1999
DOI: 10.1016/s0165-5728(99)00092-2
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Increased serum levels of soluble PECAM-1 in multiple sclerosis patients with brain gadolinium-enhancing lesions

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Cited by 65 publications
(43 citation statements)
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“…The migration of inflammatory cells is facilitated by the upregulation of adhesion molecules, such as intercellular adhesion molecule 1, vascular-cell adhesion molecule 1, and platelet endothelial cell adhesion molecule 1 (10,11). On the other hand, matrix metalloproteinases (e.g., MMP-9) may degrade components of the basement membrane, and chemokines can form concentration gradients, which attract leukocytes, and activate leukocyte integrins, increasing adherence and extravasation (12,13).…”
mentioning
confidence: 99%
“…The migration of inflammatory cells is facilitated by the upregulation of adhesion molecules, such as intercellular adhesion molecule 1, vascular-cell adhesion molecule 1, and platelet endothelial cell adhesion molecule 1 (10,11). On the other hand, matrix metalloproteinases (e.g., MMP-9) may degrade components of the basement membrane, and chemokines can form concentration gradients, which attract leukocytes, and activate leukocyte integrins, increasing adherence and extravasation (12,13).…”
mentioning
confidence: 99%
“…An increase of serum levels of sPECAM-1 is well documented in MS (Losy et al, 1999;Jimenez et al, 2005;Minagar et al, 2001;Kuenz et al, 2005. ), although studies have not been able to link genetic changes in PECAM-1 with MS (Sciacca et al, 2000;Nelissen et al 2000.…”
Section: Discussionmentioning
confidence: 92%
“…Losy and Niezgoda [1] showed increased PECAM-1 in MS patients with gadolinium-enhancing lesions in comparison to patients with non-active lesions. They hypothesized direct involvement of PECAM-1 in the process of blood-brain barrier damage and secondary extravasation of leukocytes towards brain parenchyma.…”
Section: Central Nervous Systemmentioning
confidence: 93%
“…Because the native and soluble forms may have opposite effects [1,2]. Niezgoda and Losy hypothesized that the soluble forms are rather a sort of truncated false saturators for their natural counterpart which finally reduce the triggered inflammatory cascade [1,8]. They should be then considered a self-limiting negative feed-back mechanism of the CAM-activated inflammatory pathway (Fig.…”
Section: Cell Adhesion Molecule -Forms Timing Rolementioning
confidence: 99%