Effect of angiotensin-converting enzyme-inhibiting therapy on the expression of vascular endothelial growth factor in hyperstimulated rat ovary

Özçakır, Hasan Tayfun; Giray, Seren Gülşen; Özbilgin, Mahmut Kemal; İnceboz, Ümit; Çağlar, Hüsnü

doi:10.1016/j.fertnstert.2004.03.053

Cited by 8 publications

(7 citation statements)

References 26 publications

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“…Research suggests that VEGF is responsible for the increased vascular permeability leading to the extravasation of protein-rich fluid and subsequent OHSS progression [42,43]. In addition, high levels of VEGF have been detected in serum and follicular fluids from women with severe OHSS [44].…”

Section: Discussionmentioning

confidence: 99%

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Metformin decreases the incidence of ovarian hyperstimulation syndrome: an experimental study

Elia

Quintana²,

Carrere³

et al. 2013

J Ovarian Res

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BackgroundIn assisted reproduction cycles, gonadotropins are administered to obtain a greater number of oocytes. A majority of patients do not have an adverse response; however, approximately 3-6% develop ovarian hyperstimulation syndrome (OHSS). Metformin reduces the risk of OHSS but little is known about the possible effects and mechanisms of action involved.ObjectiveTo evaluate whether metformin attenuates some of the ovarian adverse effects caused by OHSS and to study the mechanisms involved.Material and methodsA rat OHSS model was used to investigate the effects of metformin administration. Ovarian histology and follicle counting were performed in ovarian sections stained with Masson trichrome. Vascular permeability was measured by the release of intravenously injected Evans Blue dye (EB). VEGF levels were measured by commercially immunosorbent assay kit. COX-2 protein expression was evaluated by western blot and NOS levels were analyses by immunohistochemistry.ResultsAnimals of the OHSS group showed similar physiopathology characteristics to the human syndrome: increased body weight, elevated progesterone and estradiol levels (P<0.001), increased number of corpora lutea (P<0.001), higher ovarian VEGF levels and vascular permeability (P<0.001 and P<0.01); and treatment with metformin prevented this effect (OHSS+M group; P<0.05). The vasoactive factors: COX-2 and NOS were increased in the ovaries of the OHSS group (P<0.05 and P<0.01) and metformin normalized their expression (P<0.05); suggesting that metformin has a role preventing the increased in vascular permeability caused by the syndrome.ConclusionMetformin has a beneficial effect preventing OHSS by reducing the increase in: body weight, circulating progesterone and estradiol and vascular permeability. These effects of metformin are mediated by inhibiting the increased of the vasoactive molecules: VEGF, COX-2 and partially NOS. Molecules that are increased in OHSS and are responsible for a variety of the symptoms related to OHSS.

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Section: Discussionmentioning

confidence: 99%

“…Moreover, the vascular permeability in mouse skin induced by VEGF, was mediated by modulation of NOS and COX-2 [7]. Although the importance of COX-2 in the ovulatory process has been documented, the exact functions of this prostaglandin in human ovaries, fertilization, and implantation are not completely understood [43]. …”

Section: Discussionmentioning

confidence: 99%

Metformin decreases the incidence of ovarian hyperstimulation syndrome: an experimental study

Elia

Quintana²,

Carrere³

et al. 2013

J Ovarian Res

View full text Add to dashboard Cite

show abstract

“…Research suggests that VEGF is responsible for the increased capillary permeability leading to the extravasation of protein-rich fluid and subsequent OHSS progression (3,17). In addition, high levels of VEGF have been detected in both serum and follicular fluids (FF) of women with severe OHSS (18).…”

Section: Quintana Cox-2 Inhibition In Ovarian Hyperstimulation Fertmentioning

confidence: 99%

“…Similarly, COX-2 inhibition prevents hypoxic up-regulation of VEGF in human prostate cancer cells (15,16). Although the importance of COX-2 in the ovulatory process has been documented, the exact functions of prostaglandins in human ovary, fertilization, and implantation are not completely understood (17).…”

mentioning

confidence: 99%

Inhibition of cyclooxygenase-2 (COX-2) by meloxicam decreases the incidence of ovarian hyperstimulation syndrome in a rat model

Quintana¹,

Kopcow²,

Marconi³

et al. 2008

Fertility and Sterility

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“…RAS components have been detected in endothelial and ovarian cells (Dzau 1988, Harata et al 2006. Furthermore, angiotensin II has been described to influence reproductive processes such as ovulation (Mitsube et al 2003, Ozcakir et al 2004, Ferreira et al 2007). …”

Section: Introductionmentioning

confidence: 99%

Regulation of endothelial proliferation by the renin–angiotensin system in human umbilical vein endothelial cells

Herr

Rodewald²,

Fraser³

et al. 2008

Reproduction

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This study was performed in order to evaluate the role of angiotensin II in physiological angiogenesis. Human umbilical vein endothelial cells (HUVEC) were stained for angiotensin II type 1 receptor (AGTR1) immunocytochemically and for gene expression of renin-angiotensin system (RAS) components. The regulation of the angiogenesis-associated genes vascular endothelial growth factor (VEGF) and angiopoietins (ANGPT1 and ANGPT2) were studied using quantitative RT-PCR. Furthermore, we examined the effect of angiotensin II on the proliferation of HUVEC using Ki-67 as well as BrdU immunocytochemistry and investigated whether the administration of the AGTR1 blocker candesartan or the VEGF antagonist FLT1-Fc could suppress the observed angiotensin II-dependent proangiogenic effect. AGTR1 was expressed in HUVEC and the administration of angiotensin II significantly increased the gene expression of VEGF and decreased the gene expression of ANGPT1. Since the expression of ANGPT2 was not affected significantly the ratio of ANGPT1/ANGPT2 was decreased. In addition, a significantly increased endothelial cell proliferation was observed after stimulation with angiotensin II, which was suppressed by the simultaneous administration of candesartan or the VEGF antagonist FLT1-Fc. These results indicate the potential capacity of angiotensin II in influencing angiogenesis by the regulation of angiogenesis-associated genes via AGTR1. Since VEGF blockade opposed the effect of angiotensin II on cell proliferation, it is hypothesised that VEGF mediates the angiotensin II-dependent effect in concert with the changes in angiopoietin expression. This is the first report of the RAS on the regulation of angiogenesis-associated genes in physiology. Reproduction (2008) 136 125-130

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Effect of angiotensin-converting enzyme-inhibiting therapy on the expression of vascular endothelial growth factor in hyperstimulated rat ovary

Cited by 8 publications

References 26 publications

Metformin decreases the incidence of ovarian hyperstimulation syndrome: an experimental study

Metformin decreases the incidence of ovarian hyperstimulation syndrome: an experimental study

Inhibition of cyclooxygenase-2 (COX-2) by meloxicam decreases the incidence of ovarian hyperstimulation syndrome in a rat model

Regulation of endothelial proliferation by the renin–angiotensin system in human umbilical vein endothelial cells

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