Differences in nitric oxide production by superficial and deep human articular chondrocytes: Implications for proteoglycan turnover in inflammatory joint diseases

H. J. Häuselmann, M. Stefanovic-Racic, B. A. Michel, Christopher H Evans

Research output: Contribution to journalArticle

64 Citations (Scopus)

Abstract

During inflammatory joint diseases, chondrocytes are exposed to cytokines such as IL-1 that induce the synthesis of nitric oxide (NO). Chondrocytes from different zones of the articular cartilage are known to have different metabolic properties. In the present study, we have demonstrated that chondrocytes recovered from the superficial zone of normal, human, articular cartilage synthesize approximately 2 to 3 times as much NO in response to IL-1 as chondrocytes recovered from the deep zone of the same cartilage. Production of NO by normal cartilage in response to IL-1 was also found to decrease with age. Addition of the NO synthase inhibitor N(G)- monomethyl-L-arginine (L-NMA, 1 mM) blocked NO production by cells of both zones. L-NMA completely reversed the suppression of proteoglycan synthesis imposed by IL-1 in deep chondrocytes, but produced only partial reversal in superficial cells. As noted previously, IL-1 failed to elicit a strong catabolic response in cultures of human cartilage. In the presence of L-NMA, however, IL-1 reduced the metabolic t( 1/4 ) of proteoglycans by approximately 50 % in both the superficial and deep zones. This suggests that NO has, directly or indirectly, an anticatabolic effect in human cartilage. These data confirm the metabolic heterogeneity of human chondrocytes, and suggest that NO may be involved to different degrees as an endogenous modulator of the turnover of the cartilaginous matrix in different zones of articular cartilage.

Original languageEnglish (US)
Pages (from-to)1444-1448
Number of pages5
JournalJournal of Immunology
Volume160
Issue number3
StatePublished - Feb 1 1998
Externally publishedYes

Fingerprint

Joint Diseases
Proteoglycans
Chondrocytes
Interleukin-1
Nitric Oxide
Joints
Cartilage
Articular Cartilage
Nitric Oxide Synthase
Arginine
Cytokines

ASJC Scopus subject areas

  • Immunology

Cite this

Differences in nitric oxide production by superficial and deep human articular chondrocytes : Implications for proteoglycan turnover in inflammatory joint diseases. / Häuselmann, H. J.; Stefanovic-Racic, M.; Michel, B. A.; Evans, Christopher H.

In: Journal of Immunology, Vol. 160, No. 3, 01.02.1998, p. 1444-1448.

Research output: Contribution to journalArticle

@article{57ae7e56f52e458f98e127da1e46bcee,
title = "Differences in nitric oxide production by superficial and deep human articular chondrocytes: Implications for proteoglycan turnover in inflammatory joint diseases",
abstract = "During inflammatory joint diseases, chondrocytes are exposed to cytokines such as IL-1 that induce the synthesis of nitric oxide (NO). Chondrocytes from different zones of the articular cartilage are known to have different metabolic properties. In the present study, we have demonstrated that chondrocytes recovered from the superficial zone of normal, human, articular cartilage synthesize approximately 2 to 3 times as much NO in response to IL-1 as chondrocytes recovered from the deep zone of the same cartilage. Production of NO by normal cartilage in response to IL-1 was also found to decrease with age. Addition of the NO synthase inhibitor N(G)- monomethyl-L-arginine (L-NMA, 1 mM) blocked NO production by cells of both zones. L-NMA completely reversed the suppression of proteoglycan synthesis imposed by IL-1 in deep chondrocytes, but produced only partial reversal in superficial cells. As noted previously, IL-1 failed to elicit a strong catabolic response in cultures of human cartilage. In the presence of L-NMA, however, IL-1 reduced the metabolic t( 1/4 ) of proteoglycans by approximately 50 {\%} in both the superficial and deep zones. This suggests that NO has, directly or indirectly, an anticatabolic effect in human cartilage. These data confirm the metabolic heterogeneity of human chondrocytes, and suggest that NO may be involved to different degrees as an endogenous modulator of the turnover of the cartilaginous matrix in different zones of articular cartilage.",
author = "H{\"a}uselmann, {H. J.} and M. Stefanovic-Racic and Michel, {B. A.} and Evans, {Christopher H}",
year = "1998",
month = "2",
day = "1",
language = "English (US)",
volume = "160",
pages = "1444--1448",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "3",

