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Cartilage degradation by polymorphonuclear leucocytes: in vitro assessment of the pathogenic mechanisms
Polymorphonuclear leucocytes (PMNs), which predominate in inflammatory synovial fluid, can degrade cartilage. This was measured by a novel in vitro model; PMNs were incubated for up to one hour with 2 or 3 microns sections of cartilage and the glycosaminoglycan loss determined by microdensitometry a...
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Published in: | Annals of the rheumatic diseases 1993-01, Vol.52 (1), p.27-31 |
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creator | Moore, A R Iwamura, H Larbre, J P Scott, D L Willoughby, D A |
description | Polymorphonuclear leucocytes (PMNs), which predominate in inflammatory synovial fluid, can degrade cartilage. This was measured by a novel in vitro model; PMNs were incubated for up to one hour with 2 or 3 microns sections of cartilage and the glycosaminoglycan loss determined by microdensitometry after alcian blue staining. Glycosaminoglycan loss could be as a result of damage from reactive oxygen species, proteolytic enzymes, or a combination of the two. The relative contributions of these mechanisms were evaluated using selective inhibitors. The results show that activated PMNs will degrade cartilage and that this degradation is due to proteolytic enzymes and not reactive oxygen species. There is a specificity involving elastase but not other serine proteases. It is suggested that enzyme inhibition may play a part in reducing PMN mediated cartilage damage. |
doi_str_mv | 10.1136/ard.52.1.27 |
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Psychology</topic><topic>Glycosaminoglycans - metabolism</topic><topic>Inflammation</topic><topic>Kinetics</topic><topic>Male</topic><topic>Models, Biological</topic><topic>Molecular and cellular biology</topic><topic>Neutrophils - metabolism</topic><topic>Pancreatic Elastase - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reactive Oxygen Species - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Moore, A R</creatorcontrib><creatorcontrib>Iwamura, H</creatorcontrib><creatorcontrib>Larbre, J P</creatorcontrib><creatorcontrib>Scott, D L</creatorcontrib><creatorcontrib>Willoughby, D A</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Science Database (ProQuest)</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Annals of the rheumatic diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Moore, A R</au><au>Iwamura, H</au><au>Larbre, J P</au><au>Scott, D L</au><au>Willoughby, D A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cartilage degradation by polymorphonuclear leucocytes: in vitro assessment of the pathogenic mechanisms</atitle><jtitle>Annals of the rheumatic diseases</jtitle><addtitle>Ann Rheum Dis</addtitle><date>1993-01</date><risdate>1993</risdate><volume>52</volume><issue>1</issue><spage>27</spage><epage>31</epage><pages>27-31</pages><issn>0003-4967</issn><eissn>1468-2060</eissn><coden>ARDIAO</coden><abstract>Polymorphonuclear leucocytes (PMNs), which predominate in inflammatory synovial fluid, can degrade cartilage. This was measured by a novel in vitro model; PMNs were incubated for up to one hour with 2 or 3 microns sections of cartilage and the glycosaminoglycan loss determined by microdensitometry after alcian blue staining. Glycosaminoglycan loss could be as a result of damage from reactive oxygen species, proteolytic enzymes, or a combination of the two. The relative contributions of these mechanisms were evaluated using selective inhibitors. The results show that activated PMNs will degrade cartilage and that this degradation is due to proteolytic enzymes and not reactive oxygen species. There is a specificity involving elastase but not other serine proteases. It is suggested that enzyme inhibition may play a part in reducing PMN mediated cartilage damage.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and European League Against Rheumatism</pub><pmid>8427510</pmid><doi>10.1136/ard.52.1.27</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Arthritis, Rheumatoid - metabolism Biological and medical sciences Cartilage - metabolism Cattle Culture Techniques Fundamental and applied biological sciences. Psychology Glycosaminoglycans - metabolism Inflammation Kinetics Male Models, Biological Molecular and cellular biology Neutrophils - metabolism Pancreatic Elastase - metabolism Rats Rats, Wistar Reactive Oxygen Species - metabolism |
title | Cartilage degradation by polymorphonuclear leucocytes: in vitro assessment of the pathogenic mechanisms |
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