Signaling of Prostaglandin E Receptors, EP3 and EP4 Facilitates Wound Healing and Lymphangiogenesis with Enhanced Recruitment of M2 Macrophages in Mice
Identifieur interne : 008878 ( Ncbi/Checkpoint ); précédent : 008877; suivant : 008879Signaling of Prostaglandin E Receptors, EP3 and EP4 Facilitates Wound Healing and Lymphangiogenesis with Enhanced Recruitment of M2 Macrophages in Mice
Auteurs : Kanako Hosono [Japon] ; Risa Isonaka [Japon] ; Tadashi Kawakami [Japon] ; Shuh Narumiya [Japon] ; Masataka Majima [Japon]Source :
- PLoS ONE [ 1932-6203 ] ; 2016.
Abstract
Lymphangiogenesis plays an important role in homeostasis, metabolism, and immunity, and also occurs during wound-healing. Here, we examined the roles of prostaglandin E2 (PGE2) receptor (EP) signaling in enhancement of lymphangiogenesis in wound healing processes. The hole-punch was made in the ears of male C57BL/6 mice using a metal ear punch. Healing process and lymphangiogenesis together with macrophage recruitment were analyzed in EP knockout mice. Lymphangiogenesis was up-regulated in the granulation tissues at the margins of punched-hole wounds in mouse ears, and this increase was accompanied by increased expression levels of COX-2 and microsomal prostaglandin E synthase-1. Administration of celecoxib, a COX-2 inhibitor, suppressed lymphangiogenesis in the granulation tissues and reduced the induction of the pro-lymphangiogenic factors, vascular endothelial growth factor (VEGF) -C and VEGF-D. Topical applications of selective EP receptor agonists enhanced the expressions of lymphatic vessel endothelial hyaluronan receptor-1 and VEGF receptor-3. The wound-healing processes and recruitment of CD11b-positive macrophages, which produced VEGF-C and VEGF-D, were suppressed under COX-2 inhibition. Mice lacking either EP3 or EP4 exhibited reduced wound-healing, lymphangiogenesis and recruitment of M2 macrophages, compared with wild type mice. Proliferation of cultured human lymphatic endothelial cells was not detected under PGE2 stimulation. Lymphangiogenesis and recruitment of M2 macrophages that produced VEGF-C/D were suppressed in mice treated with a COX-2 inhibitor or lacking either EP3 or EP4 during wound healing. COX-2 and EP3/EP4 signaling may be novel targets to control lymphangiogenesis in vivo.
Url:
DOI: 10.1371/journal.pone.0162532
PubMed: 27711210
PubMed Central: 5053515
Affiliations:
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Kanagawa</wicri:regionArea><wicri:noRegion>Kanagawa</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="aff002"><addr-line>Department of Pharmacology, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan</addr-line></nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Pharmacology, Kitasato University School of Medicine, Sagamihara, Kanagawa</wicri:regionArea><wicri:noRegion>Kanagawa</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="aff003"><addr-line>Department of Physiology, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan</addr-line></nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Physiology, Kitasato University School of Medicine, Sagamihara, Kanagawa</wicri:regionArea><wicri:noRegion>Kanagawa</wicri:noRegion></affiliation></author><author><name sortKey="Isonaka, Risa" sort="Isonaka, Risa" uniqKey="Isonaka R" first="Risa" last="Isonaka">Risa Isonaka</name><affiliation wicri:level="1"><nlm:aff id="aff003"><addr-line>Department of Physiology, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan</addr-line></nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Physiology, Kitasato University School of Medicine, Sagamihara, Kanagawa</wicri:regionArea><wicri:noRegion>Kanagawa</wicri:noRegion></affiliation></author><author><name sortKey="Kawakami, Tadashi" sort="Kawakami, Tadashi" uniqKey="Kawakami T" first="Tadashi" last="Kawakami">Tadashi Kawakami</name><affiliation wicri:level="1"><nlm:aff id="aff003"><addr-line>Department of Physiology, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan</addr-line></nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Physiology, Kitasato University School of Medicine, Sagamihara, Kanagawa</wicri:regionArea><wicri:noRegion>Kanagawa</wicri:noRegion></affiliation></author><author><name sortKey="Narumiya, Shuh" sort="Narumiya, Shuh" uniqKey="Narumiya S" first="Shuh" last="Narumiya">Shuh Narumiya</name><affiliation wicri:level="1"><nlm:aff id="aff004"><addr-line>Center for Innovation in Immunoregulation Technology and Therapeutics, Kyoto University Graduate School of Medicine, Kyoto, Japan</addr-line></nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Center for Innovation in Immunoregulation Technology and Therapeutics, Kyoto University Graduate School of Medicine, Kyoto</wicri:regionArea><wicri:noRegion>Kyoto</wicri:noRegion></affiliation></author><author><name sortKey="Majima, Masataka" sort="Majima, Masataka" uniqKey="Majima M" first="Masataka" last="Majima">Masataka Majima</name><affiliation wicri:level="1"><nlm:aff id="aff001"><addr-line>Department of Molecular Pharmacology, Graduate School of Medical Sciences, Kitasato University, Sagamihara, Kanagawa, Japan</addr-line></nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Molecular Pharmacology, Graduate School of Medical Sciences, Kitasato