The Experts below are selected from a list of 273 Experts worldwide ranked by ideXlab platform
Hirotsugu Okamoto - One of the best experts on this subject based on the ideXlab platform.
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Roles of Thromboxane Receptor Signaling in Enhancement of Lipopolysaccharide-Induced Lymphangiogenesis and Lymphatic Drainage Function in Diaphragm.
Arteriosclerosis thrombosis and vascular biology, 2021Co-Authors: Hiromi Matsuda, Yoshiya Ito, Kanako Hosono, Seri Tsuru, Tomoyoshi Inoue, Shuji Nakamoto, Chie Kurashige, Masanori Hirashma, Shuh Narumiya, Hirotsugu OkamotoAbstract:OBJECTIVE Thromboxane is an arachidonic acid metabolite that exerts its actions through a G-protein-coupled receptor with 7 transmembrane domains. Although an arachidonic acid metabolite, prostaglandin E2 was reported to enhance lymphangiogenesis, little is known on other arachidonic acid metabolites. In the present study, we investigated the roles of TP (thromboxane prostanoid) signaling in facilitating lymphangiogenesis during inflammation. Approach and Results: Inflammation was induced by repeated intraperitoneal injections of lipopolysaccharide, and lymphangiogenesis essential for draining peritoneal fluids was estimated in the diaphragm. Lipopolysaccharide induced lymphangiogenesis in the diaphragm in a time-dependent manner in wild-type mice. Compared with wild-type mice, lipopolysaccharide-induced lymphangiogenesis in TP-deficient (TP-/-) mouse diaphragm tissues was suppressed, and this was accompanied by reduced Drainage Function from the peritoneal cavity. TP-positive macrophages and T cells were accumulated in the diaphragm and produced VEGF (vascular endothelial growth factor)-C and VEGF-D in a TP-dependent manner. Removal of macrophages and T cells resulted in reduced lymphangiogenesis and lowered expressions of VEGF-C and VEGF-D. Furthermore, TP-/- bone marrow chimeric mice exhibited reduced lymphangiogenesis. TP knockout specific to macrophages and T cells also led to reduced lymphangiogenesis and Drainage Function in mice with lipopolysaccharide injections. CONCLUSIONS The present results suggest that TP signaling exerts prolymphangiogenic activity by acting on macrophages and T cells accumulated during inflammation and that TP signaling represents a novel target for controlling lymphangiogenesis.
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roles of thromboxane receptor signaling in enhancement of lipopolysaccharide induced lymphangiogenesis and lymphatic Drainage Function in diaphragm
Arteriosclerosis Thrombosis and Vascular Biology, 2021Co-Authors: Hiromi Matsuda, Yoshiya Ito, Kanako Hosono, Seri Tsuru, Tomoyoshi Inoue, Shuji Nakamoto, Chie Kurashige, Masanori Hirashma, Shuh Narumiya, Hirotsugu OkamotoAbstract:Objective: Thromboxane is an arachidonic acid metabolite that exerts its actions through a G-protein–coupled receptor with 7 transmembrane domains. Although an arachidonic acid metabolite, prostagl...
Shuji Nakamoto - One of the best experts on this subject based on the ideXlab platform.
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Roles of Thromboxane Receptor Signaling in Enhancement of Lipopolysaccharide-Induced Lymphangiogenesis and Lymphatic Drainage Function in Diaphragm.
Arteriosclerosis thrombosis and vascular biology, 2021Co-Authors: Hiromi Matsuda, Yoshiya Ito, Kanako Hosono, Seri Tsuru, Tomoyoshi Inoue, Shuji Nakamoto, Chie Kurashige, Masanori Hirashma, Shuh Narumiya, Hirotsugu OkamotoAbstract:OBJECTIVE Thromboxane is an arachidonic acid metabolite that exerts its actions through a G-protein-coupled receptor with 7 transmembrane domains. Although an arachidonic acid metabolite, prostaglandin E2 was reported to enhance lymphangiogenesis, little is known on other arachidonic acid metabolites. In the present study, we investigated the roles of TP (thromboxane prostanoid) signaling in facilitating lymphangiogenesis during inflammation. Approach and Results: Inflammation was induced by repeated intraperitoneal injections of lipopolysaccharide, and lymphangiogenesis essential for draining peritoneal fluids was estimated in the diaphragm. Lipopolysaccharide induced lymphangiogenesis in the diaphragm in a time-dependent manner in wild-type mice. Compared with wild-type mice, lipopolysaccharide-induced lymphangiogenesis in TP-deficient (TP-/-) mouse diaphragm tissues was suppressed, and this was accompanied by reduced Drainage Function from the peritoneal cavity. TP-positive macrophages and T cells were accumulated in the diaphragm and produced VEGF (vascular endothelial growth factor)-C and VEGF-D in a TP-dependent manner. Removal of macrophages and T cells resulted in reduced lymphangiogenesis and lowered expressions of VEGF-C and VEGF-D. Furthermore, TP-/- bone marrow chimeric mice exhibited reduced lymphangiogenesis. TP knockout specific to macrophages and T cells also led to reduced lymphangiogenesis and Drainage Function in mice with lipopolysaccharide injections. CONCLUSIONS The present results suggest that TP signaling exerts prolymphangiogenic activity by acting on macrophages and T cells accumulated during inflammation and that TP signaling represents a novel target for controlling lymphangiogenesis.
