Role of EFNB2/EPHB4 signaling in spiral artery development during pregnancy: An appraisal.
EFNB2 and EPHB4, which belong to a large tyrosine kinase receptor superfamily, are molecular markers of arterial and venous blood vessels, respectively. EFNB2/EPHB4 signaling plays an important role in physiological and pathological angiogenesis, and its role in tumor vessel development has been extensively studied. Pregnancy and tumors share similar features, including continuous cell proliferation and increased demand for a blood supply. Our previous studies showed that Efnb2 and Ephb4 were expressed dynamically in the spiral arteries, uterine natural killer cells, and trophoblasts during mouse gestation Days 6.5-12.5. Moreover, uterine natural killer cells and trophoblasts are required for the modification of spiral arteries. Oxygen tension within the pregnant uterus, which contributes to the vascular development, also affects EFNB2 and EPHB4 expression. Considering the role of EFNB2/EPHB4 signaling in embryonic and tumor vascular development, and its dynamic expression in the decidua and placenta, we hypothesize that EFNB2 and EPHB4 are involved in the regulation of spiral artery remodeling. Investigating this hypothesis will help clarify the mechanisms of pathological pregnancy that may underlie abnormal spiral artery development.
Department of Forensic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.
Hongmei
H
Dong
Department of Forensic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.
Chaoran
C
Yu
Department of Forensic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.
Jiao
J
Mu
Department of Forensic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.
Ji
J
Zhang
Department of Forensic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.
Wei
W
Lin
D000818:Animals; D036388:Ephrin-B2 / Q000502:physiology*; D005260:Female; D051379:Mice; D008822:Mice, Transgenic; D009369:Neoplasms / Q000098:blood supply / Q000235:genetics; D009389:Neovascularization, Pathologic / Q000235:genetics; D018919:Neovascularization, Physiologic / Q000235:genetics; D011247:Pregnancy / Q000235:genetics / Q000502:physiology*; D036224:Receptor, EphB4 / Q000502:physiology*; D015398:Signal Transduction / Q000235:genetics / Q000502:physiology; D055988:Uterine Artery / Q000254:growth & development* / Q000378:metabolism; D014599:Uterus / Q000098:blood supply
C000601240:EFNB2 protein, mouse; D036388:Ephrin-B2; C086681:Ephb4 protein, mouse; D036224:Receptor, EphB4