P-selectin and intercellular adhesion molecule-1 expression after focal brain ischemia and reperfusion.

Okada, Yasushi; Copeland, Brian R.; Mori, Etsuro; Tung, M M; Thomas, W. S.; Zoppo, Gregory J. del

doi:10.1161/01.str.25.1.202

Cited by 394 publications

(218 citation statements)

References 57 publications

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“…The animals employed for these studies overlapped with those participating in published work on endothelial receptor up-regulation (Okada et al, 1994). Animals weighing 6.3-11.7 kg were conditioned for human contact and observed to be clinically without infection during a mandated quar antine period before entry into this study.…”

Section: Methodsmentioning

confidence: 99%

Polymorphonuclear Leukocyte Behavior in a Nonhuman Primate Focal Ischemia Model

Ember¹,

Zoppo

Mori

et al. 1994

J Cereb Blood Flow Metab

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Summary: There is increasing interest in the role of poly morphonuclear (PMN) leukocytes in the evolution of fo cal cerebral infarction. Surgical preparation of focal ce rebral ischemia models may alter leukocyte reactivity and thereby make interpretation of leukocyte function follow ing ischemiaireperfusion difficult. The effects of surgical preparation and of experimental ischemiaireperfusion on granulocyte function have been examined prospectively in a baboon model. Twenty-six adolescent male baboons underwent surgical preparation, of which 21 underwent middle cerebral artery occlusion/reperfusion. Four addi tional animals served as nonsurgical controls. Peripheral venous blood specimens were taken for performing as says of leukocyte function at defined intervals before and after both the surgical preparation (i.e., the overall pro cedure for implantation of the middle cerebral artery oc clusion device) and occlusionlreperfusion. A stress related elevation in total leukocyte number was attributed mainly to an increase in the number of circulating PMN leukocytes. Values rose from 13.9 ± 4.9 x 103 to 27.8 ± S.8 x 103/fLl, (±SD; n = 21) for total leukocyte number, withp < 0.001, and from 4.3 ± 2. 1 x 103 to IS.9 ± 4.7 x 103/fLi (n = 21) for PMN leukocytes, with p < 0.001.Polymorphonuclear (PMN) leukocytes may play an active and significant role in microvascular events (Ernst et aI

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Section: Methodsmentioning

confidence: 99%

Polymorphonuclear Leukocyte Behavior in a Nonhuman Primate Focal Ischemia Model

Ember¹,

Zoppo

Mori

et al. 1994

J Cereb Blood Flow Metab

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“…It has been reported that the expression of PECAM-1 or other cell adhesion molecules were increased in the spinal cord ischemia [4], focal cerebral ischemia [9,29], and other peripheral ischemia models [31,33,34]. The elevation of PECAM-1 immunoreactivity and its protein level in vessels increases the transmigration of lymphocytes and neutrophils [6,27].…”

Section: Discussionmentioning

confidence: 99%

Change in platelet endothelial cell adhesion molecule-1 immunoreactivity in the dentate gyrus in gerbils fed a folate-deficient diet

et al. 2007

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Folate deficiency increases stroke risk. We examined whether folate deficiency affects platelet endothelial cell adhesion molecule-1 (PECAM-1), which is an immunoglobulin-associated cell adhesion molecule and mediates the final common pathway of neutrophil transendothelial migration, in blood vessels in the gerbil dentate gyrus after transient forebrain ischemia. Gerbils were exposed to a folic acid-deficient diet (FAD) for 3 months and then subjected to common carotid artery occlusion for 5 min. In the control diet (CD)-and FAD-treated shamoperated groups, weak PECAM-1 immunoreactivity was detected in the blood vessels located in the dentate gyrus. PECAM-1 immunoreactivity in both groups was increased by 4 days after ischemic insult. PECAM-1 immunoreactivity in the FAD-treated group was twice as high that in the CD-treated-sham-operated group 4 days after ischemic insult. Western blot analyses showed that the change patterns in PECAM-1 protein levels in the dentate gyrus in both groups after ischemic insult were similar to changes in PECAM-1 immunohistochemistry in the ischemic dentate gyrus. Our results suggest that folate deficiency enhances PECAM-1 in the dentate gyrus induced by transient ischemia.

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“…In contrast, treatment with methanol resulted in an almost complete abrogation of intracellular esterase activity, resulting in loss of fluorescence upregulated on brain microvessels located within the ischaemic lesion, indicating that the selectins facilitate the adhesion of inflammatory cells and subsequently increase neuronal injury. 44,45 We hypothesised that the immunomodulatory drug MMF can influence the process of monocyte adhesion to endothelial cells, possibly by altering the glycosylation of adhesion molecules. It has been described that different adhesion molecules require glycosylation for the activation of their adhesive functions, 18 consequently, Heemann et al 46 showed that MMF treatment reduced leucocyte infiltration into transplanted kidneys.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of monocyte/endothelial cell interactions and monocyte adhesion molecule expression by the immunosuppressant mycophenolate mofetil

2003

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Study design: In vitro study on the effects of mycophenolate mofetil (MMF) on isolated human monocytes and endothelial cells. Objectives: Haematogenous macrophages play an essential role in the development of secondary damage following spinal cord injury (SCI), and there is evidence that the use of immunosuppressants such as MMF can reduce monocyte invasion and neuronal damage. Setting: University Hospital for Orthopaedic Surgery, Frankfurt am Main, Germany. Methods: The effects of MMF on the adhesion of human monocytes to human umbilical vein endothelial cells (HUVEC), monocyte binding to immobilised E-selectin, and monocyte expression of intercellular adhesion molecule (ICAM)-1, sialyl Lewis X (sLeX) and major histocompatibility complex (MHC)-II were studied. The binding of monocytes to E-selectin was examined by using purified and immobilised E-selectin fusion protein. Adhesion molecule expression was investigated by flow cytometry. Results: The binding of monocytes to HUVEC was significantly reduced by 30.1% after treatment of monocytes with MMF (10 mg/ml), whereas the pretreatment of HUVEC with MMF did not result in significant changes in monocyte adhesion. MMF forcefully inhibited monocyte binding to immobilised E-selectin by 55.7%. Furthermore, MMF significantly inhibited the upregulation of ICAM-1-and MHC-II-expression on monocytes stimulated with either lipopolysaccharide or interferon-g, whereas the expression of sLeX was not impaired. Toxic effects were excluded by propidium-iodide staining and measurement of fluoresceindiacetate metabolism. Conclusion: MMF can downregulate important monocytic adhesion molecules and inhibits monocyte adhesion to endothelial cells, thus indicating that treatment with MMF could be beneficial after SCI. Sponsorship: This study was supported by the DFG (Ha 2721/1-3), the Paul und Ursula KleinStiftung and the Stiftung Friedrichsheim.

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P-selectin and intercellular adhesion molecule-1 expression after focal brain ischemia and reperfusion.

Cited by 394 publications

References 57 publications

Polymorphonuclear Leukocyte Behavior in a Nonhuman Primate Focal Ischemia Model

Polymorphonuclear Leukocyte Behavior in a Nonhuman Primate Focal Ischemia Model

Change in platelet endothelial cell adhesion molecule-1 immunoreactivity in the dentate gyrus in gerbils fed a folate-deficient diet

Inhibition of monocyte/endothelial cell interactions and monocyte adhesion molecule expression by the immunosuppressant mycophenolate mofetil

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