}

TY - JOUR

T1 - Differences in nitric oxide production by superficial and deep human articular chondrocytes

T2 - Implications for proteoglycan turnover in inflammatory joint diseases

AU - Häuselmann, H. J.

AU - Stefanovic-Racic, M.

AU - Michel, B. A.

AU - Evans, Christopher H

PY - 1998/2/1

Y1 - 1998/2/1

N2 - During inflammatory joint diseases, chondrocytes are exposed to cytokines such as IL-1 that induce the synthesis of nitric oxide (NO). Chondrocytes from different zones of the articular cartilage are known to have different metabolic properties. In the present study, we have demonstrated that chondrocytes recovered from the superficial zone of normal, human, articular cartilage synthesize approximately 2 to 3 times as much NO in response to IL-1 as chondrocytes recovered from the deep zone of the same cartilage. Production of NO by normal cartilage in response to IL-1 was also found to decrease with age. Addition of the NO synthase inhibitor N(G)- monomethyl-L-arginine (L-NMA, 1 mM) blocked NO production by cells of both zones. L-NMA completely reversed the suppression of proteoglycan synthesis imposed by IL-1 in deep chondrocytes, but produced only partial reversal in superficial cells. As noted previously, IL-1 failed to elicit a strong catabolic response in cultures of human cartilage. In the presence of L-NMA, however, IL-1 reduced the metabolic t( 1/4 ) of proteoglycans by approximately 50 % in both the superficial and deep zones. This suggests that NO has, directly or indirectly, an anticatabolic effect in human cartilage. These data confirm the metabolic heterogeneity of human chondrocytes, and suggest that NO may be involved to different degrees as an endogenous modulator of the turnover of the cartilaginous matrix in different zones of articular cartilage.

AB - During inflammatory joint diseases, chondrocytes are exposed to cytokines such as IL-1 that induce the synthesis of nitric oxide (NO). Chondrocytes from different zones of the articular cartilage are known to have different metabolic properties. In the present study, we have demonstrated that chondrocytes recovered from the superficial zone of normal, human, articular cartilage synthesize approximately 2 to 3 times as much NO in response to IL-1 as chondrocytes recovered from the deep zone of the same cartilage. Production of NO by normal cartilage in response to IL-1 was also found to decrease with age. Addition of the NO synthase inhibitor N(G)- monomethyl-L-arginine (L-NMA, 1 mM) blocked NO production by cells of both zones. L-NMA completely reversed the suppression of proteoglycan synthesis imposed by IL-1 in deep chondrocytes, but produced only partial reversal in superficial cells. As noted previously, IL-1 failed to elicit a strong catabolic response in cultures of human cartilage. In the presence of L-NMA, however, IL-1 reduced the metabolic t( 1/4 ) of proteoglycans by approximately 50 % in both the superficial and deep zones. This suggests that NO has, directly or indirectly, an anticatabolic effect in human cartilage. These data confirm the metabolic heterogeneity of human chondrocytes, and suggest that NO may be involved to different degrees as an endogenous modulator of the turnover of the cartilaginous matrix in different zones of articular cartilage.

UR - http://www.scopus.com/inward/record.url?scp=2642661478&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=2642661478&partnerID=8YFLogxK

M3 - Article

C2 - 9570565

AN - SCOPUS:2642661478

VL - 160

SP - 1444

EP - 1448

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 3

ER -