Activation and Degradation of Protein C by Primary Rabbit Pleural Mesothelial Cells
Identifieur interne : 001D79 ( Main/Exploration ); précédent : 001D78; suivant : 001D80Activation and Degradation of Protein C by Primary Rabbit Pleural Mesothelial Cells
Auteurs : Alexei Iakhiaev [États-Unis] ; Steven Idell [États-Unis]Source :
- Lung [ 0341-2040 ] ; 2006-04-01.
Descripteurs français
- KwdFr :
- MESH :
- cytologie : Plèvre, Poumon.
- métabolisme : Cellules épithéliales, Pleurésie, Protéine C.
- physiologie : Fibroblastes, Thrombine.
- Animaux, Dépollution biologique de l'environnement, Lapins, Technique d'immunofluorescence.
English descriptors
- KwdEn :
- Activated protein C (APC), Animals, Biodegradation, Environmental, Degradation, Endocytosis, Epithelial Cells (metabolism), Fibroblasts (physiology), Fluorescent Antibody Technique, Lung (cytology), Pleura (cytology), Pleurisy (metabolism), Primary rabbit pleural mesothelial cells (RPMC), Protein C (PC), Protein C (metabolism), Rabbits, Thrombin (physiology).
- MESH :
- chemical , metabolism : Protein C.
- cytology : Lung, Pleura.
- metabolism : Epithelial Cells, Pleurisy.
- physiology : Fibroblasts, Thrombin.
- Animals, Biodegradation, Environmental, Fluorescent Antibody Technique, Rabbits.
Abstract
Abstract: The protein C (PC) anticoagulant pathway is the major mechanism that controls thrombin generation in vivo and may thereby influence pathophysiologic fibrin turnover associated with intrapleural inflammation. We hypothesized that pleural mesothelial cells could regulate local expression of PC in evolving pleurodesis where inflammation and thrombosis play an important role. To test this hypothesis, we determined the ability of rabbit pleural mesothelial cells (RPMC) to support the activation of PC as well as its binding, internalization, and degradation. Lung fibroblasts were also assessed to test the specificity of the responses. We found that both cell types could support thrombin-dependent activation of PC in vitro. Both cell types were capable of binding, internalizing, and degrading 125I-PC. Degradation of 125I-PC by these cells was prevented by the lysosomal inhibitor chloroquine but not the proteasomal inhibitor lactacystin, supporting involvement of a lysosomal mechanism of PC degradation. During evolving tetracycline (TCN)-induced pleural injury in rabbits, PC levels in pleural fluids were sustained, exhibited a trend toward progressive decline, and were temporally correlated with pleural adhesion formation in vivo. These observations indicate that sustained expression of PC during evolving pleurodesis induced by TCN is subject to regulation by resident pleural cells: both RPMC and lung fibroblasts. Both cell types support local generation of APC. Internalization and degradation of PC by RPMC and fibroblasts may regulate its intrapleural expression and influence remodeling of extravascular fibrin in the setting of evolving pleurodesis induced by TCN.
