIGN: P-selectin is a cell adhesion molecule of the selectin family. This study evaluated the effects of novel, low molecular weight P-selectin inhibitors in a cell adhesion assay and a murine model of peritonitis. MATERIALS: U937 or HL60 was used for cell adhesion assay. Human polymorphonuclear cells were studied for the production of superoxide. BALB/c mice were used for the in vivo study. TREATMENT: The thioglycollate (TG)-induced accumulation of leukocytes in mice was measured 6 h after the treatment. KF38789 or antibody (1 mg/kg) was injected intravenously prior to TG injection and at 3 h following initial injection. RESULTS: Low molecular weight, non-carbohydrate inhibitors against P-selectin- mediated cell adhesion were tested. One of the most potent inhibitors, KF38789, inhibited the binding of U937 cells to immobilized P-selectin immunoglobulin G chimeric protein (P-selectin-Ig) with an IC50 value of 1.97 microM. Cell adhesion to both E-selectin-Ig and L-selectin-Ig were not affected even by 100 microM of KF38789. Moreover, KF38789 inhibited P-selectin-induced superoxide production from human polymorphonuclear cells. Intravenously injected KF38789 significantly inhibited the TG-induced accumulation of leukocytes in the mouse peritoneal cavity (p<0.01). CONCLUSION: A novel low molecular weight compound, KF38789, specifically inhibited P-selectin-dependent cell adhesion and the leukocyte recruitment in mouse peritonitis.

Animals↗
PubMed2004

P-selectin in arterial thrombosis.

P-selectin is a transmembrane protein present in the alpha granules of platelets and the Weibel-Palade bodies of endothelial cells. Following activation, it is rapidly translocated to the cell surface. P-selectin expression in platelets has been shown to be elevated in disorders associated with arterial thrombosis such as coronary artery disease, acute myocardial infarction, stroke, and peripheral artery disease. P-selectin mediates rolling of platelets and leukocytes on activated endothelial cells as well as interactions of platelets with leukocytes. Platelet P-selectin interacts with P-selectin glycoprotein ligand-1 (PSGL-1) on leukocytes to form platelet-leukocyte aggregates. Furthermore, this interaction of P-selectin with PSGL-1 induces the upregulation of tissue factor, several cytokines in leukocytes and the production of procoagulant microparticles, thereby contributing to a prothrombotic state. P-selectin is also involved in platelet-platelet interactions, i. e. platelet aggregation which is a major factor in arterial thrombosis. P-selectin interacts with platelet sulfatides, thereby stabilizing initial platelet aggregates formed by GPIIb/IIIa-fibrinogen bridges. Inhibtion of the P-selectin-sulfatide interaction leads to a reversal of platelet aggregation. Thus, P-selectin plays a significant role in platelet aggregation and platelet- leukocyte interactions, both important mechanisms in the development of arterial thrombosis.

Animals↗
PubMed1998

Enhanced expression of selectins in human skin wounds.

The aim of the study was to characterize the vitality and age of skin wounds by the detection of selectins. A prospective study was conducted for this purpose in which 197 vital human skin wounds (time since injury ranging from 3 min to 790 days) were investigated immunohistologically. Of the samples tested, 97 were taken from autopsy material and 100 from patient material from the department of surgery at the university hospital. The selectins were detected in paraffin sections after autoclaving and using the ABC technique. The intensity was rated by a semi-quantitative evaluation using a four-stage ordinal scale. Strong positive immunohistochemical reactions were observed for the P-selectin 3 min at the earliest and 7 h at the latest after the time of injury. For the E-selectin a positive staining was evident I h at the earliest and 17 days at the latest from the time the skin was injured. The staining intensity decreased significantly after an interval of 12 h from the time of injury (P < 0.05). The L-selectin was regularly detected on leukocytes in the samples of injured skin. The immunohistochemical results for the P- and E-selectins were significantly different between injured and uninjured skin (P < 0.01). The expression of the selectins is indicative of the vitality of the wound. P-selectin was detected in a few cases (n=4) at low intensity while E-selectin could not be found in the control samples (n=31) of postmortem skin wounds. The use of P- and E-selectins for forensic purposes can help to achieve better estimates of the age of wounds with short survival times.

Female↗
PubMed2000

Serum concentration of E-selectin in patients with chronic hepatitis, liver cirrhosis and hepatocellular carcinoma.

