Serum soluble E- and L-selectin in the very early neonatal period

Giannaki, Galini; Rizos, Demetrios; Xyni, Kyriaki; Sarandakou, Angeliki; Protonotariou, Efthimia; Phocas, I.; Creatsas, George

doi:10.1016/s0378-3782(00)00115-8

Cited by 16 publications

(8 citation statements)

References 26 publications

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“…46 In addition, vascular endothelial cells from neonates may express different amounts and combinations of adhesion molecules at different developmental time points. 47 Therefore, a complete understanding of the mechanism(s) involved in stroke in sph/sph mice must address the particular complement(s) of adhesion molecules that are exposed on both erythroid and nonerythroid (eg, cerebrovascular endothelial) cells at different ages.…”

Section: Discussionmentioning

confidence: 99%

Increased erythrocyte adhesion in mice and humans with hereditary spherocytosis and hereditary elliptocytosis

Wandersee

Olson

Holzhauer

et al. 2004

Blood

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Mice with disruptions of the red blood cell (RBC) cytoskeleton provide severe hemolytic anemia models in which to study multiorgan thrombosis and infarction. The incidence of cerebral infarction ranges from 70% to 100% in mice with alpha-spectrin deficiency. To determine whether mutant RBCs abnormally bind adhesive vascular components, we measured adhesion of mouse and human RBCs to immobilized human thrombospondin (TSP) and laminin (LM) under controlled flow conditions. Mutant RBCs had at least 10-fold higher adhesion to TSP compared with normal RBCs (P <.006). Mutant relative to unaffected RBC adhesion to LM was significantly (P <.01) increased as well. Treatment of RBCs with the anionic polysaccharide dextran sulfate inhibited mutant RBC adhesion to TSP (P <.001). Treatment of RBCs with antibodies to CD47 or the CD47-binding TSP peptide 4N1K did not inhibit TSP adhesion of RBCs. Previously, we have shown that infarcts in alpha-spectrin-deficient sph/sph mice become histologically evident beginning at 6 weeks of age. TSP adhesion of RBCs from 3- to 4- and 6- to 8-week-old sph/sph mice was significantly higher than RBCs from adult mice (> 12 weeks old; P <.005). While the mechanism of infarction in these mice is unknown, we speculate that changes in RBC adhesive characteristics contribute to this pathology.

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Section: Discussionmentioning

confidence: 99%

Increased erythrocyte adhesion in mice and humans with hereditary spherocytosis and hereditary elliptocytosis

Wandersee

Olson

Holzhauer

et al. 2004

Blood

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“…I/R-induced microcirculator y dysfunction and subsequent tissue injury are a complicated process consisting of multiple reactions, among which leukocyte recruitment is a crucial step mediated by the expression of a group of adhesion molecules on neutrophils and endothelial cells. It was reported that peroxide produced by SMA I/R degrades I-κB for activation of NF-κB and induces the expression of vascular endothelial E-selectin and ICAM-1 [6][7][8][9][10] , and also transfers L-selectin and adhesion molecules CD11b and CD18 from leukocyte cytoplasm to the cell surface [11][12][13]38] , which initiates leukocyte rolling and adhesion ultimately. The ability of R1 to attenuate gut I/R-induced leukocyte rolling and adhesion in hepatic venules found in the present study is most probably due to its inhibiting effect on the expression of adhesion molecules on both leukocytes and endothelial cells, as suggested by the fact that pretreatment with R1 could significantly blunt SMA I/Rinduced expression of E-selectin on endothelium and CD18 on neutrophils.…”

Section: Applicationsmentioning

confidence: 99%

“…Oxygen free radicals produced by gut I/R activate nuclear factor kappa-B (NF-κB) [6,7] , initiate expression of selectin and adhesion molecules [8][9][10] , and elicit release of proinfl ammatory mediators like tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) [10] . The expression of L-selectin on leukocytes and E-selectin on endothelial cells induces the rolling of leukocytes along the vascular endothelium [11,12] , which further promotes the expression of adhesion molecules CD11b, CD18 on leukocytes and intercellular adhesion molecule-1 (ICAM-1) on endothelial cells, resulting in adhesion of leukocytes to vascular endothelial cells [2,4,13,14] . In addition, proinfl ammatory mediators produced by I/R enhance the expression of selectins and adhesion molecules, and aggravate the rolling and adhesion of leukocytes [8,15] .…”

Section: Introductionmentioning

confidence: 99%

Effect of notoginsenoside R1 on hepatic microcirculation disturbance induced by gut ischemia and reperfusion