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roles of thromboxane receptor signaling in enhancement of lipopolysaccharide induced lymphangiogenesis and lymphatic Drainage Function in diaphragm
Arteriosclerosis Thrombosis and Vascular Biology, 2021Co-Authors: Hiromi Matsuda, Yoshiya Ito, Kanako Hosono, Seri Tsuru, Tomoyoshi Inoue, Shuji Nakamoto, Chie Kurashige, Masanori Hirashma, Shuh Narumiya, Hirotsugu OkamotoAbstract:Objective: Thromboxane is an arachidonic acid metabolite that exerts its actions through a G-protein–coupled receptor with 7 transmembrane domains. Although an arachidonic acid metabolite, prostagl...
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Lymphangiogenesis and accumulation of reparative macrophages contribute to liver repair after hepatic ischemia–reperfusion injury
Angiogenesis, 2020Co-Authors: Shuji Nakamoto, Yoshiya Ito, Nobuyuki Nishizawa, Takuya Goto, Ken Kojo, Yusuke Kumamoto, Masahiko Watanabe, Masataka MajimaAbstract:Hepatic tissue repair plays a critical role in determining the outcome of hepatic ischemia–reperfusion (I/R) injury. Hepatic lymphatics participate in the clearance of dead tissues and contribute to the reparative process after acute hepatic injury; however, it remains unknown whether lymphangiogenesis in response to hepatic inflammation is involved in liver repair. Herein, we determined if hepatic lymphangiogenesis improves liver repair after hepatic I/R injury. Using a mouse model of hepatic I/R injury, we investigated hepatic lymphatic structure, growth, and Function in injured murine livers. Hepatic I/R injury enhanced lymphangiogenesis around the portal tract and this was associated with increased expression of pro-lymphangiogenic growth factors including vascular endothelial growth factor (VEGF)-C and VEGF-D. Recombinant VEGF-D treatment facilitated liver repair in association with the expansion of lymphatic vessels and increased expression of genes related to the reparative macrophage phenotype. Treatment with a VEGF receptor 3 (VEGFR3) inhibitor suppressed liver repair, lymphangiogenesis, Drainage Function, and accumulation of VEGFR3-expressing reparative macrophages. VEGF-C and VEGF-D upregulated expression of genes related to lymphangiogenic factors and the reparative macrophage phenotype in cultured macrophages. These results suggest that activation of VEGFR3 signaling increases lymphangiogenesis and the number of reparative macrophages, both of which play roles in liver repair. Expanded lymphatics and induction of reparative macrophage accumulation may be therapeutic targets to enhance liver repair after hepatic injury.
Hiromi Matsuda - One of the best experts on this subject based on the ideXlab platform.
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Roles of Thromboxane Receptor Signaling in Enhancement of Lipopolysaccharide-Induced Lymphangiogenesis and Lymphatic Drainage Function in Diaphragm.
Arteriosclerosis thrombosis and vascular biology, 2021Co-Authors: Hiromi Matsuda, Yoshiya Ito, Kanako Hosono, Seri Tsuru, Tomoyoshi Inoue, Shuji Nakamoto, Chie Kurashige, Masanori Hirashma, Shuh Narumiya, Hirotsugu OkamotoAbstract:OBJECTIVE Thromboxane is an arachidonic acid metabolite that exerts its actions through a G-protein-coupled receptor with 7 transmembrane domains. Although an arachidonic acid metabolite, prostaglandin E2 was reported to enhance lymphangiogenesis, little is known on other arachidonic acid metabolites. In the present study, we investigated the roles of TP (thromboxane prostanoid) signaling in facilitating lymphangiogenesis during inflammation. Approach and Results: Inflammation was induced by repeated intraperitoneal injections of lipopolysaccharide, and lymphangiogenesis essential for draining peritoneal fluids was estimated in the diaphragm. Lipopolysaccharide induced lymphangiogenesis in the diaphragm in a time-dependent manner in wild-type mice. Compared with wild-type mice, lipopolysaccharide-induced lymphangiogenesis in TP-deficient (TP-/-) mouse diaphragm tissues was suppressed, and this was accompanied by reduced Drainage Function from the peritoneal cavity. TP-positive macrophages and T cells were accumulated in the diaphragm and produced VEGF (vascular endothelial growth factor)-C and VEGF-D in a TP-dependent manner. Removal of macrophages and T cells resulted in reduced lymphangiogenesis and lowered expressions of VEGF-C and VEGF-D. Furthermore, TP-/- bone marrow chimeric mice exhibited reduced lymphangiogenesis. TP knockout specific to macrophages and T cells also led to reduced lymphangiogenesis and Drainage Function in mice with lipopolysaccharide injections. CONCLUSIONS The present results suggest that TP signaling exerts prolymphangiogenic activity by acting on macrophages and T cells accumulated during inflammation and that TP signaling represents a novel target for controlling lymphangiogenesis.
