scholarly journals Vascular Endothelial Cadherin Regulates Vascular Permeability: Implications for Ovarian Hyperstimulation Syndrome

2007 ◽  
Vol 92 (1) ◽  
pp. 314-321 ◽  
Author(s):  
A. Villasante ◽  
A. Pacheco ◽  
A. Ruiz ◽  
A. Pellicer ◽  
J. A. Garcia-Velasco
Keyword(s):  
Vascular Permeability ◽  
Ovarian Hyperstimulation Syndrome ◽  
Ovarian Hyperstimulation ◽  
Vascular Endothelial ◽  
Vascular Endothelial Cadherin

scholarly journals Ginkgo Biloba Extract 761 Reduces Vascular Permeability of the Ovary and Improves the Symptom of Ovarian Hyperstimulation Syndrome in a Rat Model

2021 ◽  
Author(s):  
Jie Zhang ◽  
Jie Huang ◽  
Xinhuan He ◽  
Ning Li ◽  
Yu Miao ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Treatment Group ◽  
Vascular Permeability ◽  
Chorionic Gonadotropin ◽  
Rat Model ◽  
Ovarian Hyperstimulation Syndrome ◽  
Ovarian Hyperstimulation ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Abstract BackgroundGinkgo biloba extract (EGb) has been widely applied in the treatment of cerebrovascular and neurological diseases. However, the effect of EGb761 on ovarian hyperstimulation syndrome (OHSS), a vascular disorder and life-threatening complication of In vitro fertilization and Intracytoplasmic sperm injection therapy (IVF/ICSI), has not been evaluated. MethodsForty female Wistar rats aged 22-days old (D22) were divided into eight groups: Control rats received intraperitoneal injection of saline for 5 consecutive days (D22-D26); OHSS-model group received 10 IU equine chorionic gonadotropin (eCG) for 4 consecutive days (D22-D25) and 30 IU of human chorionic gonadotropin (hCG) on the 5th day (D26); Prophylactic treatment group received three doses of EGb761 (50mg/kg/d, 100mg/kg/d, 200mg/kg/d) one hour before injection of eCG (hCG) for 7 consecutive days; Therapeutic treatment group received three doses of EGb761 (50mg/kg/d, 100mg/kg/d, 200mg/kg/d) 48 hours after injection of eCG (hCG) for 7 consecutive days. ResultsWe found the therapeutic treatment group exhibited the lowest ovarian and renal mass index, vascular permeability, estradiol and progesterone concentrations, vascular endothelial growth factor (VEGF) and vascular endothelial growth factor receptor (VEGFR) protein expression. ConclusionsEGb761 decreases vascular permeability in OHSS rat model by inhibiting VEGF and VEGFR expression, which may contribute to the prevention and treatment of OHSS. Furthermore, therapeutic medication is superior to prophylactic medication.

scholarly journals The kallikrein-kinin system, but not vascular endothelial growth factor, plays a role in the increased vascular permeability associated with ovarian hyperstimulation syndrome

1998 ◽  
Vol 20 (3) ◽  
pp. 363-374 ◽  
Author(s):  
H Kobayashi ◽  
Y Okada ◽  
T Asahina ◽  
J Gotoh ◽  
T Terao
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Ovarian Carcinoma ◽  
Vascular Permeability ◽  
Ovarian Hyperstimulation Syndrome ◽  
Ovarian Hyperstimulation ◽  
Vascular Endothelial ◽  
Kinin System ◽  
Kallikrein Kinin System ◽  
Endothelial Growth Factor

