Binary regulation of interleukin(IL)-6 production by EP1 and EP2/EP4 subtypes of PGE2 receptors in IL-1β-stimulated human gingival fibroblasts
Prostaglandin E2(PGE2) exerts its biological actions via EP receptors, which are divided into four subtypes of EP1, EP2, EP3 and EP4. In the present study, we investigated whether PGE2 regulated interleukin(IL)-6 production in human gingival fibroblasts (HGF) stimulated with IL-1β and if so, which s...
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Gespeichert in:
| Autor*in: |
Noguchi, Kazuyuki [verfasserIn] Shitashige, Miki [verfasserIn] Endo, Hirahito [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Copenhagen: Munksgaard International Publishers ; 2002 |
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| Schlagwörter: |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2008 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Journal of periodontal research - Oxford [u.a.] : Wiley-Blackwell, 1966, 37(2002), 1, Seite 0 |
| Übergeordnetes Werk: |
volume:37 ; year:2002 ; number:1 ; pages:0 |
| Links: |
|---|
| DOI / URN: |
10.1034/j.1600-0765.2002.00641.x |
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| 520 | |a Prostaglandin E2(PGE2) exerts its biological actions via EP receptors, which are divided into four subtypes of EP1, EP2, EP3 and EP4. In the present study, we investigated whether PGE2 regulated interleukin(IL)-6 production in human gingival fibroblasts (HGF) stimulated with IL-1β and if so, which subtype(s) of PGE2 receptors were involved. Indomethacin, a cyclooxygenase inhibitor, significantly enhanced IL-1β-induced IL-6 production by HGF, although it completely inhibited IL-1β-induced PGE2 production. Exogenous PGE2 suppressed the IL-1β-induced IL-6 production. Reverse transcription-polymerase chain reaction analysis demonstrated that mRNA of EP1, EP2 and EP4, but not EP3 mRNA, was expressed in unstimulated and IL-1β-stimulated HGF. 11-deoxy-PGE1, a selective EP2/EP3/EP4 agonist, and butaprost, a selective EP2 agonist, inhibited IL-1β-induced IL-6 production, although butaprost was less potent than 11-deoxy-PGE1. 17-phenyl-ω-trinor PGE2, an EP1 agonist, enhanced IL-1β-induced IL-6 production. Based on these data, we suggest that PGE2 can up- or downregulate IL-1β-induced IL-6 production via EP1 receptors or via EP2/EP4 receptors in HGF, respectively. Expression and function of EP1, EP2 and EP4 receptors in HGF may play critical roles in controlling inflammatory jreiodontal conditions. | ||
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10.1034/j.1600-0765.2002.00641.x doi (DE-627)NLEJ242985440 DE-627 ger DE-627 rakwb Noguchi, Kazuyuki verfasserin aut Binary regulation of interleukin(IL)-6 production by EP1 and EP2/EP4 subtypes of PGE2 receptors in IL-1β-stimulated human gingival fibroblasts Copenhagen Munksgaard International Publishers 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Prostaglandin E2(PGE2) exerts its biological actions via EP receptors, which are divided into four subtypes of EP1, EP2, EP3 and EP4. In the present study, we investigated whether PGE2 regulated interleukin(IL)-6 production in human gingival fibroblasts (HGF) stimulated with IL-1β and if so, which subtype(s) of PGE2 receptors were involved. Indomethacin, a cyclooxygenase inhibitor, significantly enhanced IL-1β-induced IL-6 production by HGF, although it completely inhibited IL-1β-induced PGE2 production. Exogenous PGE2 suppressed the IL-1β-induced IL-6 production. Reverse transcription-polymerase chain reaction analysis demonstrated that mRNA of EP1, EP2 and EP4, but not EP3 mRNA, was expressed in unstimulated and IL-1β-stimulated HGF. 11-deoxy-PGE1, a selective EP2/EP3/EP4 agonist, and butaprost, a selective EP2 agonist, inhibited IL-1β-induced IL-6 production, although butaprost was less potent than 11-deoxy-PGE1. 17-phenyl-ω-trinor PGE2, an EP1 agonist, enhanced IL-1β-induced IL-6 production. Based on these data, we suggest that PGE2 can up- or downregulate IL-1β-induced IL-6 production via EP1 receptors or via EP2/EP4 receptors in HGF, respectively. Expression and function of EP1, EP2 and EP4 receptors in HGF may play critical roles in controlling inflammatory jreiodontal conditions. 2008 Blackwell Publishing Journal Backfiles 1879-2005 |2008|||||||||| gingival fibroblasts Shitashige, Miki verfasserin aut Endo, Hirahito verfasserin aut Kondo, Hirobumi oth Ishikawa, Isao oth In Journal of periodontal research Oxford [u.a.] : Wiley-Blackwell, 1966 37(2002), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927452 (DE-600)2025633-4 1600-0765 nnns volume:37 year:2002 number:1 pages:0 http://dx.doi.org/10.1034/j.1600-0765.2002.00641.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 37 2002 1 0 |
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10.1034/j.1600-0765.2002.00641.x doi (DE-627)NLEJ242985440 DE-627 ger DE-627 rakwb Noguchi, Kazuyuki verfasserin aut Binary regulation of interleukin(IL)-6 production by EP1 and EP2/EP4 subtypes of PGE2 receptors in IL-1β-stimulated human gingival fibroblasts Copenhagen Munksgaard International Publishers 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Prostaglandin E2(PGE2) exerts its biological actions via EP receptors, which are divided into four subtypes of EP1, EP2, EP3 and EP4. In the present study, we investigated whether PGE2 regulated interleukin(IL)-6 production in human gingival fibroblasts (HGF) stimulated with IL-1β and if so, which subtype(s) of PGE2 receptors were involved. Indomethacin, a cyclooxygenase inhibitor, significantly enhanced IL-1β-induced IL-6 production by HGF, although it completely inhibited IL-1β-induced PGE2 production. Exogenous PGE2 suppressed the IL-1β-induced IL-6 production. Reverse transcription-polymerase chain reaction analysis demonstrated that mRNA of EP1, EP2 and EP4, but not EP3 mRNA, was expressed in unstimulated and IL-1β-stimulated HGF. 11-deoxy-PGE1, a selective EP2/EP3/EP4 agonist, and butaprost, a selective EP2 agonist, inhibited IL-1β-induced IL-6 production, although butaprost was less potent than 11-deoxy-PGE1. 17-phenyl-ω-trinor PGE2, an EP1 agonist, enhanced IL-1β-induced IL-6 production. Based on these data, we suggest that PGE2 can up- or downregulate IL-1β-induced IL-6 production via EP1 receptors or via EP2/EP4 receptors in HGF, respectively. Expression and function of EP1, EP2 and EP4 receptors in HGF may play critical roles in controlling inflammatory jreiodontal conditions. 2008 Blackwell Publishing Journal Backfiles 1879-2005 |2008|||||||||| gingival fibroblasts Shitashige, Miki verfasserin aut Endo, Hirahito verfasserin aut Kondo, Hirobumi oth Ishikawa, Isao oth In Journal of periodontal research Oxford [u.a.] : Wiley-Blackwell, 1966 37(2002), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927452 (DE-600)2025633-4 1600-0765 nnns volume:37 year:2002 number:1 pages:0 http://dx.doi.org/10.1034/j.1600-0765.2002.00641.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 37 2002 1 0 |
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10.1034/j.1600-0765.2002.00641.x doi (DE-627)NLEJ242985440 DE-627 ger DE-627 rakwb Noguchi, Kazuyuki verfasserin aut Binary regulation of interleukin(IL)-6 production by EP1 and EP2/EP4 subtypes of PGE2 receptors in IL-1β-stimulated human gingival fibroblasts Copenhagen Munksgaard International Publishers 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Prostaglandin E2(PGE2) exerts its biological actions via EP receptors, which are divided into four subtypes of EP1, EP2, EP3 and EP4. In the present study, we investigated whether PGE2 regulated interleukin(IL)-6 production in human gingival fibroblasts (HGF) stimulated with IL-1β and if so, which subtype(s) of PGE2 receptors were involved. Indomethacin, a cyclooxygenase inhibitor, significantly enhanced IL-1β-induced IL-6 production by HGF, although it completely inhibited IL-1β-induced PGE2 production. Exogenous PGE2 suppressed the IL-1β-induced IL-6 production. Reverse transcription-polymerase chain reaction analysis demonstrated that mRNA of EP1, EP2 and EP4, but not EP3 mRNA, was expressed in unstimulated and IL-1β-stimulated HGF. 11-deoxy-PGE1, a selective EP2/EP3/EP4 agonist, and butaprost, a selective EP2 agonist, inhibited IL-1β-induced IL-6 production, although butaprost was less potent than 11-deoxy-PGE1. 17-phenyl-ω-trinor PGE2, an EP1 agonist, enhanced IL-1β-induced IL-6 production. Based on these data, we suggest that PGE2 can up- or downregulate IL-1β-induced IL-6 production via EP1 receptors or via EP2/EP4 receptors in HGF, respectively. Expression and function of EP1, EP2 and EP4 receptors in HGF may play critical roles in controlling inflammatory jreiodontal conditions. 2008 Blackwell Publishing Journal Backfiles 1879-2005 |2008|||||||||| gingival fibroblasts Shitashige, Miki verfasserin aut Endo, Hirahito verfasserin aut Kondo, Hirobumi oth Ishikawa, Isao oth In Journal of periodontal research Oxford [u.a.] : Wiley-Blackwell, 1966 37(2002), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927452 (DE-600)2025633-4 1600-0765 nnns volume:37 year:2002 number:1 pages:0 http://dx.doi.org/10.1034/j.1600-0765.2002.00641.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 37 2002 1 0 |
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10.1034/j.1600-0765.2002.00641.x doi (DE-627)NLEJ242985440 DE-627 ger DE-627 rakwb Noguchi, Kazuyuki verfasserin aut Binary regulation of interleukin(IL)-6 production by EP1 and EP2/EP4 subtypes of PGE2 receptors in IL-1β-stimulated human gingival fibroblasts Copenhagen Munksgaard International Publishers 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Prostaglandin E2(PGE2) exerts its biological actions via EP receptors, which are divided into four subtypes of EP1, EP2, EP3 and EP4. In the present study, we investigated whether PGE2 regulated interleukin(IL)-6 production in human gingival fibroblasts (HGF) stimulated with IL-1β and if so, which subtype(s) of PGE2 receptors were involved. Indomethacin, a cyclooxygenase inhibitor, significantly enhanced IL-1β-induced IL-6 production by HGF, although it completely inhibited IL-1β-induced PGE2 production. Exogenous PGE2 suppressed the IL-1β-induced IL-6 production. Reverse transcription-polymerase chain reaction analysis demonstrated that mRNA of EP1, EP2 and EP4, but not EP3 mRNA, was expressed in unstimulated and IL-1β-stimulated HGF. 11-deoxy-PGE1, a selective EP2/EP3/EP4 agonist, and butaprost, a selective EP2 agonist, inhibited IL-1β-induced IL-6 production, although butaprost was less potent than 11-deoxy-PGE1. 17-phenyl-ω-trinor PGE2, an EP1 agonist, enhanced IL-1β-induced IL-6 production. Based on these data, we suggest that PGE2 can up- or downregulate IL-1β-induced IL-6 production via EP1 receptors or via EP2/EP4 receptors in HGF, respectively. Expression and function of EP1, EP2 and EP4 receptors in HGF may play critical roles in controlling inflammatory jreiodontal conditions. 2008 Blackwell Publishing Journal Backfiles 1879-2005 |2008|||||||||| gingival fibroblasts Shitashige, Miki verfasserin aut Endo, Hirahito verfasserin aut Kondo, Hirobumi oth Ishikawa, Isao oth In Journal of periodontal research Oxford [u.a.] : Wiley-Blackwell, 1966 37(2002), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927452 (DE-600)2025633-4 1600-0765 nnns volume:37 year:2002 number:1 pages:0 http://dx.doi.org/10.1034/j.1600-0765.2002.00641.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 37 2002 1 0 |
