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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

In vivo blockade of Ca+2-dependent nitric oxide synthases impairs expressions of L-selectin and PECAM-1

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Author(s):
Hebeda, Cristina B. [1] ; Teixeira, Simone A. [2] ; Muscara, Marcelo N. [2] ; Vinolo, Marco Antonio R. [3] ; Curi, Rui [3] ; de Mello, Suzana B. V. [4] ; Farsky, Sandra H. P. [1]
Total Authors: 7
Affiliation:
[1] Univ Sao Paulo, Sch Pharmaceut Sci, Dept Clin & Toxicol Anal, BR-0550900 Sao Paulo - Brazil
[2] Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, BR-0550900 Sao Paulo - Brazil
[3] Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, BR-0550900 Sao Paulo - Brazil
[4] Univ Sao Paulo, Sch Med, Dept Internal Med, Div Rheumatol, BR-0550900 Sao Paulo - Brazil
Total Affiliations: 4
Document type: Journal article
Source: Biochemical and Biophysical Research Communications; v. 377, n. 2, p. 694-698, DEC 12 2008.
Web of Science Citations: 8
Abstract

Interactions of leukocytes with endothelium play a role for the immune system modulated by endogenous agents, such as glucocorticoids and nitric oxide (NO). Glucocorticoids inhibit leukocyte-endothelial interactions whereas the role of NO is still controversial. In this study, the activity of Ca(+2)-dependent nitric oxide synthases was in vivo blocked in male Wistar rats by given L-NAME, 20 mg kg(-1) for 14 days dissolved in drinking water and expression of adhesion molecules involved in leukocyte-endothelial interactions was investigated. Expressions of L-selectin and PECAM-I in peripheral leukocytes and PECAM-1 in endothelial cells were reduced by L-NAME treatment. Only L-selectin expression was controlled at transcriptional levels. These effects were not dependent on endogenous glucocorticoids, as corticosterone levels were not altered in NAME-treated rats. Our results show that NO, produced at physiological levels, controls expression of constitutive adhesion molecules expressions in cell membranes by different mechanisms of action. Published by Elsevier Inc. (AU)