Anti-Inflammatory Pharmacotherapy with Ketoprofen Ameliorates Experimental Lymphatic Vascular Insufficiency in Mice
Identifieur interne : 006397 ( Main/Exploration ); précédent : 006396; suivant : 006398Anti-Inflammatory Pharmacotherapy with Ketoprofen Ameliorates Experimental Lymphatic Vascular Insufficiency in Mice
Auteurs : Kenta Nakamura ; Kavita Radhakrishnan ; Yat Man Wong ; Stanley G. RocksonSource :
- PLoS ONE [ 1932-6203 ] ; 2009.
Descripteurs français
- KwdFr :
- Animaux, Anti-inflammatoires (usage thérapeutique), Anti-inflammatoires non stéroïdiens (usage thérapeutique), Cytokines (métabolisme), Kétoprofène (pharmacologie), Kétoprofène (usage thérapeutique), Lymphoedème (), Lymphoedème (génétique), Lymphoedème (traitement médicamenteux), Modèles immunologiques, Médiateurs de l'inflammation (métabolisme), RT-PCR, Récepteur au facteur de nécrose tumorale de type I (pharmacologie), Régulation de l'expression des gènes (), Solubilité (), Souris, Spécificité d'organe, Vaisseaux lymphatiques (), Vaisseaux lymphatiques (anatomopathologie).
- MESH :
- anatomopathologie : Vaisseaux lymphatiques.
- génétique : Lymphoedème.
- métabolisme : Cytokines, Médiateurs de l'inflammation.
- pharmacologie : Kétoprofène, Récepteur au facteur de nécrose tumorale de type I.
- traitement médicamenteux : Lymphoedème.
- usage thérapeutique : Anti-inflammatoires, Anti-inflammatoires non stéroïdiens, Kétoprofène.
- Animaux, Lymphoedème, Modèles immunologiques, RT-PCR, Régulation de l'expression des gènes, Solubilité, Souris, Spécificité d'organe, Vaisseaux lymphatiques.
English descriptors
- KwdEn :
- Animals, Anti-Inflammatory Agents (therapeutic use), Anti-Inflammatory Agents, Non-Steroidal (therapeutic use), Cytokines (metabolism), Gene Expression Regulation (drug effects), Inflammation Mediators (metabolism), Ketoprofen (pharmacology), Ketoprofen (therapeutic use), Lymphatic Vessels (drug effects), Lymphatic Vessels (pathology), Lymphedema (chemically induced), Lymphedema (drug therapy), Lymphedema (genetics), Lymphedema (prevention & control), Mice, Models, Immunological, Organ Specificity, Receptors, Tumor Necrosis Factor, Type I (pharmacology), Reverse Transcriptase Polymerase Chain Reaction, Solubility (drug effects).
- MESH :
- chemical , metabolism : Cytokines, Inflammation Mediators.
- chemical , pharmacology : Ketoprofen, Receptors, Tumor Necrosis Factor, Type I.
- chemical , therapeutic use : Anti-Inflammatory Agents, Anti-Inflammatory Agents, Non-Steroidal, Ketoprofen.
- chemically induced : Lymphedema.
- drug effects : Gene Expression Regulation, Lymphatic Vessels, Solubility.
- drug therapy : Lymphedema.
- genetics : Lymphedema.
- pathology : Lymphatic Vessels.
- prevention & control : Lymphedema.
- Animals, Mice, Models, Immunological, Organ Specificity, Reverse Transcriptase Polymerase Chain Reaction.
Abstract
Disruption of the lymphatic vasculature causes edema, inflammation, and end-tissue destruction. To assess the therapeutic efficacy of systemic anti-inflammatory therapy in this disease, we examined the impact of a nonsteroidal anti-inflammatory drug (NSAID), ketoprofen, and of a soluble TNF-α receptor (sTNF-R1) upon tumor necrosis factor (TNF)-α activity in a mouse model of acquired lymphedema.
Lymphedema was induced by microsurgical ablation of major lymphatic conduits in the murine tail. Untreated control mice with lymphedema developed significant edema and extensive histopathological inflammation compared to sham surgical controls. Short-term ketoprofen treatment reduced tail edema and normalized the histopathology while paradoxically increasing TNF-α gene expression and cytokine levels. Conversely, sTNF-R1 treatment increased tail volume, exacerbated the histopathology, and decreased TNF-α gene expression. Expression of vascular endothelial growth factor-C (VEGF-C), which stimulates lymphangiogenesis, closely correlated with TNF-α expression.
Ketoprofen therapy reduces experimental post-surgical lymphedema, yet direct TNF-α inhibition does not. Reducing inflammation while preserving TNF-α activity appears to optimize the repair response. It is possible that the observed favorable responses, at least in part, are mediated through enhanced VEGF-C signaling.
Url:
DOI: 10.1371/journal.pone.0008380
PubMed: 20027220
PubMed Central: 2791214
Affiliations:
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Le document en format XML
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Rockson</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author></analytic><series><title level="j">PLoS ONE</title><idno type="eISSN">1932-6203</idno><imprint><date when="2009">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Anti-Inflammatory Agents (therapeutic use)</term><term>Anti-Inflammatory Agents, Non-Steroidal (therapeutic use)</term><term>Cytokines (metabolism)</term><term>Gene Expression Regulation (drug effects)</term><term>Inflammation Mediators (metabolism)</term><term>Ketoprofen (pharmacology)</term><term>Ketoprofen (therapeutic use)</term><term>Lymphatic Vessels (drug effects)</term><term>Lymphatic Vessels (pathology)</term><term>Lymphedema (chemically induced)</term><term>Lymphedema (drug therapy)</term><term>Lymphedema (genetics)</term><term>Lymphedema (prevention & control)</term><term>Mice</term><term>Models, Immunological</term><term>Organ Specificity</term><term>Receptors, Tumor Necrosis Factor, Type I (pharmacology)</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>Solubility (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Anti-inflammatoires (usage thérapeutique)</term><term>Anti-inflammatoires non stéroïdiens (usage thérapeutique)</term><term>Cytokines (métabolisme)</term><term>Kétoprofène (pharmacologie)</term><term>Kétoprofène (usage thérapeutique)</term><term>Lymphoedème ()</term><term>Lymphoedème (génétique)</term><term>Lymphoedème (traitement médicamenteux)</term><term>Modèles immunologiques</term><term>Médiateurs de l'inflammation (métabolisme)</term><term>RT-PCR</term><term>Récepteur au facteur de nécrose tumorale de type I (pharmacologie)</term><term>Régulation de l'expression des gènes ()</term><term>Solubilité ()</term><term>Souris</term><term>Spécificité d'organe</term><term>Vaisseaux lymphatiques ()</term><term>Vaisseaux lymphatiques (anatomopathologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term><term>Inflammation Mediators</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Ketoprofen</term><term>Receptors, Tumor Necrosis Factor, Type I</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Anti-Inflammatory Agents</term><term>Anti-Inflammatory Agents, Non-Steroidal</term><term>Ketoprofen</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Vaisseaux lymphatiques</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Gene Expression Regulation</term><term>Lymphatic Vessels</term><term>Solubility</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Lymphoedème</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cytokines</term><term>Médiateurs de l'inflammation</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lymphatic Vessels</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Kétoprofène</term><term>Récepteur au facteur de nécrose tumorale de type I</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Lymphoedème</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Anti-inflammatoires</term><term>Anti-inflammatoires non stéroïdiens</term><term>Kétoprofène</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Mice</term><term>Models, Immunological</term><term>Organ Specificity</term><term>Reverse Transcriptase Polymerase Chain Reaction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Lymphoedème</term><term>Modèles immunologiques</term><term>RT-PCR</term><term>Régulation de l'expression des gènes</term><term>Solubilité</term><term>Souris</term><term>Spécificité d'organe</term><term>Vaisseaux lymphatiques</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Background</title><p>Disruption of the lymphatic vasculature causes edema, inflammation, and end-tissue destruction. To assess the therapeutic efficacy of systemic anti-inflammatory therapy in this disease, we examined the impact of a nonsteroidal anti-inflammatory drug (NSAID), ketoprofen, and of a soluble TNF-α receptor (sTNF-R1) upon tumor necrosis factor (TNF)-α activity in a mouse model of acquired lymphedema.</p></sec><sec><title>Methods and Findings</title><p>Lymphedema was induced by microsurgical ablation of major lymphatic conduits in the murine tail. Untreated control mice with lymphedema developed significant edema and extensive histopathological inflammation compared to sham surgical controls. Short-term ketoprofen treatment reduced tail edema and normalized the histopathology while paradoxically increasing TNF-α gene expression and cytokine levels. Conversely, sTNF-R1 treatment increased tail volume, exacerbated the histopathology, and decreased TNF-α gene expression. Expression of vascular endothelial growth factor-C (VEGF-C), which stimulates lymphangiogenesis, closely correlated with TNF-α expression.