Thromboxane A2 receptor signaling inhibits angiogenesis and lymphangiogenesis in the endometriotic lesions in mice

Akiko Furue, Yoshiya Ito, Masako Honda, Kyoko Hattori, Kazuki Sekiguti, Atsushi Yamashita, Mayuko Osada, Mina Tanabe, Kanako Hosono, Ko Hatanaka, Masataka Majima, Kazuyoshi Kato, Hideki Amano
In: Proceedings for Annual Meeting of The Japanese Pharmacological Society · 2022 · vol. 96(0) , pp. 2–B · doi:10.1254/jpssuppl.96.0_2-b-p-091 · W4313198437
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Thromboxane A2 receptor signaling inhibits endometriosis lesion growth by suppressing angiogenesis and lymphangiogenesis in mouse models.

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The paper investigated whether signaling through the thromboxane A2 receptor (TP) regulates angiogenesis and lymphangiogenesis during endometriosis development using wild-type mice and TP knockout mice. In a mouse ectopic endometriosis model, endometrial tissue fragments from donor mice (WT or TPKO) were transplanted into the peritoneal wall of host mice (WT or TPKO), and lesion size plus vessel density and gene expression were assessed; TPKO→TPKO implants showed increased implant size and higher density and mRNA levels of blood/lymphatic markers (CD31, LYVE-1) and angiogenic/lymphangiogenic growth factors (VEGF-A and VEGF-C/D) versus WT→WT. Immunostaining indicated TP expression in F4/80-positive macrophages rather than in blood or lymphatic vessels, and genes associated with M2 macrophages were higher in TPKO→TPKO implants without a significant change in M1-associated genes. This paper is centrally about endometriosis — it shows that TP signaling inhibits angiogenesis and lymphangiogenesis in endometriotic lesions in mice.

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Abstract

Angiogenesis and lymphangiogenesis contribute to the development of endometriosis. We recently reported that thromboxane A2 (TXA2) receptor signaling involves in angiogenesis in critical limb ischemia and lymphangiogenesis in inflamed diaphragm. In the present study, using wild-type mice (WT) and thromboxane prostanoid receptor (TP) knockout mice (TPKO), we examined whether TP signaling 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 (WT or TPKO) into the peritoneal wall of host mice (WT or TPKO). The implant sizes and density of blood and lymphatic vessels in the TPKO implants from host TPKO (TPKO→TPKO) were increased as compared with the WT→WT. The mRNA levels of markers for blood (CD31) and lymphatic vessels (LYVE-1) and of growth factors for angiogenesis (VEGF-A) and lymphangiogenesis (VEGF-C/D) in the TPKO→TPKO were higher than those in the WT→WT. Immunostaining showed that TP was expressed in F4/80-positive macrophages, but not in blood and lymphatic vessels in endometriosis lesions. The levels of M2 macrophage-related genes were higher in the TPKO→TPKO than in the WT→WT, while no statistically significant difference in M1 macrophage-related genes was observed. These results suggest that TP signaling inhibits the growth of endometriosis by reducing angiogenesis and lymphangiogenesis.
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第96回日本薬理学会年会 セッションID: 96_2-B-P-091 会議情報 主催: 公益社団法人日本薬理学会 会議名: 第96回日本薬理学会年会 回次: 96 開催地: 横浜 開催日: 2022/11/30 - 2022/12/03 一般演題（ポスター） トロンボキサンA2受容体シグナルは子宮内膜症の血管およびリンパ管新生を抑制する 詳細 抄録 Angiogenesis and lymphangiogenesis contribute to the development of endometriosis. We recently reported that thromboxane A2 (TXA2) receptor signaling involves in angiogenesis in critical limb ischemia and lymphangiogenesis in inflamed diaphragm. In the present study, using wild-type mice (WT) and thromboxane prostanoid receptor (TP) knockout mice (TPKO), we examined whether TP signaling 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 (WT or TPKO) into the peritoneal wall of host mice (WT or TPKO). The implant sizes and density of blood and lymphatic vessels in the TPKO implants from host TPKO (TPKO→TPKO) were increased as compared with the WT→WT. The mRNA levels of markers for blood (CD31) and lymphatic vessels (LYVE-1) and of growth factors for angiogenesis (VEGF-A) and lymphangiogenesis (VEGF-C/D) in the TPKO→TPKO were higher than those in the WT→WT. Immunostaining showed that TP was expressed in F4/80-positive macrophages, but not in blood and lymphatic vessels in endometriosis lesions. The levels of M2 macrophage-related genes were higher in the TPKO→TPKO than in the WT→WT, while no statistically significant difference in M1 macrophage-related genes was observed. These results suggest that TP signaling inhibits the growth of endometriosis by reducing angiogenesis and lymphangiogenesis. © 2022 本論文著者

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