OBJECTIVES: High levels of soluble E-selectin have been reported in acute and chronic inflammatory disorders. Moreover, in some types of tumor elevated values have been found while in other types reduced levels have been reported. Our aims were to determine whether soluble E-selectin levels might be useful in monitoring the progression of chronic liver disease, including hepatocellular carcinoma. METHODS: Circulating soluble E-selectin was measured by an enzyme-linked immunosorbent assay in the sera of 18 patients with chronic hepatitis, 44 with liver cirrhosis, and 38 with hepatocellular-carcinoma-associated liver cirrhosis. Immunohistochemical localization of E-selectin was also performed on liver tissue specimens of patients with chronic hepatitis, liver cirrhosis and hepatocellular carcinoma. RESULTS: Serum levels of soluble E-selectin were higher in the chronic hepatitis and liver cirrhosis patients than in the hepatocellular carcinoma patients and healthy controls. Levels in the hepatocellular carcinoma patients and controls were not significantly different. In the liver cirrhosis group, divided according to the Child-Pugh classification, soluble E-selectin decreased with disease severity. Similarly, in patients with liver cirrhosis who developed hepatocellular carcinoma, soluble E-selectin decreased as the disease progressed. Immunohistochemical localization showed strong membrane staining on endothelial cells in areas rich in inflammatory cells in severe chronic hepatitis. In some hepatocellular carcinoma tissues a marked E-selectin staining was observed on endothelial cells of tumor-associated small vessels. CONCLUSIONS: The results obtained suggest that high serum levels of soluble E-selectin are associated with chronic hepatitis and liver cirrhosis, and that levels decrease in liver cirrhosis patients as the disease progresses. Patients with hepatocellular carcinoma have different types of soluble E-selectin behaviour the significance of which requires further investigation.

Adult↗
PubMed1996

Expression and functional characterization of the P-selectin glycoprotein ligand-1 in various cells.

We have examined the expression and function of P-selectin glycoprotein ligand-1 (PSGL-1), which is a high affinity ligand for P-selectin. Northern blot and flow cytometric analysis demonstrated that a variety of hematopoietic cells and cell lines expressed PSGL-1. However, P-selectin binding ability was dependent on the additional expression of a carbohydrate structure, sialyl Lewis x (sLex). All the peripheral lymphocytes expressed PSGL-1 and subpopulation expressed sLex. Two color analysis showed that the majority of the cells that bound P-selectin were sLex-negative I lymphocytes, and most of the sLex-positive cells were B lymphocytes that did not blind P-selectin, indicating that the carbohydrate on T lymphocytes recognized by P-selectin is not sLex, and that the sLex on B lymphocytes is not readily presented for P-selectin recognition. Transfected 293 cells detectably bound P-selectin only when the cells expressed both PSGL-1 and sLex. When cysteine 310 of PSGL-1 was mutated to alanine, P-selectin binding was markedly reduced, suggesting the importance of dimerization of PSGL-1. These findings indicate that a preferable conformation of both carbohydrate and protein structure is necessary for a functional P-selectin ligand.

B-Lymphocytes↗
PubMed2005

P-selectin expression, neutrophil infiltration, and histologic injury in neonates with necrotizing enterocolitis.

BACKGROUND/PURPOSE: P-selectin promotes adherence of leukocytes to the endothelium in inflammatory processes. The aim of this study was to investigate the expression of P-selectin and its role in the development of inflammation in neonates with necrotizing enterocolitis (NEC). METHODS: Twenty-nine intestinal specimens from 13 neonates with NEC and 7 control neonates with congenital gastrointestinal abnormalities were studied. Histologic damage, immunohistochemical expression of P-selectin, and polymorphonuclear cell infiltrate were graded blindly. Mann-Whitney U and Spearman rank tests were used to compare grades. RESULTS: Expression of P-selectin was increased in NEC compared with controls in both medium-sized vessels (P = .03) and in the microcirculation (P = .03). P-selectin expression on medium-sized vessels correlated with the degree of histologic injury (P = .02, r = 0.425). P-selectin expression was greatest in areas of active inflammation but markedly lower in necrotic areas. The degree of polymorphonuclear cell infiltration strongly correlated with P-selectin expression on both medium-sized vessels (P = .004, r = 0.513) and the microcirculation (P = .001, r = 0.578). CONCLUSIONS: Expression of P-selectin is increased in medium-sized vessels and in the microcirculation in intestinal specimens of neonates with NEC compared with neonatal controls. Expression of P-selectin is associated with the recruitment of polymorphonuclear cells and the severity of histologic injury, although P-selectin expression is lost in necrotic tissue.