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10.1034/j.1600-0765.2002.00641.x doi (DE-627)NLEJ242985440 DE-627 ger DE-627 rakwb Noguchi, Kazuyuki verfasserin aut Binary regulation of interleukin(IL)-6 production by EP1 and EP2/EP4 subtypes of PGE2 receptors in IL-1β-stimulated human gingival fibroblasts Copenhagen Munksgaard International Publishers 2002 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Prostaglandin E2(PGE2) exerts its biological actions via EP receptors, which are divided into four subtypes of EP1, EP2, EP3 and EP4. In the present study, we investigated whether PGE2 regulated interleukin(IL)-6 production in human gingival fibroblasts (HGF) stimulated with IL-1β and if so, which subtype(s) of PGE2 receptors were involved. Indomethacin, a cyclooxygenase inhibitor, significantly enhanced IL-1β-induced IL-6 production by HGF, although it completely inhibited IL-1β-induced PGE2 production. Exogenous PGE2 suppressed the IL-1β-induced IL-6 production. Reverse transcription-polymerase chain reaction analysis demonstrated that mRNA of EP1, EP2 and EP4, but not EP3 mRNA, was expressed in unstimulated and IL-1β-stimulated HGF. 11-deoxy-PGE1, a selective EP2/EP3/EP4 agonist, and butaprost, a selective EP2 agonist, inhibited IL-1β-induced IL-6 production, although butaprost was less potent than 11-deoxy-PGE1. 17-phenyl-ω-trinor PGE2, an EP1 agonist, enhanced IL-1β-induced IL-6 production. Based on these data, we suggest that PGE2 can up- or downregulate IL-1β-induced IL-6 production via EP1 receptors or via EP2/EP4 receptors in HGF, respectively. Expression and function of EP1, EP2 and EP4 receptors in HGF may play critical roles in controlling inflammatory jreiodontal conditions. 2008 Blackwell Publishing Journal Backfiles 1879-2005 |2008|||||||||| gingival fibroblasts Shitashige, Miki verfasserin aut Endo, Hirahito verfasserin aut Kondo, Hirobumi oth Ishikawa, Isao oth In Journal of periodontal research Oxford [u.a.] : Wiley-Blackwell, 1966 37(2002), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927452 (DE-600)2025633-4 1600-0765 nnns volume:37 year:2002 number:1 pages:0 http://dx.doi.org/10.1034/j.1600-0765.2002.00641.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 37 2002 1 0 |
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verfasserin |
| title_sort |
binary regulation of interleukin(il)-6 production by ep1 and ep2/ep4 subtypes of pge2 receptors in il-1β-stimulated human gingival fibroblasts |
| title_auth |
Binary regulation of interleukin(IL)-6 production by EP1 and EP2/EP4 subtypes of PGE2 receptors in IL-1β-stimulated human gingival fibroblasts |
| abstract |
Prostaglandin E2(PGE2) exerts its biological actions via EP receptors, which are divided into four subtypes of EP1, EP2, EP3 and EP4. In the present study, we investigated whether PGE2 regulated interleukin(IL)-6 production in human gingival fibroblasts (HGF) stimulated with IL-1β and if so, which subtype(s) of PGE2 receptors were involved. Indomethacin, a cyclooxygenase inhibitor, significantly enhanced IL-1β-induced IL-6 production by HGF, although it completely inhibited IL-1β-induced PGE2 production. Exogenous PGE2 suppressed the IL-1β-induced IL-6 production. Reverse transcription-polymerase chain reaction analysis demonstrated that mRNA of EP1, EP2 and EP4, but not EP3 mRNA, was expressed in unstimulated and IL-1β-stimulated HGF. 11-deoxy-PGE1, a selective EP2/EP3/EP4 agonist, and butaprost, a selective EP2 agonist, inhibited IL-1β-induced IL-6 production, although butaprost was less potent than 11-deoxy-PGE1. 