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Inhibition of nitric oxide can ameliorate apoptosis and modulate matrix protein gene expression in bacteria infected chondrocytes in vitro
Author(s) -
Lee M. S.,
Tu Y. K.,
Chao C. C. K.,
Chen S. C.,
Chen C. Y.,
Chan Y. S.,
Yeh W. L.,
Ueng S. W. N.
Publication year - 2005
Publication title -
journal of orthopaedic research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.041
H-Index - 155
eISSN - 1554-527X
pISSN - 0736-0266
DOI - 10.1016/j.orthres.2004.06.011
Subject(s) - chondrocyte , apoptosis , aggrecan , nitric oxide , gene expression , downregulation and upregulation , microbiology and biotechnology , cartilage , type ii collagen , in vitro , matrix (chemical analysis) , chemistry , immunology , gene , biology , medicine , osteoarthritis , biochemistry , pathology , endocrinology , anatomy , articular cartilage , alternative medicine , chromatography
Bacterial infection stimulates nitric oxide (NO) production in chondrocytes. However, the role of NO in chondrocyte apoptosis after infection remains unclear. The purpose of the study was to test if inhibition of NO could ameliorate apoptosis and modulate matrix protein gene expression in bacteria‐infected chondrocytes. It was shown that pre‐treating chondrocytes with L‐NAME (1 mM) significantly decreased the release of NO (from 72 to 14 μM) and the extent of apoptosis (from 52.9% to 18.9%). Pre‐treatment with L‐NAME also counteracted the bacteria‐induced downregulation of Type II collagen (from 26% to 79%) and aggrecan (from 63% to 105%) mRNA levels. Inhibition of NO after the induction of infection could not decrease the extent of apoptosis and modulate matrix protein gene expression. The results of this study support the hypothesis that NO has an important role in bacteriainduced chondrocyte apoptosis. Pre‐treatment but not post‐treatment could ameliorate the extent of apoptosis and reestablish the cartilage matrix protein gene expression. This study suggests that in addition to NO, other mechanisms may be responsible for the sustained destruction of articular cartilage in the post‐infectious arthropathy. © 2004 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved.