Soluble urokinase receptor (uPAR, CD 87) is present in serum and cerebrospinal fluid in patients with neurologic diseases

被引:46
作者
Garcia-Monco, JC [1 ]
Coleman, JL
Benach, JL
机构
[1] Hosp Galdacano, Dept Neurol, Galdakao 48960, Vizcaya, Spain
[2] SUNY Stony Brook, Ctr Infect Dis, Stony Brook, NY 11794 USA
[3] SUNY Stony Brook, New York State Dept Hlth, Stony Brook, NY 11794 USA
关键词
urokinase; urokinase receptor; uPAR; suPAR;
D O I
10.1016/S0165-5728(02)00186-8
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Background: The receptor for urokinase plasminogen activator (uPAR) promotes invasion by neoplastic or inflammatory cells by focusing proteolysis of urokinase to the cell surface. In pathologic conditions, soluble forms of the receptor (suPAR) are released. and activate cell receptors to promote chemotaxis. In the CNS, suPAR and other components of the plasminogen activation system (PAS) could be associated with an increase of the blood-brain barrier (BBB) permeability and subsequent neural damage. Objective: To detect suPAR in the serum and cerebrospinal fluid (CSF) of patients with diverse neurologic conditions. Patients and methods: Serum anti CSF from 121 patients with cancer, bacterial and viral infection, stroke, demyelinating disease and peripheral neuropathy were examined for the presence of suPAR. Results: suPAR was elevated in the serum of patients with paraneoplastic syndromes, and carcinomatous meningitis, and inflections, but less in stroke and demyelinating disease patients. CSF suPAR was present in the cancer and CNS infection groups, but not in the other groups. The levels of serum and CSF suPAR were correlated, and CSF suPAR correlated with the albumin index. Conclusions: suPAR is present in serum and CSF of patients with carcinomatous meningitis, paraneoplastic disorders and bacterial anti viral infection of the CNS. suPAR could be associated with BBB disruption and with promotion of CNS invasion by chemotactically active cells, macromolecules, and microbes. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:216 / 223
页数:8
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