17-phenyl-ω-trinor PGE2, an EP1 agonist, enhanced IL-1β-induced IL-6 production. Based on these data, we suggest that PGE2 can up- or downregulate IL-1β-induced IL-6 production via EP1 receptors or via EP2/EP4 receptors in HGF, respectively. Expression and function of EP1, EP2 and EP4 receptors in HGF may play critical roles in controlling inflammatory jreiodontal conditions. |
| abstractGer |
Prostaglandin E2(PGE2) exerts its biological actions via EP receptors, which are divided into four subtypes of EP1, EP2, EP3 and EP4. In the present study, we investigated whether PGE2 regulated interleukin(IL)-6 production in human gingival fibroblasts (HGF) stimulated with IL-1β and if so, which subtype(s) of PGE2 receptors were involved. Indomethacin, a cyclooxygenase inhibitor, significantly enhanced IL-1β-induced IL-6 production by HGF, although it completely inhibited IL-1β-induced PGE2 production. Exogenous PGE2 suppressed the IL-1β-induced IL-6 production. Reverse transcription-polymerase chain reaction analysis demonstrated that mRNA of EP1, EP2 and EP4, but not EP3 mRNA, was expressed in unstimulated and IL-1β-stimulated HGF. 11-deoxy-PGE1, a selective EP2/EP3/EP4 agonist, and butaprost, a selective EP2 agonist, inhibited IL-1β-induced IL-6 production, although butaprost was less potent than 11-deoxy-PGE1. 17-phenyl-ω-trinor PGE2, an EP1 agonist, enhanced IL-1β-induced IL-6 production. Based on these data, we suggest that PGE2 can up- or downregulate IL-1β-induced IL-6 production via EP1 receptors or via EP2/EP4 receptors in HGF, respectively. Expression and function of EP1, EP2 and EP4 receptors in HGF may play critical roles in controlling inflammatory jreiodontal conditions. |
| abstract_unstemmed |
Prostaglandin E2(PGE2) exerts its biological actions via EP receptors, which are divided into four subtypes of EP1, EP2, EP3 and EP4. In the present study, we investigated whether PGE2 regulated interleukin(IL)-6 production in human gingival fibroblasts (HGF) stimulated with IL-1β and if so, which subtype(s) of PGE2 receptors were involved. Indomethacin, a cyclooxygenase inhibitor, significantly enhanced IL-1β-induced IL-6 production by HGF, although it completely inhibited IL-1β-induced PGE2 production. Exogenous PGE2 suppressed the IL-1β-induced IL-6 production. Reverse transcription-polymerase chain reaction analysis demonstrated that mRNA of EP1, EP2 and EP4, but not EP3 mRNA, was expressed in unstimulated and IL-1β-stimulated HGF. 11-deoxy-PGE1, a selective EP2/EP3/EP4 agonist, and butaprost, a selective EP2 agonist, inhibited IL-1β-induced IL-6 production, although butaprost was less potent than 11-deoxy-PGE1. 17-phenyl-ω-trinor PGE2, an EP1 agonist, enhanced IL-1β-induced IL-6 production. Based on these data, we suggest that PGE2 can up- or downregulate IL-1β-induced IL-6 production via EP1 receptors or via EP2/EP4 receptors in HGF, respectively. Expression and function of EP1, EP2 and EP4 receptors in HGF may play critical roles in controlling inflammatory jreiodontal conditions. |
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Binary regulation of interleukin(IL)-6 production by EP1 and EP2/EP4 subtypes of PGE2 receptors in IL-1β-stimulated human gingival fibroblasts |
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Shitashige, Miki Endo, Hirahito Kondo, Hirobumi Ishikawa, Isao |
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