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roles of thromboxane receptor signaling in enhancement of lipopolysaccharide induced lymphangiogenesis and lymphatic Drainage Function in diaphragm
Arteriosclerosis Thrombosis and Vascular Biology, 2021Co-Authors: Hiromi Matsuda, Yoshiya Ito, Kanako Hosono, Seri Tsuru, Tomoyoshi Inoue, Shuji Nakamoto, Chie Kurashige, Masanori Hirashma, Shuh Narumiya, Hirotsugu OkamotoAbstract:Objective: Thromboxane is an arachidonic acid metabolite that exerts its actions through a G-protein–coupled receptor with 7 transmembrane domains. Although an arachidonic acid metabolite, prostagl...
Yoshiya Ito - One of the best experts on this subject based on the ideXlab platform.
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Roles of Thromboxane Receptor Signaling in Enhancement of Lipopolysaccharide-Induced Lymphangiogenesis and Lymphatic Drainage Function in Diaphragm.
Arteriosclerosis thrombosis and vascular biology, 2021Co-Authors: Hiromi Matsuda, Yoshiya Ito, Kanako Hosono, Seri Tsuru, Tomoyoshi Inoue, Shuji Nakamoto, Chie Kurashige, Masanori Hirashma, Shuh Narumiya, Hirotsugu OkamotoAbstract:OBJECTIVE Thromboxane is an arachidonic acid metabolite that exerts its actions through a G-protein-coupled receptor with 7 transmembrane domains. Although an arachidonic acid metabolite, prostaglandin E2 was reported to enhance lymphangiogenesis, little is known on other arachidonic acid metabolites. In the present study, we investigated the roles of TP (thromboxane prostanoid) signaling in facilitating lymphangiogenesis during inflammation. Approach and Results: Inflammation was induced by repeated intraperitoneal injections of lipopolysaccharide, and lymphangiogenesis essential for draining peritoneal fluids was estimated in the diaphragm. Lipopolysaccharide induced lymphangiogenesis in the diaphragm in a time-dependent manner in wild-type mice. Compared with wild-type mice, lipopolysaccharide-induced lymphangiogenesis in TP-deficient (TP-/-) mouse diaphragm tissues was suppressed, and this was accompanied by reduced Drainage Function from the peritoneal cavity. TP-positive macrophages and T cells were accumulated in the diaphragm and produced VEGF (vascular endothelial growth factor)-C and VEGF-D in a TP-dependent manner. Removal of macrophages and T cells resulted in reduced lymphangiogenesis and lowered expressions of VEGF-C and VEGF-D. Furthermore, TP-/- bone marrow chimeric mice exhibited reduced lymphangiogenesis. TP knockout specific to macrophages and T cells also led to reduced lymphangiogenesis and Drainage Function in mice with lipopolysaccharide injections. CONCLUSIONS The present results suggest that TP signaling exerts prolymphangiogenic activity by acting on macrophages and T cells accumulated during inflammation and that TP signaling represents a novel target for controlling lymphangiogenesis.
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roles of thromboxane receptor signaling in enhancement of lipopolysaccharide induced lymphangiogenesis and lymphatic Drainage Function in diaphragm
Arteriosclerosis Thrombosis and Vascular Biology, 2021Co-Authors: Hiromi Matsuda, Yoshiya Ito, Kanako Hosono, Seri Tsuru, Tomoyoshi Inoue, Shuji Nakamoto, Chie Kurashige, Masanori Hirashma, Shuh Narumiya, Hirotsugu OkamotoAbstract:Objective: Thromboxane is an arachidonic acid metabolite that exerts its actions through a G-protein–coupled receptor with 7 transmembrane domains. Although an arachidonic acid metabolite, prostagl...
