VEGFR1 signaling plays a critical role in endometriosis through increasing lymphangiogenesis

Kyoko Hattori, Yoshiya Ito, Masako Honda, Kazuki Sekiguchi, Nobuya Unno, 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-57 · W3010970854
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VEGFR1 signaling in macrophages and fibroblasts promotes endometriosis growth and lymphangiogenesis by increasing VEGF-C and VEGF-D.

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This paper investigated how VEGFR1 signaling regulates lymphangiogenesis and growth of endometrial tissue in an endometriosis mouse model. Endometrial fragments were implanted into the peritoneal wall of wild-type versus VEGFR1 tyrosine kinase–deficient (TK-/-) mice, and the authors quantified implant size, lymphatic vessel density, and pro-lymphangiogenic factors VEGF-C and VEGF-D, with immunofluorescence localizing VEGF-C/VEGF-D expression to CD11b+ and S100A4+ cells. They found that WT→WT implants showed increased lymphangiogenesis and VEGF-C/VEGF-D expression, while TK-/-→TK-/- hosts had reduced implant size and lymphangiogenesis, and that PlGF increased VEGF-C/VEGF-D mRNA in a VEGFR1-dependent manner in bone-marrow–derived macrophages and fibroblasts. A VEGFR3 kinase inhibitor significantly suppressed implant size, lymphangiogenesis, VEGF-C/VEGF-D, and accumulation of CD11b+ and S100A4+ cells, though the study’s explicit limitation is that it uses an animal model and reports findings based on peritoneal implantation. This paper is centrally about endometriosis — it focuses on VEGFR1 signaling’s role in promoting lymphangiogenesis and endometrial tissue growth.

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Abstract

Lymphangiogenesis is associated with the growth of endometriosis. In this study, we examined the role of vascular endothelial growth factor (VEGF) receptor 1 (VEGFR1) signaling in lymphangiogenesis and tissue growth in an endometriosis model. Using wild-type (WT) and VEGFR1 tyrosine kinase (TK) deficient mice, endometrial fragments were implanted into the peritoneal wall of mice. Endometrial tissue growth and lymphangiogenesis as indicated by lymphatic vessel density were determined. Endometrial fragments from wild-type (WT) mice transplanted into in host WT mice (WT→WT) grew with increased lymphangiogenesis accompanied by increases in pro-lymphangiogenic factors, VEGF-C and VEGF-D. The implant size and lymphangiogenesis were reduced in the TK-/-→TK-/-. Immunofluorescence demonstrated that both VEGF-C and VEGF-D were expressed in both CD11b+ and S100A4+ cells. When cultured bone marrow-derived macrophages and fibroblasts were stimulated with placental growth factor (PlGF), a specific agonist for VEGFR1, the mRNA levels of VEGF-C and VEGF-D were increased in a VEGFR1 dependent manner. A VEGFR3 kinase inhibitor significantly suppressed the size of implants, lymphangiogenesis, pro-lymphangiogenic factors, and accumulation of CD11b+ and S100A4+ cells. These results suggest that VEGFR1 signaling in macrophages and fibroblasts promote the growth and lymphangiogenesis in endometrial tissue. Therefore, VEGFR1 blockade is a potential treatment for endometriosis.
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第93回日本薬理学会年会 セッションID: 93_2-YIA-57 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 子宮内膜症におけるリンパ管新生を制御するVEGFR1の役割解明 詳細 抄録 Lymphangiogenesis is associated with the growth of endometriosis. In this study, we examined the role of vascular endothelial growth factor (VEGF) receptor 1 (VEGFR1) signaling in lymphangiogenesis and tissue growth in an endometriosis model. Using wild-type (WT) and VEGFR1 tyrosine kinase (TK) deficient mice, endometrial fragments were implanted into the peritoneal wall of mice. Endometrial tissue growth and lymphangiogenesis as indicated by lymphatic vessel density were determined. Endometrial fragments from wild-type (WT) mice transplanted into in host WT mice (WT→WT) grew with increased lymphangiogenesis accompanied by increases in pro-lymphangiogenic factors, VEGF-C and VEGF-D. The implant size and lymphangiogenesis were reduced in the TK-/-→TK-/-. Immunofluorescence demonstrated that both VEGF-C and VEGF-D were expressed in both CD11b+ and S100A4+ cells. When cultured bone marrow-derived macrophages and fibroblasts were stimulated with placental growth factor (PlGF), a specific agonist for VEGFR1, the mRNA levels of VEGF-C and VEGF-D were increased in a VEGFR1 dependent manner. A VEGFR3 kinase inhibitor significantly suppressed the size of implants, lymphangiogenesis, pro-lymphangiogenic factors, and accumulation of CD11b+ and S100A4+ cells. These results suggest that VEGFR1 signaling in macrophages and fibroblasts promote the growth and lymphangiogenesis in endometrial tissue. Therefore, VEGFR1 blockade is a potential treatment for endometriosis. © 2020 本論文著者

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