Histamine promotes angiogenesis through a histamine H1 receptor-PKC-VEGF-mediated pathway in human endothelial cells
Histamine is a well-known inflammatory mediator, but how histamine induces angiogenesis remains poorly understood. In the present study, we demonstrated a dose-dependent dynamic tube formation in the human endothelial cell line EA.hy926 in the presence of histamine that was completely blocked by his...
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| Autor*in: |
Omer Faruk Hatipoglu [verfasserIn] Takashi Nishinaka [verfasserIn] Masahiro Nishibori [verfasserIn] Masahiro Watanabe [verfasserIn] Takao Toyomura [verfasserIn] Shuji Mori [verfasserIn] Kursat Oguz Yaykasli [verfasserIn] Hidenori Wake [verfasserIn] Hideo Takahashi [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2023 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
In: Journal of Pharmacological Sciences - Elsevier, 2017, 151(2023), 4, Seite 177-186 |
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| Übergeordnetes Werk: |
volume:151 ; year:2023 ; number:4 ; pages:177-186 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.jphs.2023.02.006 |
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| Katalog-ID: |
DOAJ088553973 |
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| 520 | |a Histamine is a well-known inflammatory mediator, but how histamine induces angiogenesis remains poorly understood. In the present study, we demonstrated a dose-dependent dynamic tube formation in the human endothelial cell line EA.hy926 in the presence of histamine that was completely blocked by histamine H1 receptor (H1R) and protein kinase C (PKC) inhibitors. However, histamine H2, H3, and H4 receptor inhibitors did not inhibit tube formation, suggesting that H1R–PKC signaling is involved in histamine-induced tube formation. Moreover, we found an H1-specific induction of vascular endothelial growth factor (VEGF) expression. Inhibition of VEGF receptor 2 (VEGFR2) suppressed the histamine-induced tube formation, indicating that VEGF is downstream of histamine signaling. Additionally, we demonstrated that histamine stimulation induces the expression of critical regulators of angiogenesis such as matrix metalloproteinase (MMP)-9 and MMP-14 metalloproteases, as histamine-induced tube formation is blocked by MMP inhibitors. In summary, our study indicates that histamine can activate the H1R in human endothelial cells and thereby promote tube formation through the PKC, MMP, and VEGF signaling pathways. | ||
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10.1016/j.jphs.2023.02.006 doi (DE-627)DOAJ088553973 (DE-599)DOAJ10c6c25a6cfb413aa2241db4b3d45e50 DE-627 ger DE-627 rakwb eng RM1-950 Omer Faruk Hatipoglu verfasserin aut Histamine promotes angiogenesis through a histamine H1 receptor-PKC-VEGF-mediated pathway in human endothelial cells 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Histamine is a well-known inflammatory mediator, but how histamine induces angiogenesis remains poorly understood. In the present study, we demonstrated a dose-dependent dynamic tube formation in the human endothelial cell line EA.hy926 in the presence of histamine that was completely blocked by histamine H1 receptor (H1R) and protein kinase C (PKC) inhibitors. However, histamine H2, H3, and H4 receptor inhibitors did not inhibit tube formation, suggesting that H1R–PKC signaling is involved in histamine-induced tube formation. Moreover, we found an H1-specific induction of vascular endothelial growth factor (VEGF) expression. Inhibition of VEGF receptor 2 (VEGFR2) suppressed the histamine-induced tube formation, indicating that VEGF is downstream of histamine signaling. Additionally, we demonstrated that histamine stimulation induces the expression of critical regulators of angiogenesis such as matrix metalloproteinase (MMP)-9 and MMP-14 metalloproteases, as histamine-induced tube formation is blocked by MMP inhibitors. In summary, our study indicates that histamine can activate the H1R in human endothelial cells and thereby promote tube formation through the PKC, MMP, and VEGF signaling pathways. Histamine H1R MMPs Tube formation VEGF Therapeutics. Pharmacology Takashi Nishinaka verfasserin aut Masahiro