Url:
DOI: 10.1007/s00408-005-2566-z
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream Istex, to step Corpus: 000A41
- to stream Istex, to step Curation: 000A41
- to stream Istex, to step Checkpoint: 000C47
- to stream PubMed, to step Corpus: 000438
- to stream PubMed, to step Curation: 000438
- to stream PubMed, to step Checkpoint: 000682
- to stream Ncbi, to step Merge: 000085
- to stream Ncbi, to step Curation: 000085
- to stream Ncbi, to step Checkpoint: 000085
- to stream Main, to step Merge: 001D91
- to stream Main, to step Curation: 001D79
Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Activation and Degradation of Protein C by Primary Rabbit Pleural Mesothelial Cells</title>
<author><name sortKey="Iakhiaev, Alexei" sort="Iakhiaev, Alexei" uniqKey="Iakhiaev A" first="Alexei" last="Iakhiaev">Alexei Iakhiaev</name>
</author>
<author><name sortKey="Idell, Steven" sort="Idell, Steven" uniqKey="Idell S" first="Steven" last="Idell">Steven Idell</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">ISTEX</idno>
<idno type="RBID">ISTEX:4A77F12087A43F1AAA219F3366C82C3270F513BA</idno>
<date when="2006" year="2006">2006</date>
<idno type="doi">10.1007/s00408-005-2566-z</idno>
<idno type="url">https://api.istex.fr/ark:/67375/VQC-5L1D3GMV-V/fulltext.pdf</idno>
<idno type="wicri:Area/Istex/Corpus">000A41</idno>
<idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000A41</idno>
<idno type="wicri:Area/Istex/Curation">000A41</idno>
<idno type="wicri:Area/Istex/Checkpoint">000C47</idno>
<idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">000C47</idno>
<idno type="wicri:doubleKey">0341-2040:2006:Iakhiaev A:activation:and:degradation</idno>
<idno type="wicri:source">PubMed</idno>
<idno type="RBID">pubmed:16622777</idno>
<idno type="wicri:Area/PubMed/Corpus">000438</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000438</idno>
<idno type="wicri:Area/PubMed/Curation">000438</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000438</idno>
<idno type="wicri:Area/PubMed/Checkpoint">000682</idno>
<idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000682</idno>
<idno type="wicri:Area/Ncbi/Merge">000085</idno>
<idno type="wicri:Area/Ncbi/Curation">000085</idno>
<idno type="wicri:Area/Ncbi/Checkpoint">000085</idno>
<idno type="wicri:doubleKey">0341-2040::Iakhiaev A:activation:and:degradation</idno>
<idno type="wicri:Area/Main/Merge">001D91</idno>
<idno type="wicri:Area/Main/Curation">001D79</idno>
<idno type="wicri:Area/Main/Exploration">001D79</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Activation and Degradation of Protein C by Primary Rabbit Pleural Mesothelial Cells</title>
<author><name sortKey="Iakhiaev, Alexei" sort="Iakhiaev, Alexei" uniqKey="Iakhiaev A" first="Alexei" last="Iakhiaev">Alexei Iakhiaev</name>
<affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Departments of Medicine and Biomedical Research, The University of Texas Health Center at Tyler, 75708, Tyler, Texas</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
<affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Lab C-6, The University of Texas Health Center at Tyler, 11937 US Hwy 271, 75708, Tyler, TX</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
<affiliation wicri:level="1"><country wicri:rule="url">États-Unis</country>
</affiliation>
</author>
<author><name sortKey="Idell, Steven" sort="Idell, Steven" uniqKey="Idell S" first="Steven" last="Idell">Steven Idell</name>
<affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Departments of Medicine and Biomedical Research, The University of Texas Health Center at Tyler, 75708, Tyler, Texas</wicri:regionArea>
<placeName><region type="state">Texas</region>
</placeName>
</affiliation>
</author>
</analytic>
<monogr></monogr>
<series><title level="j">Lung</title>
<title level="j" type="sub">An International Journal on Lungs, Airways and Breathing</title>
<title level="j" type="abbrev">Lung</title>
<idno type="ISSN">0341-2040</idno>
<idno type="eISSN">1432-1750</idno>
<imprint><publisher>Springer-Verlag; www.springer-ny.com</publisher>
<pubPlace>New York</pubPlace>
<date type="published" when="2006-04-01">2006-04-01</date>
<biblScope unit="volume">184</biblScope>
<biblScope unit="issue">2</biblScope>
<biblScope unit="page" from="81">81</biblScope>
<biblScope unit="page" to="88">88</biblScope>
</imprint>
<idno type="ISSN">0341-2040</idno>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><idno type="ISSN">0341-2040</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Activated protein C (APC)</term>
<term>Animals</term>
<term>Biodegradation, Environmental</term>
<term>Degradation</term>
<term>Endocytosis</term>
<term>Epithelial Cells (metabolism)</term>
