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Article: Increasing expression of tissue plasminogen activator and plasminogen activator inhibitor type 2 in dog gingival tissues with progressive inflammation

TitleIncreasing expression of tissue plasminogen activator and plasminogen activator inhibitor type 2 in dog gingival tissues with progressive inflammation
Authors
Issue Date2001
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/archoralbio
Citation
Archives Of Oral Biology, 2001, v. 46 n. 1, p. 23-31 How to Cite?
AbstractUrokinase and tissue-type plasminogen activators (u-PA and t-PA) are serine proteases that convert plasminogen into plasmin, which degrades matrix proteins and activates metalloproteinases. The PAs are balanced by specific inhibitors (PAI-1 and PAI-2). Local production of t-PA and PAI-2 was recently demonstrated in human gingival tissues. The aim now was to investigate the production and localization of t-PA and PAI-2 in gingival tissues from dogs in three well-defined periodontal conditions; clinically healthy gingiva, chronic gingivitis and an initial stage of ligature-induced loss of attachment. At the start of the experiment the gingiva showed clear signs of inflammation. Clinically healthy gingiva were obtained after 21 days period of intense oral hygiene. Attachment loss was induced by placing rubber ligatures around the neck of some teeth. Biopsies were taken from areas representing the different conditions and prepared for in situ hybridization and immunohistochemistry. In clinically healthy gingiva both t-PA mRNA and antigen were expressed in a thin outer layer of the sulcular and junctional epithelia. No t-PA signals or staining were seen in connective tissue. Both mRNA signaling and immunostaining for t-PA were stronger in chronic gingivitis. In areas with loss of attachment, t-PA mRNA as well as antigen were found in the sulcular and junctional epithelia to a similar degree as in gingivitis. Occasionally the connective tissue was involved, especially in connection with vessels. PAI-2 mRNA was seen in a thin outer layer of the sulcular and junctional epithelia in clinically healthy gingiva, but no signals were seen in connective tissue. PAI-2 antigen was found primarily in the outer layer of the sulcular and junctional epithelia. Some cells in the connective tissue were stained. In gingivitis, PAI-2 signals were mainly found in the same locations, but more intense and extending towards the connective tissue. Immunostaining was seen in the outer half of the sulcular and junctional epithelia as well as in the upper part of the connective tissue, close to the sulcular epithelium. In sites with loss of attachment, PAI-2 mRNA was found throughout the sulcular and junctional epithelia, as was the antigen, which stained intensely. No PAI-2 mRNA was seen in connective tissue; the antigen was found scattered, especially near vessels. This study shows that the expression of both t-PA and PAI-2 increases with experimental gingival inflammation in the dog, and furthermore, the two techniques demonstrate a strong correlation between the topographical distribution of the site of protein synthesis and the tissue location of the antigens for both t-PA and PIA-2. The distribution correlates well with previous findings in humans. © 2000 Elsevier Science Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/154141
ISSN
2015 Impact Factor: 1.733
2015 SCImago Journal Rankings: 0.713
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLindberg, Pen_US
dc.contributor.authorKinnby, Ben_US
dc.contributor.authorLecander, Ien_US
dc.contributor.authorLang, NPen_US
dc.contributor.authorMatsson, Len_US
dc.date.accessioned2012-08-08T08:23:28Z-
dc.date.available2012-08-08T08:23:28Z-
dc.date.issued2001en_US
dc.identifier.citationArchives Of Oral Biology, 2001, v. 46 n. 1, p. 23-31en_US
dc.identifier.issn0003-9969en_US
dc.identifier.urihttp://hdl.handle.net/10722/154141-