Nishibori verfasserin aut Masahiro Watanabe verfasserin aut Takao Toyomura verfasserin aut Shuji Mori verfasserin aut Kursat Oguz Yaykasli verfasserin aut Hidenori Wake verfasserin aut Hideo Takahashi verfasserin aut In Journal of Pharmacological Sciences Elsevier, 2017 151(2023), 4, Seite 177-186 (DE-627)1760631620 13478613 nnns volume:151 year:2023 number:4 pages:177-186 https://doi.org/10.1016/j.jphs.2023.02.006 kostenfrei https://doaj.org/article/10c6c25a6cfb413aa2241db4b3d45e50 kostenfrei http://www.sciencedirect.com/science/article/pii/S1347861323000130 kostenfrei https://doaj.org/toc/1347-8613 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 151 2023 4 177-186 |
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10.1016/j.jphs.2023.02.006 doi (DE-627)DOAJ088553973 (DE-599)DOAJ10c6c25a6cfb413aa2241db4b3d45e50 DE-627 ger DE-627 rakwb eng RM1-950 Omer Faruk Hatipoglu verfasserin aut Histamine promotes angiogenesis through a histamine H1 receptor-PKC-VEGF-mediated pathway in human endothelial cells 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Histamine is a well-known inflammatory mediator, but how histamine induces angiogenesis remains poorly understood. In the present study, we demonstrated a dose-dependent dynamic tube formation in the human endothelial cell line EA.hy926 in the presence of histamine that was completely blocked by histamine H1 receptor (H1R) and protein kinase C (PKC) inhibitors. However, histamine H2, H3, and H4 receptor inhibitors did not inhibit tube formation, suggesting that H1R–PKC signaling is involved in histamine-induced tube formation. Moreover, we found an H1-specific induction of vascular endothelial growth factor (VEGF) expression. Inhibition of VEGF receptor 2 (VEGFR2) suppressed the histamine-induced tube formation, indicating that VEGF is downstream of histamine signaling. Additionally, we demonstrated that histamine stimulation induces the expression of critical regulators of angiogenesis such as matrix metalloproteinase (MMP)-9 and MMP-14 metalloproteases, as histamine-induced tube formation is blocked by MMP inhibitors. In summary, our study indicates that histamine can activate the H1R in human endothelial cells and thereby promote tube formation through the PKC, MMP, and VEGF signaling pathways. Histamine H1R MMPs Tube formation VEGF Therapeutics. Pharmacology Takashi Nishinaka verfasserin aut Masahiro Nishibori verfasserin aut Masahiro Watanabe verfasserin aut Takao Toyomura verfasserin aut Shuji Mori verfasserin aut Kursat Oguz Yaykasli verfasserin aut Hidenori Wake verfasserin aut Hideo Takahashi verfasserin aut In Journal of Pharmacological Sciences Elsevier, 2017 151(2023), 4, Seite 177-186 (DE-627)1760631620 13478613 nnns volume:151 year:2023 number:4 pages:177-186 https://doi.org/10.1016/j.jphs.2023.02.006 kostenfrei https://doaj.org/article/10c6c25a6cfb413aa2241db4b3d45e50 kostenfrei http://www.sciencedirect.com/science/article/pii/S1347861323000130 kostenfrei https://doaj.org/toc/1347-8613 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ AR 151 2023 4 177-186 |
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RM1-950 Histamine promotes angiogenesis through a histamine H1 receptor-PKC-VEGF-mediated pathway in human endothelial cells Histamine H1R MMPs Tube formation VEGF |
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Histamine promotes angiogenesis through a histamine H1 receptor-PKC-VEGF-mediated pathway in human endothelial cells |
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Histamine promotes angiogenesis through a histamine H1 receptor-PKC-VEGF-mediated pathway in human endothelial cells |
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Omer Faruk Hatipoglu |
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Journal of Pharmacological Sciences |
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Omer Faruk Hatipoglu Takashi Nishinaka Masahiro Nishibori Masahiro Watanabe Takao Toyomura Shuji Mori Kursat Oguz Yaykasli Hidenori Wake Hideo Takahashi |
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10.1016/j.jphs.2023.02.006 |
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histamine promotes angiogenesis through a histamine h1 receptor-pkc-vegf-mediated pathway in human endothelial cells |