University, Sagamihara, Kanagawa</wicri:regionArea><wicri:noRegion>Kanagawa</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="aff002"><addr-line>Department of Pharmacology, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan</addr-line></nlm:aff><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Pharmacology, Kitasato University School of Medicine, Sagamihara, Kanagawa</wicri:regionArea><wicri:noRegion>Kanagawa</wicri:noRegion></affiliation></author></analytic><series><title level="j">PLoS ONE</title><idno type="eISSN">1932-6203</idno><imprint><date when="2016">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Lymphangiogenesis plays an important role in homeostasis, metabolism, and immunity, and also occurs during wound-healing. Here, we examined the roles of prostaglandin E<sub>2</sub> (PGE<sub>2</sub>) receptor (EP) signaling in enhancement of lymphangiogenesis in wound healing processes. The hole-punch was made in the ears of male C57BL/6 mice using a metal ear punch. Healing process and lymphangiogenesis together with macrophage recruitment were analyzed in EP knockout mice. Lymphangiogenesis was up-regulated in the granulation tissues at the margins of punched-hole wounds in mouse ears, and this increase was accompanied by increased expression levels of COX-2 and microsomal prostaglandin E synthase-1. Administration of celecoxib, a COX-2 inhibitor, suppressed lymphangiogenesis in the granulation tissues and reduced the induction of the pro-lymphangiogenic factors, vascular endothelial growth factor (VEGF) -C and VEGF-D. Topical applications of selective EP receptor agonists enhanced the expressions of lymphatic vessel endothelial hyaluronan receptor-1 and VEGF receptor-3. The wound-healing processes and recruitment of CD11b-positive macrophages, which produced VEGF-C and VEGF-D, were suppressed under COX-2 inhibition. Mice lacking either EP3 or EP4 exhibited reduced wound-healing, lymphangiogenesis and recruitment of M2 macrophages, compared with wild type mice. Proliferation of cultured human lymphatic endothelial cells was not detected under PGE<sub>2</sub> stimulation. Lymphangiogenesis and recruitment of M2 macrophages that produced VEGF-C/D were suppressed in mice treated with a COX-2 inhibitor or lacking either EP3 or EP4 during wound healing. COX-2 and EP3/EP4 signaling may be novel targets to control lymphangiogenesis in vivo.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Kim, H" uniqKey="Kim H">H Kim</name></author><author><name sortKey="Kataru, Rp" uniqKey="Kataru R">RP Kataru</name></author><author><name sortKey="Koh, Gy" uniqKey="Koh G">GY Koh</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Paavonen, K" uniqKey="Paavonen K">K Paavonen</name></author><author><name sortKey="Puolakkainen, P" uniqKey="Puolakkainen P">P Puolakkainen</name></author><author><name sortKey="Jussila, L" uniqKey="Jussila L">L Jussila</name></author><author><name sortKey="Jahkola, T" uniqKey="Jahkola T">T Jahkola</name></author><author><name sortKey="Alitalo, K" uniqKey="Alitalo K">K Alitalo</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kurashige, C" uniqKey="Kurashige C">C Kurashige</name></author><author><name 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Machura</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhang, Mz" uniqKey="Zhang M">MZ Zhang</name></author><author><name sortKey="Yao, B" uniqKey="Yao B">B Yao</name></author><author><name sortKey="Wang, Y" uniqKey="Wang Y">Y Wang</name></author><author><name sortKey="Yang, S" uniqKey="Yang S">S Yang</name></author><author><name sortKey="Wang, S" uniqKey="Wang S">S Wang</name></author><author><name sortKey="Fan, X" uniqKey="Fan X">X Fan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Binger, Kj" uniqKey="Binger K">KJ Binger</name></author><author><name sortKey="Gebhardt, M" uniqKey="Gebhardt M">M Gebhardt</name></author><author><name sortKey="Heinig, M" uniqKey="Heinig M">M Heinig</name></author><author><name sortKey="Rintisch, C" uniqKey="Rintisch C">C Rintisch</name></author><author><name sortKey="Schroeder, A" uniqKey="Schroeder A">A Schroeder</name></author><author><name sortKey="Neuhofer, W" uniqKey="Neuhofer W">W Neuhofer</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Japon</li></country></list><tree><country name="Japon"><noRegion><name sortKey="Hosono, Kanako" sort="Hosono, Kanako" uniqKey="Hosono K" first="Kanako" last="Hosono">Kanako Hosono</name></noRegion><name sortKey="Hosono, Kanako" sort="Hosono, Kanako" uniqKey="Hosono K" first="Kanako" last="Hosono">Kanako Hosono</name><name sortKey="Hosono, Kanako" sort="Hosono, Kanako" uniqKey="Hosono K" first="Kanako" last="Hosono">Kanako Hosono</name><name sortKey="Isonaka, Risa" sort="Isonaka, Risa" uniqKey="Isonaka R" first="Risa" last="Isonaka">Risa Isonaka</name><name sortKey="Kawakami, Tadashi" sort="Kawakami, Tadashi" uniqKey="Kawakami T" first="Tadashi" last="Kawakami">Tadashi Kawakami</name><name sortKey="Majima, Masataka" sort="Majima, Masataka" uniqKey="Majima M" first="Masataka" last="Majima">Masataka Majima</name><name sortKey="Majima, Masataka" sort="Majima, Masataka" uniqKey="Majima M" first="Masataka" last="Majima">Masataka Majima</name><name sortKey="Narumiya, Shuh" sort="Narumiya, Shuh" uniqKey="Narumiya S" first="Shuh" last="Narumiya">Shuh Narumiya</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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