dc.description.abstractUrokinase and tissue-type plasminogen activators (u-PA and t-PA) are serine proteases that convert plasminogen into plasmin, which degrades matrix proteins and activates metalloproteinases. The PAs are balanced by specific inhibitors (PAI-1 and PAI-2). Local production of t-PA and PAI-2 was recently demonstrated in human gingival tissues. The aim now was to investigate the production and localization of t-PA and PAI-2 in gingival tissues from dogs in three well-defined periodontal conditions; clinically healthy gingiva, chronic gingivitis and an initial stage of ligature-induced loss of attachment. At the start of the experiment the gingiva showed clear signs of inflammation. Clinically healthy gingiva were obtained after 21 days period of intense oral hygiene. Attachment loss was induced by placing rubber ligatures around the neck of some teeth. Biopsies were taken from areas representing the different conditions and prepared for in situ hybridization and immunohistochemistry. In clinically healthy gingiva both t-PA mRNA and antigen were expressed in a thin outer layer of the sulcular and junctional epithelia. No t-PA signals or staining were seen in connective tissue. Both mRNA signaling and immunostaining for t-PA were stronger in chronic gingivitis. In areas with loss of attachment, t-PA mRNA as well as antigen were found in the sulcular and junctional epithelia to a similar degree as in gingivitis. Occasionally the connective tissue was involved, especially in connection with vessels. PAI-2 mRNA was seen in a thin outer layer of the sulcular and junctional epithelia in clinically healthy gingiva, but no signals were seen in connective tissue. PAI-2 antigen was found primarily in the outer layer of the sulcular and junctional epithelia. Some cells in the connective tissue were stained. In gingivitis, PAI-2 signals were mainly found in the same locations, but more intense and extending towards the connective tissue. Immunostaining was seen in the outer half of the sulcular and junctional epithelia as well as in the upper part of the connective tissue, close to the sulcular epithelium. In sites with loss of attachment, PAI-2 mRNA was found throughout the sulcular and junctional epithelia, as was the antigen, which stained intensely. No PAI-2 mRNA was seen in connective tissue; the antigen was found scattered, especially near vessels. This study shows that the expression of both t-PA and PAI-2 increases with experimental gingival inflammation in the dog, and furthermore, the two techniques demonstrate a strong correlation between the topographical distribution of the site of protein synthesis and the tissue location of the antigens for both t-PA and PIA-2. The distribution correlates well with previous findings in humans. © 2000 Elsevier Science Ltd.en_US
dc.languageengen_US
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/archoralbioen_US
dc.relation.ispartofArchives of Oral Biologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshChronic Diseaseen_US
dc.subject.meshDogsen_US
dc.subject.meshEpithelial Attachment - Metabolismen_US
dc.subject.meshFemaleen_US
dc.subject.meshGingiva - Metabolismen_US
dc.subject.meshGingivitis - Metabolismen_US
dc.subject.meshImmunoenzyme Techniquesen_US
dc.subject.meshIn Situ Hybridizationen_US
dc.subject.meshPeriodontal Attachment Loss - Metabolismen_US
dc.subject.meshPlasminogen Activator Inhibitor 2 - Biosynthesisen_US
dc.subject.meshRna, Messenger - Analysisen_US
dc.subject.meshTissue Plasminogen Activator - Biosynthesisen_US
dc.titleIncreasing expression of tissue plasminogen activator and plasminogen activator inhibitor type 2 in dog gingival tissues with progressive inflammationen_US
dc.typeArticleen_US
dc.identifier.emailLang, NP:nplang@hkucc.hku.hken_US
dc.identifier.authorityLang, NP=rp00031en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0003-9969(00)00098-4en_US
dc.identifier.pmid11163592-
dc.identifier.scopuseid_2-s2.0-0035151396en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035151396&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume46en_US
dc.identifier.issue1en_US
dc.identifier.spage23en_US
dc.identifier.epage31en_US
dc.identifier.isiWOS:000166491300003-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLindberg, P=35839845500en_US
dc.identifier.scopusauthoridKinnby, B=6603743700en_US
dc.identifier.scopusauthoridLecander, I=21646056000en_US
dc.identifier.scopusauthoridLang, NP=7201577367en_US
dc.identifier.scopusauthoridMatsson, L=7005134462en_US

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