Enterocolitis, Necrotizing↗
PubMed2004

Independent pathways of P-selectin and complement-mediated renal ischemia/reperfusion injury.

Evidence from in vitro studies indicates that complement activation regulates the expression of P-selectin on endothelial cells. This suggests that in disorders such as ischemia/reperfusion injury, in which both complement and P-selectin have been shown to play a role, complement activation is a primary event and the effects of P-selectin are secondary. To test this hypothesis in vivo, we examined a mouse kidney model of ischemia/reperfusion injury. Surprisingly, the time course and extent of expression of P-selectin was unaltered in C3-deficient mice compared with wild-type mice, in which there was rapid but transient up-regulation of P-selectin on capillary walls and slower accumulation of complement split product on the tubular epithelium. In addition, treatment with anti-P-selectin antibody to reduce the neutrophil-mediated reperfusion damage was equally effective in the absence of C3. These data imply that complement and P-selectin-mediated pathways of renal reperfusion injury are mutually independent, a conclusion that is possibly explained by the differences in the location and time kinetics of complement activation and P-selectin expression. We conclude that in vivo interaction between complement and P-selectin is limited because of time and spatial considerations. Consequently, complement and P-selectin pose distinct targets for therapy.

Animals↗
PubMed1997

Quantifying rolling adhesion with a cell-free assay: E-selectin and its carbohydrate ligands.

Rolling of neutrophils over stimulated endothelial cells is a prerequisite to firm attachment and subsequent transendothelial migration during the inflammatory response. The selectin family of adhesion molecules are thought to mediate rolling by binding counter-receptors that present carbohydrates, such as sialyl Lewis(x) (sLe[x]). Recently we described a cell-free system for rolling using sLe(x)-coated microspheres and E-selectin molecules on inert substrates. We showed that sLe(x)-coated microspheres rolled over E-selectin-IgG chimera substrates with dynamics that are similar to those of leukocytes rolling over stimulated endothelium. In this paper we provide a thorough quantitative description of the dynamics of adhesion for this system. We find that particle rolling velocity increases with increasing wall shear stress and decreases with increasing E-selectin or sLe(x) surface densities. Large changes in the average rolling velocity can occur with small changes in sLe(x) or E-selectin density; however, rolling velocity is more sensitive to E-selectin surface coverage than to the number of sLe(x) molecules on the microspheres. Aided by dimensional analysis, we show that decreasing the wall shear stress or increasing either receptor (E-selectin) or ligand (sLe[x]) surface coverage results in an equivalent decrease in particle rolling velocity. In addition, we find that different Lewis carbohydrates are more effective in mediating rolling on E-selectin, with effectiveness following the trend sialyl Lewis(a) > sialyl Lewis(x) >> sulfated Lewis(x) >> Lewis(x). Rolling velocity fluctuated with time for all carbohydrate-selectin pairs tested, and the magnitude of the velocity fluctuations was linearly proportional to the mean rolling velocity for all combinations of E-selectin site density, sLe(x) site density, wall shear stress, and carbohydrate chemistry tested.

Biophysical Phenomena↗
PubMed2000

Oxidized lipoprotein(a) enhanced the expression of P-selectin in cultured human umbilical vein endothelial cells.

Lipoprotein(a) [Lp(a)] has been demonstrated to be an independent risk factor for coronary heart disease. However, the precise mechanism by which it contributes to the development of atherosclerosis remains unclear. P-selectin is one of the major adhesion molecules to mediate the interaction between monocytes, platelets and endothelial cells. Increased expression of P-selectin has been frequently found in atherosclerotic lesions. The present study assessed the effects of native and oxidized LDL (n-LDL and ox-LDL) and Lp(a) (n-Lp(a) and ox-Lp(a)) on the expression of P-selectin in cultured human umbilical vein endothelial cells (HUVECs). Cell ELISA was used to measure the expression of P-selectin in HUVECs and monocyte adhesion assay was used to detect whether the P-selectin expressed in HUVECs was functional. P-selectin mRNA expression in HUVECs was determined by Northern blot. Results showed that P-selectin protein expression was not influenced by n-LDL, but was moderately increased by ox-LDL and n-Lp(a). ox-Lp(a) was the most potent stimulus for P-selectin expression, increasing it in HUVECs by 144 +/- 10% at 10 nmol/l and 202 +/- 22% at 20 nmol/l. In addition, it showed that dose dependency induced monocyte adherence to endothelial cells after incubation of HUVECs with ox-Lp(a). Northern blot analysis demonstrated that the amount of P-selectin mRNA was markedly increased after treatment with ox-Lp(a) but not with n-LDL, ox-LDL and n-Lp(a). These results demonstrate that ox-Lp(a) can induce P-selectin expression in HUVECs, which may thereby influence the pathogenesis of athersclerosis.