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Lymphangiogenesis and accumulation of reparative macrophages contribute to liver repair after hepatic ischemia–reperfusion injury
Angiogenesis, 2020Co-Authors: Shuji Nakamoto, Yoshiya Ito, Nobuyuki Nishizawa, Takuya Goto, Ken Kojo, Yusuke Kumamoto, Masahiko Watanabe, Masataka MajimaAbstract:Hepatic tissue repair plays a critical role in determining the outcome of hepatic ischemia–reperfusion (I/R) injury. Hepatic lymphatics participate in the clearance of dead tissues and contribute to the reparative process after acute hepatic injury; however, it remains unknown whether lymphangiogenesis in response to hepatic inflammation is involved in liver repair. Herein, we determined if hepatic lymphangiogenesis improves liver repair after hepatic I/R injury. Using a mouse model of hepatic I/R injury, we investigated hepatic lymphatic structure, growth, and Function in injured murine livers. Hepatic I/R injury enhanced lymphangiogenesis around the portal tract and this was associated with increased expression of pro-lymphangiogenic growth factors including vascular endothelial growth factor (VEGF)-C and VEGF-D. Recombinant VEGF-D treatment facilitated liver repair in association with the expansion of lymphatic vessels and increased expression of genes related to the reparative macrophage phenotype. Treatment with a VEGF receptor 3 (VEGFR3) inhibitor suppressed liver repair, lymphangiogenesis, Drainage Function, and accumulation of VEGFR3-expressing reparative macrophages. VEGF-C and VEGF-D upregulated expression of genes related to lymphangiogenic factors and the reparative macrophage phenotype in cultured macrophages. These results suggest that activation of VEGFR3 signaling increases lymphangiogenesis and the number of reparative macrophages, both of which play roles in liver repair. Expanded lymphatics and induction of reparative macrophage accumulation may be therapeutic targets to enhance liver repair after hepatic injury.
Shuh Narumiya - One of the best experts on this subject based on the ideXlab platform.
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Roles of Thromboxane Receptor Signaling in Enhancement of Lipopolysaccharide-Induced Lymphangiogenesis and Lymphatic Drainage Function in Diaphragm.
Arteriosclerosis thrombosis and vascular biology, 2021Co-Authors: Hiromi Matsuda, Yoshiya Ito, Kanako Hosono, Seri Tsuru, Tomoyoshi Inoue, Shuji Nakamoto, Chie Kurashige, Masanori Hirashma, Shuh Narumiya, Hirotsugu OkamotoAbstract:OBJECTIVE Thromboxane is an arachidonic acid metabolite that exerts its actions through a G-protein-coupled receptor with 7 transmembrane domains. Although an arachidonic acid metabolite, prostaglandin E2 was reported to enhance lymphangiogenesis, little is known on other arachidonic acid metabolites. In the present study, we investigated the roles of TP (thromboxane prostanoid) signaling in facilitating lymphangiogenesis during inflammation. Approach and Results: Inflammation was induced by repeated intraperitoneal injections of lipopolysaccharide, and lymphangiogenesis essential for draining peritoneal fluids was estimated in the diaphragm. Lipopolysaccharide induced lymphangiogenesis in the diaphragm in a time-dependent manner in wild-type mice. Compared with wild-type mice, lipopolysaccharide-induced lymphangiogenesis in TP-deficient (TP-/-) mouse diaphragm tissues was suppressed, and this was accompanied by reduced Drainage Function from the peritoneal cavity. TP-positive macrophages and T cells were accumulated in the diaphragm and produced VEGF (vascular endothelial growth factor)-C and VEGF-D in a TP-dependent manner. Removal of macrophages and T cells resulted in reduced lymphangiogenesis and lowered expressions of VEGF-C and VEGF-D. Furthermore, TP-/- bone marrow chimeric mice exhibited reduced lymphangiogenesis. TP knockout specific to macrophages and T cells also led to reduced lymphangiogenesis and Drainage Function in mice with lipopolysaccharide injections. CONCLUSIONS The present results suggest that TP signaling exerts prolymphangiogenic activity by acting on macrophages and T cells accumulated during inflammation and that TP signaling represents a novel target for controlling lymphangiogenesis.
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roles of thromboxane receptor signaling in enhancement of lipopolysaccharide induced lymphangiogenesis and lymphatic Drainage Function in diaphragm
Arteriosclerosis Thrombosis and Vascular Biology, 2021Co-Authors: Hiromi Matsuda, Yoshiya Ito, Kanako Hosono, Seri Tsuru, Tomoyoshi Inoue, Shuji Nakamoto, Chie Kurashige, Masanori Hirashma, Shuh Narumiya, Hirotsugu OkamotoAbstract:Objective: Thromboxane is an arachidonic acid metabolite that exerts its actions through a G-protein–coupled receptor with 7 transmembrane domains. Although an arachidonic acid metabolite, prostagl...
