| RRC ID |
63790
|
| 著者 |
Hattori K, Ito Y, Honda M, Sekiguchi K, Hosono K, Shibuya M, Unno N, Majima M.
|
| タイトル |
Lymphangiogenesis induced by vascular endothelial growth factor receptor 1 signaling contributes to the progression of endometriosis in mice.
|
| ジャーナル |
J Pharmacol Sci
|
| Abstract |
Lymphangiogenesis is related to the growth of endometriosis. Here, we examined whether vascular endothelial growth factor (VEGF) receptor 1 (VEGFR1) signaling plays a role in lymphangiogenesis during endometriosis. Endometrial fragments from wild-type (WT) mice transplanted into the peritoneal wall of host WT mice (WT→WT) developed well and displayed enhanced lymphangiogenesis associated with increases in mRNA levels of VEGF-C and VEGF-D. Compared with WT mice, the implant size and lymphangiogenesis were reduced, when endometrial fragments from mice lacking the VEGFR1 tyrosine kinase (TK) domain (TK-/-) were transplanted into host TK-/- mice (TK-/-→TK-/-). Treatment of WT→WT mice with the VEGFR3 kinase inhibitor suppressed the size of implants and lymphangiogenesis. Immunofluorescence analyses demonstrated that VEGF-C and VEGF-D were expressed in both CD11b+ and S100A4+ cells. TK-/-→TK-/- mice had lower numbers of CD11b+ and S100A4+ cells than WT→WT mice. When isolated bone marrow (BM)-derived macrophages or culture murine fibroblasts were stimulated with placental growth factor (PlGF), a specific agonist of VEGFR1, the levels of VEGF-C and VEGF-D were increased in a VEGFR1-dependent manner. These results suggest that VEGFR1 signaling in macrophages and fibroblasts contributes to the growth of endometrial implants and lymphangiogenesis.
|
| 巻・号 |
143(4)
|
| ページ |
255-263
|
| 公開日 |
2020-8-1
|
| DOI |
10.1016/j.jphs.2020.05.003
|
| PII |
S1347-8613(20)30047-5
|
| PMID |
32487450
|
| MeSH |
Animals
Disease Progression
Endometriosis / etiology*
Female
Lymphangiogenesis / genetics*
Mice
Mice, Inbred C57BL
Signal Transduction*
Vascular Endothelial Growth Factor Receptor-1*
|
| IF |
2.835
|
| リソース情報 |
| ヒト・動物細胞 |
L929 |