Ovarian hyperstimulation syndrome (OHSS) is a severe complication arising from controlled stimulation treatment. Vascular endothelial growth factor (VEGF) has recently emerged as an important factor which may be responsible for the hyperpermeability seen in OHSS. The purpose of the present study was to investigate and compare the mechanisms by which ascites in patients with OHSS and ovarian carcinoma induce increases in vascular permeability in an in vitro assay and an in vivo animal experiment. We found 8-fold lower VEGF levels in ascites from patients with OHSS than in those from patients with ovarian carcinoma. Although VEGF is produced by the ovaries, it is not necessarily the factor responsible for hyperpermeability. We also demonstrated that the vascular hyperpermeability produced by OHSS ascites was not abolished by specific neutralizing anti-VEGF antibodies, and that not all of the VEGF found in the ascites fluid is biologically active. Moreover, our results strongly suggest that the vascular permeability produced by OHSS ascites may depend on activation of the kallikrein-kinin system. Possible evidence for this phenomenon was obtained by demonstrating that the hyperpermeability caused by the ascites could be blocked by Trasylol (known to inhibit bradykinin synthesis) and potentiated by captopril (a kininase II inhibitor). Taken together, the results suggest that, although VEGF is found in ascites fluid from patients with OHSS, it is unlikely that the cause of OHSS involves VEGF production by the ovaries. The kallikrein-kinin system may be more important in the hyperpermeability seen in OHSS.

scholarly journals Lysophosphatidic Acid Up-Regulates Expression of Interleukin-8 and -6 in Granulosa-Lutein Cells through Its Receptors and Nuclear Factor-κB Dependent Pathways: Implications for Angiogenesis of Corpus Luteum and Ovarian Hyperstimulation Syndrome

2008 ◽  
Vol 93 (3) ◽  
pp. 935-943 ◽  
Author(s):  
Shee-Uan Chen ◽  
Chia-Hung Chou ◽  
Hsinyu Lee ◽  
Chi-Hong Ho ◽  
Chung-Wu Lin ◽  
...  
Keyword(s):  
Growth Factor ◽  
Lysophosphatidic Acid ◽  
Ovarian Hyperstimulation Syndrome ◽  
Umbilical Vein ◽  
Nuclear Factor Κb ◽  
Ovarian Hyperstimulation ◽  
Vascular Endothelial ◽  
Nuclear Factor ◽  
Lpa Receptors ◽  
Endothelial Growth Factor

Abstract Context: Lysophosphatidic acid (LPA) was found at significant amounts in follicular fluid of preovulatory follicle. The lysophospholipase D activity of serum from women receiving ovarian stimulation was higher than women with natural cycles. Angiogenic cytokines, including IL-6, IL-8, and vascular endothelial growth factor, increased in plasma and ascites of patients with ovarian hyperstimulation syndrome. The role of LPA in ovarian follicles is unclear. Objective: Our objective was to investigate the expression of LPA receptors and function of LPA in granulosa-lutein cells. Design: Granulosa-lutein cells were obtained from women undergoing in vitro fertilization. We examined the expression of LPA receptors using RT-PCR. The effects of LPA on the expression of IL-6, IL-8, and vascular endothelial growth factor were examined. Signal pathways of LPA were delineated. The functions of secretory angiogenic factors were tested using human umbilical vein endothelial cells. Results: The LPA1, LPA2, and LPA3 receptors’ mRNA was identified in granulosa-lutein cells. LPA enhanced IL-8 and IL-6 expressions in a dose- and time-dependent manner. LPA functioned via LPA receptors, Gi protein, MAPK/ERK, p38, phosphatidylinositol 3-kinase/Akt, and nuclear factor-κB, and transactivation of epidermal growth factor receptor. LPA induced IL-8 and IL-6 through different pathways. LPA-induced IL-8 and IL-6 increased permeability of human umbilical vein endothelial cell monolayer. Conclusions: LPA induces IL-8 and IL-6 expressions through LPA receptors and nuclear factor-κB dependent pathways in granulosa-lutein cells. The LPA in preovulatory follicles may play a role in the angiogenesis of corpus luteum. Large amounts of LPA-induced IL-8 and IL-6 from multiple corpora luteae of stimulated ovaries may be one of the pathophysiological causes of ovarian hyperstimulation syndrome.

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