Chen¹,

Wang²,

Liu³

et al. 2008

WJG

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AIM:To assess the effect of notoginsenoside R1 on hepatic microcirculatory disturbance induced by gut ischemia/reperfusion (I/R) in mice. METHODS:The superior mesenteric artery (SMA) of C57/BL mice was ligated for 15 min to induce gut ischemia followed by 30-min reperfusion. In another set of experiments, R1 was continuously infused (10 mg/kg per hour) from 10 min before I/R until the end of the investigation to study the influence of R1 on hepatic microcirculatory disturbance induced by gut I/R. Hepatic microcirculation was observed by inverted microscopy, and the vascular diameter, red blood cell (RBC) velocity and sinusoid perfusion were estimated. Leukocyte rolling and adhesion were observed under a laser confocal microscope. Thirty and 60 min after reperfusion, lactate dehydrogenase (LDH), alanine aminotransferase (ALT) and aspartate transaminase (AST) in peripheral blood were determined. The expression of adhesion molecules CD11b/CD18 in neutrophils and tumor necrosis factoralpha (TNF-α), interleukin-6 (IL-6) and monocyte chemotactic protein-1 (MCP-1) in plasma were evaluated by fl ow cytometry. E-selectin and intercellular adhesion molecule-1 (ICAM-1) in hepatic tissue were examined by immunofl uorescence.www.wjgnet.com RESULTS: After gut I/R, the diameters of terminal portal venules and central veins, RBC velocity and the number of perfused sinusoids were decreased, while the leukocyte rolling and adhesion, the expression of E-selectin in hepatic vessels and CD18 in neutrophils, IL-6, MCP-1, LDH, ALT and AST were increased. R1 treatment attenuated these alterations except for IL-6 and MCP-1. CONCLUSION:R1 prevents I/R-induced hepatic microcirculation disturbance and hepatocyte injury. The effect of R1 is related to its inhibition of leukocyte rolling and adhesion by inhibiting the expression of E-selectin in endothelium and CD18 in neutrophils.

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“…In newborn infants, levels have been shown to be highly elevated in comparison to that in adults. 13 A significant decrease in plasma sE-selectin concentrations occurs between the second and fifth postnatal days, reflecting its transient expression, which peaks and begins to decline before the appearance of CD35 ϩ cells. 13,14 Term-born infants have higher levels than do premature newborns.…”

mentioning

confidence: 99%

“…13 A significant decrease in plasma sE-selectin concentrations occurs between the second and fifth postnatal days, reflecting its transient expression, which peaks and begins to decline before the appearance of CD35 ϩ cells. 13,14 Term-born infants have higher levels than do premature newborns. 14,15 The time at which adult plasma levels are reached has not been investigated.…”

mentioning

confidence: 99%

Plasma sE-selectin in Premature Infants: A Possible Surrogate Marker of Retinopathy of Prematurity

Pieh¹,

Krüger

Lagrèze³

et al. 2010

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. To prospectively study plasma levels of soluble E-selectin (sE-selectin) in premature infants and to identify their relationship to retinopathy of prematurity (ROP) on the background of known clinical risk factors. METHODS. Eighty-five sE-selectin plasma samples from 42 preterm infants born at 23 to 32 weeks of gestational age (GA) were analyzed. Twenty-two of the infants did not have ROP, eight had stage I, seven stage II, and five stage III. Infants having no ROP or stage I were designated as the no-ROP group, and infants with stage II or III formed the ROP group. RESULTS. In ROP infants, sE-selectin levels were significantly increased, with a median plasma level of 74.7 ng/mL (range, 28.5-222.0) compared with that in the no-ROP infants, with a median sE-selectin plasma level of 39.7 ng/mL (range, 11.9-130.0, P = 0.005). Children with ROP were born with lower birth weight and at lower GA. They were ventilated and needed surfactant therapy more often. However, multivariate analysis identified only sE-selectin level and GA as independent predictors. An increase of 10 ng/mL in sE-selectin increased the risk of ROP 1.6-fold. Receiver operating characteristic curve analysis confirmed the clinical usefulness of sE-selectin plasma levels in the prediction of ROP. CONCLUSIONS. Elevated sE-selectin plasma levels are associated with the development of ROP and are an independent risk predictor in addition to other known risk factors. A score based on the infant's GA and sE-selectin plasma concentrations would improve ROP prediction. Plasma concentrations in premature infants should be assessed 2 to 3 weeks after birth.

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Serum soluble E- and L-selectin in the very early neonatal period

Cited by 16 publications

References 26 publications

Increased erythrocyte adhesion in mice and humans with hereditary spherocytosis and hereditary elliptocytosis

Increased erythrocyte adhesion in mice and humans with hereditary spherocytosis and hereditary elliptocytosis

Effect of notoginsenoside R1 on hepatic microcirculation disturbance induced by gut ischemia and reperfusion

Plasma sE-selectin in Premature Infants: A Possible Surrogate Marker of Retinopathy of Prematurity

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