Cell Adhesion↗
PubMed1995

Cleaved L-selectin concentrations in meningeal leukaemia.

Involvement of the central nervous system has important therapeutic implications in acute leukaemia. Because the identification of blast cells in cerebrospinal fluid (CSF) is often difficult, there is a need for sensitive markers of leukaemic infiltration. Since the shed form of L-selectin (sL-selectin) is frequently increased in acute leukaemia (sL-selectin+ leukaemia), we examined whether assay of sL-selectin in CSF could improve our ability to detect such meningeal involvement. CSF sL-selectin was significantly (p < 0.001) higher in 15 patients with sL-selectin+ meningeal leukaemia (median 60 ng/mL, range 34-150) than in 20 patients with acute leukaemia without meningeal involvement (12 ng/mL, 1-39) or 88 control patients (14 ng/mL, 0-37). Serial measurements of sL-selectin in patients with sL-selectin+ leukaemic meningitis showed increased CSF concentrations of the cleaved receptor in 4 patients with therapy-resistant meningeal leukaemia and sustained normal concentrations in 9 patients in remission. Our results suggest that CSF sL-selectin may be a useful marker in the detection of meningeal involvement by blast cells in patients with sL-selectin+ leukaemia.

Adult↗
PubMed2001

Serum L-selectin and ICAM-1 in patients with Graves' ophthalmopathy during treatment with corticosteroids.

UNLABELLED: Circulating forms of L-selectin were found to be elevated in several autoimmune diseases. ICAM-1 has been suggested a predictor of the onset of GO. The aim of the study was an estimation of serum L-selectin and ICAM-1 in patients with Graves' disease with ophthalmopathy during treatment with corticosteroids to assess their potential as a guideline of immunosuppressive therapy. We detected serum L-selectin and ICAM-1 in three groups of subjects: 20 patients with Graves' disease without ophthalmopathy (Gd), 17 patients with clinical symptoms of ophthalmopathy (CAS> or =3, anamnesis of GO> or =1 year) and 24 healthy volunteers. Corticosteroid therapy consisted of intravenous infusions of methyloprednisolone (MP) and subsequent treatment with oral prednisone (P). The serum samples were collected 24 h before MP, 24 h after MP, 12+/-2 days of treatment with prednisone and after the end of the corticosteroid therapy. The levels of soluble L-selectin and ICAM-1 in the serum were determined by the ELISA method. The statistical significance was estimated by the Mann-Whitney U-test. Serum L-selectin and ICAM-1 were significantly increased in patients with GO (respectively 1182+/-222 and 438+/-68 ng/ml) and in patients with Graves' disease without ophthalmopathy (respectively: 1168+/-130 and 343+/-109) in relation to the controls. After MP treatment in corticosteroid-responsive patients (improvement in CAS < or =1) serum concentration of L-selectin and ICAM-1 decreased significantly and gradually increased during subsequent treatment with prednisone. In corticosteroid-responsive patients serum L-selectin was significantly higher before MP administration and after P treatment in relation to corticosteroid-resistant subjects. CONCLUSIONS: 1. Serum L-selectin and ICAM-1 were elevated in patients with active GO 2. Methyloprednisolone decreased levels of the studied adhesion molecules in corticosteroid-responsive patients with GO 3. Lack of clinical results in corticosteroid therapy in patients with a low starting L-selectin level would suggest the possibility of serum L-selectin estimation as a prognostic for immunotherapy efficacy.

Adult↗
PubMed2001

Soluble P-selectin and the success of thrombolysis in acute myocardial infarction.

