RAMP1 signaling facilitates angiogenesis and lymphangiogenesis in the endometriotic lesions in mice

Masako Honda, Yoshiya Ito, Kyoko Hattori, Kanako Hosono, Shuji Nakamoto, Fumisato Otaka, Seri Tsuru, Masataka Majima
In: Proceedings for Annual Meeting of The Japanese Pharmacological Society · 2020 · vol. 93(0) , pp. 2–YIA · doi:10.1254/jpssuppl.93.0_2-yia-59 · W3011946847
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⚙ AI-generated summary by claude@2026-06, 2026-06-13 ⓘ

RAMP1 signaling in macrophages and fibroblasts promotes angiogenesis and lymphangiogenesis, reducing the growth of ectopic endometriotic lesions in RAMP1 deficient mice.

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The study investigated whether receptor activity-modifying protein 1 (RAMP1) signaling promotes endometriosis growth by stimulating angiogenesis and lymphangiogenesis. Using a mouse ectopic endometriosis model, the authors compared implants generated in wild-type versus RAMP1-deficient (RAMP1-/-) mice and measured vessel size/density, vascular and lymphatic marker mRNA, angiogenic/lymphangiogenic growth factor expression, and cell localization by immunofluorescence. Vessel density and expression of blood/lymphatic vessel markers and angiogenic/lymphangiogenic growth factors were reduced in RAMP1-/-→RAMP1-/- implants, while RAMP1-expressing CD11b+ and S100A4+ cells colocalized with VEGF-A, VEGF-C, and VEGF-D; cultured macrophages and fibroblasts increased VEGF-A/C/D expression in a RAMP1-dependent manner. The main limitation is that the work relies on a peritoneal ectopic model and molecular/marker readouts of vascular growth rather than direct demonstration of systemic RAMP1 effects in humans. This paper is centrally about endometriosis — it tests how RAMP1-dependent signaling drives angiogenesis and lymphangiogenesis in endometriotic lesions in mice.

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Abstract

Newly formation of blood and lymphatic vessels is involved in the development of endometriosis. We have demonstrated that calcitonin gene-related peptide (CGRP) promotes wound healing and wound-associated formation of blood and lymphatic vessels via receptor activity-modifying protein 1 (RAMP1), a subunit of the CGRP receptor. In the present study, using wild-type (WT) mice and RAMP1 deficient (RAMP1-/-) mice, we examined whether RAMP1 plays a role in the growth of endometriosis by angiogenic responses. Ectopic endometriosis model was created by transplantation of endometrial tissue fragments from donor mice into the peritoneal wall of host mice. The sizes and density of blood and lymphatic vessels in the RAMP1-/- implants from host RAMP1-/- mice (RAMP1-/-→RAMP1-/-) were reduced as compared with the WT→WT. The mRNA levels of markers for blood and lymphatic vessels as well as growth factors for angiogenesis and lymphangiogenesis in the RAMP1-/-→RAMP1-/- were lower than those in the WT→WT. Immunofluorescence demonstrated that RAMP1 was expressed in CD11b+ and S100A4+ cells, and these cells also co-localized with VEGF-A, VEGF-C, and VEGF-D. Cultured macrophages and fibroblasts increased the mRNA levels of VEGF-A, VEGF-C, and VEGF-D in a RAMP1 dependent manner. These results suggest that RAMP1 signaling in macrophages and fibroblasts is critical for the growth of endometriosis by promoting angiogenesis and lymphangiogenesis.
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第93回日本薬理学会年会 セッションID: 93_2-YIA-59 会議情報 主催: 第93回日本薬理学会年会 会議名: 第93回日本薬理学会年会 回次: 93 開催地: Yokohama 開催日: 2020/03/16 - 2020/03/18 年会優秀発表賞（YIA）候補演題 RAMP1によるマウス子宮内膜症における血管・リンパ管新生促進作用 キーワード: endometrium 詳細 抄録 Newly formation of blood and lymphatic vessels is involved in the development of endometriosis. We have demonstrated that calcitonin gene-related peptide (CGRP) promotes wound healing and wound-associated formation of blood and lymphatic vessels via receptor activity-modifying protein 1 (RAMP1), a subunit of the CGRP receptor. In the present study, using wild-type (WT) mice and RAMP1 deficient (RAMP1-/-) mice, we examined whether RAMP1 plays a role in the growth of endometriosis by angiogenic responses. Ectopic endometriosis model was created by transplantation of endometrial tissue fragments from donor mice into the peritoneal wall of host mice. The sizes and density of blood and lymphatic vessels in the RAMP1-/- implants from host RAMP1-/- mice (RAMP1-/-→RAMP1-/-) were reduced as compared with the WT→WT. The mRNA levels of markers for blood and lymphatic vessels as well as growth factors for angiogenesis and lymphangiogenesis in the RAMP1-/-→RAMP1-/- were lower than those in the WT→WT. Immunofluorescence demonstrated that RAMP1 was expressed in CD11b+ and S100A4+ cells, and these cells also co-localized with VEGF-A, VEGF-C, and VEGF-D. Cultured macrophages and fibroblasts increased the mRNA levels of VEGF-A, VEGF-C, and VEGF-D in a RAMP1 dependent manner. These results suggest that RAMP1 signaling in macrophages and fibroblasts is critical for the growth of endometriosis by promoting angiogenesis and lymphangiogenesis. © 2020 本論文著者

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