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Histamine promotes angiogenesis through a histamine H1 receptor-PKC-VEGF-mediated pathway in human endothelial cells |
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Histamine is a well-known inflammatory mediator, but how histamine induces angiogenesis remains poorly understood. In the present study, we demonstrated a dose-dependent dynamic tube formation in the human endothelial cell line EA.hy926 in the presence of histamine that was completely blocked by histamine H1 receptor (H1R) and protein kinase C (PKC) inhibitors. However, histamine H2, H3, and H4 receptor inhibitors did not inhibit tube formation, suggesting that H1R–PKC signaling is involved in histamine-induced tube formation. Moreover, we found an H1-specific induction of vascular endothelial growth factor (VEGF) expression. Inhibition of VEGF receptor 2 (VEGFR2) suppressed the histamine-induced tube formation, indicating that VEGF is downstream of histamine signaling. Additionally, we demonstrated that histamine stimulation induces the expression of critical regulators of angiogenesis such as matrix metalloproteinase (MMP)-9 and MMP-14 metalloproteases, as histamine-induced tube formation is blocked by MMP inhibitors. In summary, our study indicates that histamine can activate the H1R in human endothelial cells and thereby promote tube formation through the PKC, MMP, and VEGF signaling pathways. |
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Histamine is a well-known inflammatory mediator, but how histamine induces angiogenesis remains poorly understood. In the present study, we demonstrated a dose-dependent dynamic tube formation in the human endothelial cell line EA.hy926 in the presence of histamine that was completely blocked by histamine H1 receptor (H1R) and protein kinase C (PKC) inhibitors. However, histamine H2, H3, and H4 receptor inhibitors did not inhibit tube formation, suggesting that H1R–PKC signaling is involved in histamine-induced tube formation. Moreover, we found an H1-specific induction of vascular endothelial growth factor (VEGF) expression. Inhibition of VEGF receptor 2 (VEGFR2) suppressed the histamine-induced tube formation, indicating that VEGF is downstream of histamine signaling. Additionally, we demonstrated that histamine stimulation induces the expression of critical regulators of angiogenesis such as matrix metalloproteinase (MMP)-9 and MMP-14 metalloproteases, as histamine-induced tube formation is blocked by MMP inhibitors. In summary, our study indicates that histamine can activate the H1R in human endothelial cells and thereby promote tube formation through the PKC, MMP, and VEGF signaling pathways. |
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Histamine is a well-known inflammatory mediator, but how histamine induces angiogenesis remains poorly understood. In the present study, we demonstrated a dose-dependent dynamic tube formation in the human endothelial cell line EA.hy926 in the presence of histamine that was completely blocked by histamine H1 receptor (H1R) and protein kinase C (PKC) inhibitors. However, histamine H2, H3, and H4 receptor inhibitors did not inhibit tube formation, suggesting that H1R–PKC signaling is involved in histamine-induced tube formation. Moreover, we found an H1-specific induction of vascular endothelial growth factor (VEGF) expression. Inhibition of VEGF receptor 2 (VEGFR2) suppressed the histamine-induced tube formation, indicating that VEGF is downstream of histamine signaling. Additionally, we demonstrated that histamine stimulation induces the expression of critical regulators of angiogenesis such as matrix metalloproteinase (MMP)-9 and MMP-14 metalloproteases, as histamine-induced tube formation is blocked by MMP inhibitors. In summary, our study indicates that histamine can activate the H1R in human endothelial cells and thereby promote tube formation through the PKC, MMP, and VEGF signaling pathways. |
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Histamine promotes angiogenesis through a histamine H1 receptor-PKC-VEGF-mediated pathway in human endothelial cells |
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