BACKGROUND: P-Selectin mediates adhesive interactions between platelets, leukocytes and endothelium to form thrombi. Our purpose was to investigate plasma soluble(s) P-selectin levels in patients with acute myocardial infarction (aMI) and the effect of thrombolysis on P-selectin levels. METHODS: Patients with aMI within the first 6 h of chest pain were enrolled prospectively. sP-selectin levels were determined by ELISA in the plasma of patients with aMI (n=32), stable angina (n=18), and healthy controls (n=15). Samples were obtained before, 3 and 24 h after reperfusion therapy with tissue plasminogen activator. Seven patients showed recurrent angina or failure to reperfuse. RESULTS: sP-selectin levels were significantly higher in aMI group than other groups (86.7+/-8.7 ng/ml, P<0.05). sP-selectin levels were similar in stable angina and control groups (28.8+/-4.4 vs. 25.4+/-7.3 ng/ml, P=NS). A significant increase in sP-selectin levels was observed 3 h after successful thrombolysis and this was followed by a decrease to near the baseline level late after reperfusion. But patients with failed reperfusion showed sustained high sP-selectin levels after 24 h of thrombolysis (P<0.05). CONCLUSION: The plasma sP-selectin level is elevated in aMI and it increases further following thrombolytic therapy. This increase is probably induced by activation of endothelial cells or platelets after myocardial ischemia and reperfusion during aMI. As the elevated levels are sustained in patients with failed reperfusion, serial P-selectin levels may be used as a non-invasive indicator of successful thrombolysis in aMI.

Angina Pectoris↗
PubMed2004

Increase in soluble E-selectin level after PTCA and stent implantation: a potential marker of restenosis.

BACKGROUND: E-Selectin is expressed only on activated endothelial cells, and may be used as a marker of endothelial activation. The relationship between soluble form of E-selectin (sE-selectin) and development of restenosis after balloon angioplasty (PTCA) is controversial, and there are no data for after stent implantation. We evaluated the role of serially measured sE-selectin levels in predicting the development of restenosis after PTCA and stent implantation. METHODS: In sixty-one patients with stable angina pectoris who underwent PTCA (n=20) or stent implantation (n=41), peripheral blood samples were taken just before (baseline), at 3 and at 24 h after the intervention. sE-Selectin levels were measured by ELISA. Coronary angiography was repeated at 4-6 months after the intervention, and > or =50% stenosis at the site of the intervention was regarded as restenosis. Levels and time course of sE-selectin after the intervention were compared in patients with and those without restenosis. RESULTS: sE-Selectin levels of the patients with and those without restenosis were similar at each of the three measurements, and significantly increased after the intervention both in the PTCA and stent groups (P<0.001 for both groups). Posthoc analysis showed that sE-selectin levels increased significantly at 3 h after PTCA (P=0.024) and stent implantation (P=0.018), and did not change thereafter in patients with restenosis. In the nonrestenotic group, sE-selectin did not change significantly in the 24 h following PTCA, however, a significant difference was observed only by comparing the values at baseline with those at 24 h after stent implantation (P=0.021). CONCLUSIONS: A substantial increase in sE-selectin levels early (at 3 h) after PTCA and stent implantation may predict development of restenosis.

Analysis of Variance↗
PubMed1998

[The correlation between salivary endothelial expression of E-selectin and clinical and biological parameters in systemic scleroderma].

OBJECTIVES: A body of evidence suggests the pivotal role of endothelial cells in the pathophysiology of systemic sclerosis. E-selectin is an adhesion molecule specifically expressed by activated endothelial cells. In previous studies we noticed that E-selectin was frequently expressed in the salivary gland tissue of patients with systemic sclerosis. Moreover, E-selectin expression was detectable very early in the course of the disease. To better define the role of E-selectin in the pathogenesis of systemic sclerosis, we conducted a study aimed at determining whether E-selectin expression was correlated to clinical and biological features in patients with systemic sclerosis. METHODS: Thirty-one patients presenting with systemic sclerosis were included in the study. The following parameters were systematically assessed: duration and cutaneous extent of the disease, presence of secondary Sjögren's syndrome, antinuclear antibodies, and pulmonary and esophagus involvement. E-selectin expression was assessed by immunocytochemistry on minor labial salivary glands. RESULTS: E-selectin expression was detected in 21 out of 31 patients (67%). The disease duration was significantly shorter in patients with E-selectin expression (mean 9.1 +/- 8.5 years versus 4.2 +/- 3.3 years, P < 0.05). No significant difference was found for other features. CONCLUSIONS: This study shows that endothelial E-selectin expression is mainly detectable early in the course of systemic sclerosis, when active and non-cicatrical sclerosis may be evidenced. No correlation was found between E-selectin expression and immunological disorders (antinuclear antibodies, secondary Sjögren's syndrome).

Adolescent↗