</p></sec><sec><title>Conclusions</title><p>Ketoprofen therapy reduces experimental post-surgical lymphedema, yet direct TNF-α inhibition does not. Reducing inflammation while preserving TNF-α activity appears to optimize the repair response. It is possible that the observed favorable responses, at least in part, are mediated through enhanced VEGF-C signaling.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Nakamura, K" uniqKey="Nakamura K">K Nakamura</name></author><author><name sortKey="Rockson, Sg" uniqKey="Rockson S">SG Rockson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Rockson, Sg" uniqKey="Rockson S">SG Rockson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Szuba, A" uniqKey="Szuba A">A Szuba</name></author><author><name sortKey="Skobe, M" uniqKey="Skobe M">M Skobe</name></author><author><name sortKey="Karkkainen, Mj" uniqKey="Karkkainen M">MJ Karkkainen</name></author><author><name sortKey="Shin, Ws" uniqKey="Shin W">WS Shin</name></author><author><name sortKey="Beynet, Dp" uniqKey="Beynet D">DP Beynet</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cheung, L" uniqKey="Cheung L">L Cheung</name></author><author><name sortKey="Han, J" uniqKey="Han J">J Han</name></author><author><name sortKey="Beilhack, A" uniqKey="Beilhack A">A Beilhack</name></author><author><name sortKey="Joshi, S" uniqKey="Joshi S">S Joshi</name></author><author><name sortKey="Wilburn, P" uniqKey="Wilburn P">P Wilburn</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tabibiazar, R" uniqKey="Tabibiazar R">R Tabibiazar</name></author><author><name sortKey="Cheung, L" uniqKey="Cheung L">L Cheung</name></author><author><name sortKey="Han, J" uniqKey="Han J">J Han</name></author><author><name sortKey="Swanson, J" uniqKey="Swanson J">J Swanson</name></author><author><name sortKey="Beilhack, A" uniqKey="Beilhack A">A Beilhack</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Saito, Y" uniqKey="Saito Y">Y Saito</name></author><author><name sortKey="Nakagami, H" uniqKey="Nakagami H">H 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sortKey="Nakamura, K" uniqKey="Nakamura K">K Nakamura</name></author><author><name sortKey="Rockson, Sg" uniqKey="Rockson S">SG Rockson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Skobe, M" uniqKey="Skobe M">M Skobe</name></author><author><name sortKey="Hamberg, Lm" uniqKey="Hamberg L">LM Hamberg</name></author><author><name sortKey="Hawighorst, T" uniqKey="Hawighorst T">T Hawighorst</name></author><author><name sortKey="Schirner, M" uniqKey="Schirner M">M Schirner</name></author><author><name sortKey="Wolf, Gl" uniqKey="Wolf G">GL Wolf</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mandriota, Sj" uniqKey="Mandriota S">SJ Mandriota</name></author><author><name sortKey="Jussila, L" uniqKey="Jussila L">L Jussila</name></author><author><name sortKey="Jeltsch, M" uniqKey="Jeltsch M">M Jeltsch</name></author><author><name sortKey="Compagni, A" uniqKey="Compagni A">A Compagni</name></author><author><name 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Romano</name></author><author><name sortKey="Jung, Ss" uniqKey="Jung S">SS Jung</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Goldman, J" uniqKey="Goldman J">J Goldman</name></author><author><name sortKey="Le, Tx" uniqKey="Le T">TX Le</name></author><author><name sortKey="Skobe, M" uniqKey="Skobe M">M Skobe</name></author><author><name sortKey="Swartz, Ma" uniqKey="Swartz M">MA Swartz</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sitzia, J" uniqKey="Sitzia J">J Sitzia</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Pan, D" uniqKey="Pan D">D Pan</name></author><author><name sortKey="Han, J" uniqKey="Han J">J Han</name></author><author><name sortKey="Wilburn, P" uniqKey="Wilburn P">P Wilburn</name></author><author><name sortKey="Rockson, Sg" uniqKey="Rockson S">SG Rockson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Sanders, Je" uniqKey="Sanders J">JE Sanders</name></author><author><name sortKey="Goldstein, Bs" uniqKey="Goldstein B">BS Goldstein</name></author><author><name sortKey="Leotta, Df" uniqKey="Leotta D">DF Leotta</name></author><author><name sortKey="Richards, Ka" uniqKey="Richards K">KA Richards</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chen, Mm" uniqKey="Chen M">MM Chen</name></author><author><name sortKey="Ashley, Ea" uniqKey="Ashley E">EA Ashley</name></author><author><name sortKey="Deng, Dx" uniqKey="Deng D">DX Deng</name></author><author><name sortKey="Tsalenko, A" uniqKey="Tsalenko A">A Tsalenko</name></author><author><name sortKey="Deng, A" uniqKey="Deng A">A Deng</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list></list><tree><noCountry><name sortKey="Nakamura, Kenta" sort="Nakamura, Kenta" uniqKey="Nakamura K" first="Kenta" last="Nakamura">Kenta Nakamura</name><name sortKey="Radhakrishnan, Kavita" sort="Radhakrishnan, Kavita" uniqKey="Radhakrishnan K" first="Kavita" last="Radhakrishnan">Kavita Radhakrishnan</name><name sortKey="Rockson, Stanley G" sort="Rockson, Stanley G" uniqKey="Rockson S" first="Stanley G." last="Rockson">Stanley G. 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