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CartBovine VEGF-A Polyclonal Antibody
Vascular endothelial growth factor (VEGF) proteins stimulate vasculogenesis and angiogenesis. They are part of the system that restores the oxygen supply to tissues when blood circulation is inadequate. The normal function of VEGF proteins is to create new blood vessels during embryonic development, new blood vessels after injury, muscle following exercise, and new vessels (collateral circulation) to bypass blocked vessels. The VEGF family has six members, including VEGF-A, VEGF-B, VEGF-C, VEGF-D, VEGF-E, and Placental Growth Factor (PGF). Activity of VEGF-A, as its name implies, has been studied mostly on cells of the vascular endothelium, although it does have effects on a number of other cell types (e.g., stimulation monocyte/macrophage migration, neurons, cancer cells, kidney epithelial cells). In vitro, VEGF-A has been shown to stimulate endothelial cell mitogenesis and cell migration. VEGF-A is also a vasodilator and increases microvascular permeability and was originally referred to as vascular permeability factor (VPF).
Reactivity - ELISA
Bovine VEGF-A - Strong
Canine VEGF-A - Strong
Equine VEGF-A - Strong
Feline VEGF-A - Strong
Mouse VEGF-A - Strong
Ovine VEGF-A - Strong
Rabbit VEGF-A - Weak
Rabbit VEGF-A (165) - Weak
Rat VEGF-A - Strong
Swine VEGF-A - Strong
Zebrafish VEGF-A - None
Bovine VEGF-A ELISA Data
Effect of ovarian steroids on vascular endothelial growth factor a expression in bovine uterine endothelial cells during adenomyosis.
Lupicka M, Zadroga A, Szczepańska A, Korzekwa AJ.
BMC Vet Res. 2019 Dec 30;15(1):473. doi: 10.1186/s12917-019-2222-0.
Applications: Measurement of bovine VEGF-A in culture media by ELISA
Abstract
BACKGROUND:
Adenomyosis is a uterine dysfunction defined as the presence of endometrial glands within the myometrium. There is evidence that proangiogenic factors may play a role during the development of adenomyosis; however, exact mechanism remains unknown. The aim of the study was to determine the action of vascular endothelial growth factor A (VEGFA) in uterine tissue and uterine vascular endothelial cells during adenomyosis.
RESULTS:
Uterine tissues were collected and examined for the presence and extent of adenomyosis. Gene and protein expression of VEGFA and its two receptors (VEGFR1 and VEGFR2) was evaluated with quantitative polymerase chain reaction and Western blotting, respectively, in endometrium and myometrium during adenomyosis. Immunolocalization of VEGFA and its receptors within uterine tissues during adenomyosis was also determined. In an in vitro experiment, endothelial cells from non-adenomyotic bovine uteri were treated with media conditioned by non-adenomyotic or adenomyotic uterine slices treated with 17-beta-oestradiol (E2) or progesterone (P4). Both gene and protein expression of VEGFR2 were elevated in endometrium in stages 3-4 of adenomyosis. Protein expression of VEGFA and VEGFR2 as well as VEGFA secretion were increased in endothelial cells treated with media conditioned by adenomyotic uterine slices after E2 treatment.
CONCLUSIONS:
Results suggest that VEGFA signalling is an important component, next to E2, that enhances VEGFA action and participates in adenomyosis development in cows.
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