<term>Fibroblasts (physiology)</term>
<term>Fluorescent Antibody Technique</term>
<term>Lung (cytology)</term>
<term>Pleura (cytology)</term>
<term>Pleurisy (metabolism)</term>
<term>Primary rabbit pleural mesothelial cells (RPMC)</term>
<term>Protein C (PC)</term>
<term>Protein C (metabolism)</term>
<term>Rabbits</term>
<term>Thrombin (physiology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Cellules épithéliales (métabolisme)</term>
<term>Dépollution biologique de l'environnement</term>
<term>Fibroblastes (physiologie)</term>
<term>Lapins</term>
<term>Pleurésie (métabolisme)</term>
<term>Plèvre (cytologie)</term>
<term>Poumon (cytologie)</term>
<term>Protéine C (métabolisme)</term>
<term>Technique d'immunofluorescence</term>
<term>Thrombine (physiologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Protein C</term>
</keywords>
<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Plèvre</term>
<term>Poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Lung</term>
<term>Pleura</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Epithelial Cells</term>
<term>Pleurisy</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules épithéliales</term>
<term>Pleurésie</term>
<term>Protéine C</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Fibroblastes</term>
<term>Thrombine</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Fibroblasts</term>
<term>Thrombin</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Biodegradation, Environmental</term>
<term>Fluorescent Antibody Technique</term>
<term>Rabbits</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Dépollution biologique de l'environnement</term>
<term>Lapins</term>
<term>Technique d'immunofluorescence</term>
</keywords>
</textClass>
<langUsage><language ident="en">en</language>
</langUsage>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Abstract: The protein C (PC) anticoagulant pathway is the major mechanism that controls thrombin generation in vivo and may thereby influence pathophysiologic fibrin turnover associated with intrapleural inflammation. We hypothesized that pleural mesothelial cells could regulate local expression of PC in evolving pleurodesis where inflammation and thrombosis play an important role. To test this hypothesis, we determined the ability of rabbit pleural mesothelial cells (RPMC) to support the activation of PC as well as its binding, internalization, and degradation. Lung fibroblasts were also assessed to test the specificity of the responses. We found that both cell types could support thrombin-dependent activation of PC in vitro. Both cell types were capable of binding, internalizing, and degrading 125I-PC. Degradation of 125I-PC by these cells was prevented by the lysosomal inhibitor chloroquine but not the proteasomal inhibitor lactacystin, supporting involvement of a lysosomal mechanism of PC degradation. During evolving tetracycline (TCN)-induced pleural injury in rabbits, PC levels in pleural fluids were sustained, exhibited a trend toward progressive decline, and were temporally correlated with pleural adhesion formation in vivo. These observations indicate that sustained expression of PC during evolving pleurodesis induced by TCN is subject to regulation by resident pleural cells: both RPMC and lung fibroblasts. Both cell types support local generation of APC. Internalization and degradation of PC by RPMC and fibroblasts may regulate its intrapleural expression and influence remodeling of extravascular fibrin in the setting of evolving pleurodesis induced by TCN.</div>
</front>
</TEI>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Texas</li>
</region>
</list>
<tree><country name="États-Unis"><region name="Texas"><name sortKey="Iakhiaev, Alexei" sort="Iakhiaev, Alexei" uniqKey="Iakhiaev A" first="Alexei" last="Iakhiaev">Alexei Iakhiaev</name>
</region>
<name sortKey="Iakhiaev, Alexei" sort="Iakhiaev, Alexei" uniqKey="Iakhiaev A" first="Alexei" last="Iakhiaev">Alexei Iakhiaev</name>
<name sortKey="Iakhiaev, Alexei" sort="Iakhiaev, Alexei" uniqKey="Iakhiaev A" first="Alexei" last="Iakhiaev">Alexei Iakhiaev</name>
<name sortKey="Idell, Steven" sort="Idell, Steven" uniqKey="Idell S" first="Steven" last="Idell">Steven Idell</name>
</country>
</tree>
</affiliations>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001D79 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 001D79 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Sante |area= ChloroquineV1 |flux= Main |étape= Exploration |type= RBID |clé= ISTEX:4A77F12087A43F1AAA219F3366C82C3270F513BA |texte= Activation and Degradation of Protein C by Primary Rabbit Pleural Mesothelial Cells }}
This area was generated with Dilib version V0.6.33. |