Expression of VEGF and VEGF-R3 receptor by placental endothelial cells in health and gestosis

Sokolov, D. N.; Kolobov, Andrey; Pecherina, L. V.; Kramareva, N. L.; Mozgovaya, Elena V.; Kvetnoĭ, I M; Selkov, S. A.

doi:10.1007/s10517-008-0088-4

Cited by 4 publications

(3 citation statements)

References 13 publications

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“…Thus, the results of immunohistochemical study of normal placenta were generally consistent with published data on the distribution of VEGF and its receptors [1,3,12]. We found predominance of nonbranching angiogenesis in the placentas from obese women.…”

Section: Resultssupporting

confidence: 91%

“…The sections were counterstained with hematoxylin. Immunohistochemical reaction to VEGF and its receptors in the syncytiotrophoblast (SCT), non-villous cytotrophoblast (NVC), vascular endothelial cells of stem villi (VEC), and endothelial cells of the terminal and mature intermediate villi (ECV) was scored using a semiquantitative scale: no response (0), weak reaction (1), moderate reaction (2), and intensive reaction (3).…”

Section: Methodsmentioning

confidence: 99%

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Vascular Endothelial Growth Factor and its Receptors in the Placenta of Pregnant Women with Obesity

et al. 2011

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Comparative morphological study of placentas from women with obesity and normal body weight was performed. Expression of vascular endothelial growth factor (VEGF) and its receptors (VEGFR-1, VEGFR-2, VEGFR-3) was detected by immunohistochemical methods. Nonbranching angiogenesis predominated in the placentas from obese women. Immunohistochemical analysis showed reduced intensity of the reaction to VEGF in the syncytiotrophoblast and vascular endothelium of stem villi and enhanced VEGF expression in non-villous cytotrophoblast and endothelial cells of capillaries of mature intermediate and terminal villi; reduced expression of VEGFR-1 and increased levels of VEGFR-2 and VEGFR-3 in the studied structures were also noted.

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Section: Resultssupporting

confidence: 91%

Section: Methodsmentioning

confidence: 99%

Vascular Endothelial Growth Factor and its Receptors in the Placenta of Pregnant Women with Obesity

et al. 2011

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“…VEGF играет важнейшую роль в таких процессах, как деградация базальной мембраны ЭК и внеклеточного матрикса, пролиферация ЭК, формирование капилляров, синтез новой базальной мембраны. Таким образом, VEGF оказывается вовлечен во все этапы ангиогенеза [39,46]. Изоформа VEGF-A существует в виде 4 различных подтипов: VEGF121, VEGF165, VEGF189 и VEGF206 [51] и считается первым ростовым фактором, характерным именно для ЭК, который появляется в ходе эмбрионального развития.…”

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Influence of VEGF deprivation upon vascular formation by endothelium in the presence of macrophages

et al. 2020

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Development of angiogenesis depends on the functional state of endothelial cells, as well as on the balanced secretion of cytokines, growth factors and chemokines by endothelial cells and cells of microenvironment. Macrophages represent an essential component of the microenvironment and take part in the formation of blood vessels both due to the production of cytokines and due to contact interactions with endothelial cells. VEGF is among the most important cytokines that control angiogenesis at all its stages. Currently, the role of VEGF in the intercellular interactions of endothelial cells and macrophages is not well described. The aim of our study was to investigate the effect of VEGF deprivation using monoclonal antibodies on angiogenesis under conditions of co-cultivation of endothelium and macrophages. Materials and methods: monoclonal antibodies to VEGF-A were used for VEGF deprivation in monoculture of endothelial cells and in co-culture of endothelial cells with macrophages. The IL-1β, IL-6 and TNFα cytokines were used as inducers. When VEGF-A was removed from the medium, endothelial cells show plasticity and form longer vessels, they modify the expression of VEGF receptors. Macrophages regulate endothelial cell activity through the secretion of cytokines, including VEGF, and through contact interactions with endothelial cells. THP-1 cells increase the sensitivity of endothelial cells to VEGF by stimulating the VEGFR1 and VEGFR3 expression, this effect is VEGF-A-independent. The IL-1β, IL-6, TNFa cytokines independently stimulate non-branching angiogenesis, increasing the length of the vessels. At the same time, IL-ip increases the VEGFR1 expression on the surface of endothelial cells. In contrast, IL-6 and TNFα decrease it, thereby regulating the sensitivity of endothelial cells to VEGF. The effects of these cytokines are not dependent on VEGF-A. The IL-1β, IL-6, TNFα cytokines promote acquisition of anti-angiogenic properties by THP-1 cells that is independent on VEGF-A, as well as on expression of its receptors by endothelial cells. Thus, VEGF is an important, but not the sole factor controlling angiogenesis. Under conditions of VEGF-A deficiency, either endothelial cells or microenvironment cells are able to compensate for its functional load due to the production of other growth factors.

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Circulating vascular endothelial growth factor receptor‐3, a pro‐lymphangiogenic and pro‐angiogenic mediator, is decreased in pre‐eclampsia

Palei,

Kaihara,

Cavalli

et al. 2024

Intl J Gynecology & Obste

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ObjectiveTo compare circulating levels of vascular endothelial growth factor receptor 3 (VEGFR‐3) in women with pregnancy‐induced hypertension (PIH) and in non‐pregnant (NP) and healthy pregnant (HP) women.MethodsWe conducted a case–control study including PIH (n = 135), HP (n = 68), and NP (n = 49) women from southeastern Brazil. PIH were diagnosed according to international guidelines, and defined as gestational hypertension (GH, n = 61) or pre‐eclampsia (n = 74). VEGFR‐3 was measured in plasma using ELISA.ResultsPlasma VEGFR‐3 was increased in HP (1207 pg/mL) compared with NP (133 pg/mL) women; however, PIH (729 pg/mL) patients exhibited lower levels than HP women (both p < 0.05). In addition, plasma VEGFR‐3 was decreased in pre‐eclampsia compared with GH (537 versus 980 pg/mL; p < 0.05). When pre‐eclampsia was classified according to different clinical presentations, plasma VEGFR‐3 was further decreased in the cases identified as pre‐eclampsia with severe features, preterm pre‐eclampsia, and pre‐eclampsia accompanied by small for gestational age (all p < 0.05).ConclusionOur data indicate reduced circulating VEGFR‐3 levels in patients with PIH, specifically in those diagnosed with pre‐eclampsia. Moreover, decreased VEGFR‐3 was associated with adverse clinical outcomes in pre‐eclampsia. These findings expand previous evidence of reduced VEGFR‐3 expression in pre‐eclampsia. Future studies should investigate whether it can be used as a predictive biomarker and/or therapeutic target for pre‐eclampsia.

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Expression of VEGF and VEGF-R3 receptor by placental endothelial cells in health and gestosis

Cited by 4 publications

References 13 publications

Vascular Endothelial Growth Factor and its Receptors in the Placenta of Pregnant Women with Obesity

Vascular Endothelial Growth Factor and its Receptors in the Placenta of Pregnant Women with Obesity

Influence of VEGF deprivation upon vascular formation by endothelium in the presence of macrophages

Circulating vascular endothelial growth factor receptor‐3, a pro‐lymphangiogenic and pro‐angiogenic mediator, is decreased in pre‐eclampsia

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