2002 Help me understand this report
Abstract: In conclusion, our studies indicate that NSAIDs preferentially inhibit tPA expression by bovine articular chondrocytes. By increasing the production of PAI-1 at therapeutical concentrations meloxicam could reduce PA activity, whereas the other NSAIDs tested mainly enhanced the release of this inhibitor from the extracellular matrix. In how far this would affect the enzyme-inhibitor balance within cartilage has to be determined in further studies.
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Cited by 10 publications
(4 citation statements)
References 28 publications
(22 reference statements)
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“…On the other hand, by using bovine chondrocytes, Sadowski and colleagues reported that indomethacin, naproxen, and tiaprofenic acid stimulated PAI-1 release, and meloxicam induced PAI-1 expression, indicating the distinct effects of each of the nonsteroidal anti-inflammatory drugs (NSAIDs) in the expression and release of PAI-1. 28 Considering these findings and the results of our present study, it can be suggested that PGE 2 might exert a catabolic effect on cartilage by suppressing PAI-1 expression, and that the activation of COX and the levels of COX product including PGE 2 might collectively regulate the expression and secretion of PAI-1 in chondrocytes. Of note, it was shown that EP4 receptor in chondrocyte was responsible to the response to PGE 2 in suppressing PAI-1 level ( Figure 3 ).…”
Section: Discussionsupporting
confidence: 78%
“…On the other hand, by using bovine chondrocytes, Sadowski and colleagues reported that indomethacin, naproxen, and tiaprofenic acid stimulated PAI-1 release, and meloxicam induced PAI-1 expression, indicating the distinct effects of each of the nonsteroidal anti-inflammatory drugs (NSAIDs) in the expression and release of PAI-1. 28 Considering these findings and the results of our present study, it can be suggested that PGE 2 might exert a catabolic effect on cartilage by suppressing PAI-1 expression, and that the activation of COX and the levels of COX product including PGE 2 might collectively regulate the expression and secretion of PAI-1 in chondrocytes. Of note, it was shown that EP4 receptor in chondrocyte was responsible to the response to PGE 2 in suppressing PAI-1 level ( Figure 3 ).…”
Section: Discussionsupporting
confidence: 78%
“…Conversion of PLG to PL by PA in cell lysates was determined by the hydrolysis of the chromogenic substrate H-D-Val-Leu-Lys-pNA (S-2251, KabiVitrum, Stockholm, Sweden) as described previously 26 . Briefly, cells were lysed by repeated freezing and thawing and then mixed with PLG (1.3 mM; Sigma, St. Louis, MO, USA), S-2251 (0.7 mM), and Tris buffer (50 mM Tris and 0.05% Tween 80, pH 8.0).…”
Section: Determination Of Pa Activitymentioning
confidence: 99%
“…Steroidal anti-inflammatory drugs (Viaje et al 1977), non-steroidal anti-inflammatory drugs (Pelletier et al 1997;Li et al 2002;Sadowski and Steinmeyer 2002;Iwamoto et al 2003), and selective COX-2 inhibitors (Li et al 2002;Berger et al 2003;Khan et al 2004;Nishikawa et al 2004) reduce the expression of the components of the PA system. For this reason, five patients medicated with non-steroidal anti-inflammatory drugs or aspirin at any moment of the 14-day period previous to the surgery were excluded from this analysis.…”
Section: Patients' Characteristics and Tissue Samplesmentioning
confidence: 98%
“…Detailed histological examination of these ''normal tissue'' fragments demonstrated that they were not contaminated with tumor cells. As it is known that inflammatory processes increase PA activity (Pelletier et al 1997;Hersze´nyi et al 2000;Sadowski and Steinmeyer 2002;Iwamoto et al 2003;Khan et al 2004), four samples were eliminated because histological studies detected inflammatory features in the ''normal'' tissue samples. So, 35 paired ''normal'' and tumor samples were finally included in this work.…”
Section: Patients' Characteristics and Tissue Samplesmentioning
confidence: 99%
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