title: Possible action of vasohibin-1 as an inhibitor in the regulation of vascularization of the bovine corpus luteum.
abstract: The development of the corpus luteum (CL), which secretes large amounts of progesterone to establish pregnancy, is accompanied by active angiogenesis, vascularization, and lymphangiogenesis. Negative feedback regulation is a critical physiological mechanism. Vasohibin-1 (VASH1) was recently discovered as a novel endothelium-derived negative feedback regulator of vascularization. We therefore investigated the expression of VASH1 in the bovine CL. Expression of VASH1 mRNA and protein was predominantly localized to luteal endothelial cells (LECs). VASH1 expression in the CL was constant through the early to late luteal phases and decreased during CL regression relating with the action of luteolytic prostaglandin F(2)(α) in vivo. To investigate the role of VASH1, we determined whether VASH1 treatment affects angiogenesis and/or lymphangiogenesis using LECs and lymphatic endothelial cells (LyECs) in vitro. Vascular endothelial growth factor A (VEGFA) stimulated the expression of VASH1 in LECs but not in LyECs, and VASH1 completely blocked VEGFA-induced formation of capillary-like tube structures of LECs and LyECs in vitro. In summary, VASH1 is predominantly located on LECs in the bovine CL and inhibits the angiogenic and lymphangiogenic actions of VEGFA. Bovine CL therefore has a VEGFA-VASH1 system that may be involved in regulation of luteal function, especially in the development of the CL. The results indicate that VASH1 has the potential to act as a negative feedback regulator of angiogenesis and lymphangiogenesis in the CL in cows.
authors.affiliation: Graduate School of Animal and Food Hygiene, Obihiro University of Agriculture and Veterinary Medicine, Obihiro 080-8555, Japan. shirasuna@jichi.ac.jp
authors.forename: Koumei
authors.initials: K
authors.lastname: Shirasuna
authors.forename: Ayumi
authors.initials: A
authors.lastname: Kobayashi
authors.forename: Akane
authors.initials: A
authors.lastname: Nitta
authors.forename: Sayo
authors.initials: S
authors.lastname: Nibuno
authors.forename: Kiemi
authors.initials: K
authors.lastname: Sasahara
authors.forename: Takashi
authors.initials: T
authors.lastname: Shimizu
authors.forename: Heinrich
authors.initials: H
authors.lastname: Bollwein
authors.forename: Akio
authors.initials: A
authors.lastname: Miyamoto
mesh_terms: D000818:Animals; D002417:Cattle; D018797:Cell Cycle Proteins / Q000378:metabolism*; D049109:Cell Proliferation; D002478:Cells, Cultured; D003338:Corpus Luteum / Q000098:blood supply / Q000254:growth & development / Q000378:metabolism*; D015237:Dinoprost; D042783:Endothelial Cells / Q000502:physiology; D030762:Estrous Cycle / Q000378:metabolism; D005260:Female; D003341:Luteolysis / Q000378:metabolism; D042583:Lymphangiogenesis; D018919:Neovascularization, Physiologic; D011247:Pregnancy; D012333:RNA, Messenger / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D018797:Cell Cycle Proteins; D012333:RNA, Messenger; D042461:Vascular Endothelial Growth Factor A; D015237:Dinoprost