scholarly journals Electroacupuncture Reduces Oocyte Number and Maintains Vascular Barrier Against Ovarian Hyperstimulation Syndrome by Regulating CD200

2021 ◽  
Vol 9 ◽  
Author(s):  
Li Chen ◽  
Xuan Huang ◽  
Li Wang ◽  
Cencen Wang ◽  
Xu Tang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Barrier Function ◽  
Ovarian Hyperstimulation Syndrome ◽  
Umbilical Vein ◽  
Ovarian Tissue ◽  
The Body ◽  
Corpora Lutea ◽  
Ovarian Hyperstimulation ◽  
Oocyte Number

Ovarian hyperstimulation syndrome (OHSS) is a common complication caused by ovulatory stimulation therapy, which manifests as an increase in ovarian volume, an increase in the number of oocytes retrieved, and increased vascular permeability throughout the body and especially in ovarian tissue. In our previous study, we found that electroacupuncture (EA) could prevent the progression of OHSS, by mainly affecting ovary. However, the specific molecules and the mechanism of this process were still unknown. In order to explore the underlying mechanism, OHSS rat model was established and EA treatment was performed, which was followed by proteomic analysis of ovaries. Results showed a significant increase in the expression level of CD200 in the ovaries of OHSS group treated with EA than those of OHSS group. Clinical data showed that the level of CD200 in follicular fluid was negatively correlated with the number of oocytes retrieved and serum E2 level. Further in vitro experiments showed a concentration-dependent role of human chorionic gonadotropin (hCG) in reducing CD200 and CD200R levels, and increasing inflammatory cytokine levels in cultured KGN cells. In human umbilical vein endothelial cells (HUVECs), the vascular barrier function was improved by CM (cultural medium from KGN cell) which treated with CD200Fc (CD200R agonist). Meanwhile, the results of in vivo experiments indicated that EA reduced the number of ovarian corpora lutea, decreased inflammatory response, and improved the vascular barrier function by increasing the expression of CD200 and CD200R in rat ovaries. These findings suggest that EA treatment may reduce oocyte number and maintain vascular barrier against OHSS through ovarian anti-inflammatory response mediated by CD200. Therefore, this study is the first to identify CD200 as a main of EA in the ovary and elucidate the possible mechanism of EA on preventing and treating OHSS, which provide a scientific basis for CD200 as an effector and indicator in EA treatment.

scholarly journals A Case with Severe Endometriosis, Ovarian Hyperstimulation Syndrome, and Isolated Unilateral Pleural Effusion after IVF

2017 ◽  
Vol 2017 ◽  
pp. 1-4
Author(s):  
Negjyp Sopa ◽  
Elisabeth Clare Larsen ◽  
Anders Nyboe Andersen
Keyword(s):  
Pleural Effusion ◽  
Ovarian Hyperstimulation Syndrome ◽  
Common Finding ◽  
Ovarian Hyperstimulation ◽  
Pleural Effusions ◽  
Luteal Support ◽  
Vitro Fertilization ◽  
Fluid Production ◽  
The Right

We present a very rare case of right-sided isolated pleural effusion in a patient with severe endometriosis who, in relation to in vitro fertilization (IVF), developed ovarian hyperstimulation syndrome (OHSS). Earlier laparotomy showed grade IV endometriosis including endometriotic implants of the diaphragm. The patient had no known risk factors for OHSS and only a moderate number of oocytes aspirated. She received, however, repeated hCG injections for luteal support. The patient did not achieve pregnancy but was hospitalized due to pain in the right side of the chest and dyspnoea. A chest computed tomography (CT) showed a pleural effusion on the right side. Total of 1000 ml of pleural fluid was drained after a single thoracentesis. After three days, the symptoms and fluid production ceased. Ascites is a common finding in OHSS, but pleural effusions are rare. Further, isolated pleural effusions have not previously been described in a patient with endometriosis. We suggest that the repeated hCG injections induced effusions from the endometriotic lesions at the diaphragm and as a consequence this patient developed isolated hydrothorax.

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.

scholarly journals Prediction of severe ovarian hyperstimulation syndrome in women undergoing in vitro fertilization using estradiol levels, collected ova, and number of follicles

2020 ◽  
Vol 48 (8) ◽  
pp. 030006052094555
Author(s):  
Ivan Madrazo ◽  
Monserrat Fabiola Vélez ◽  
Josue Jonathan Hidalgo ◽  
Ginna Ortiz ◽  
Juan José Suárez ◽  
...  
Keyword(s):  
Ovarian Hyperstimulation Syndrome ◽  
Characteristic Curve ◽  
Antral Follicle ◽  
Antral Follicle Count ◽  
Ovarian Hyperstimulation ◽  
Vitro Fertilization ◽  
American Society ◽  
Severe Ovarian Hyperstimulation Syndrome ◽  
Severe Ohss

Objective Our objective was to determine whether estradiol (E2) levels (Day 3 and fold change to Day 10), antral follicle count (AFC), and number of ova collected could predict ovarian hyperstimulation syndrome (OHSS) and culdocentesis intervention. Methods We conducted a retrospective review of patient charts between January 2008 and December 2017. OHSS was defined using American Society for Reproductive Medicine criteria. Predictability was evaluated by measuring the area under the receiver operating characteristic curve (AUC). Results The cohort included 319 women (166 controls, 153 OHSS, of whom 54 had severe OHSS). The OHSS group had higher E2Day 3 (249 ± 177 vs. 150 ± 230 ng/L), E2FoldChange (32.2 ± 29.1 vs. 20.1 ± 23.8), AFC (18.2 ± 9.1 vs. 11.6 ± 8.3), and number of ova collected (21.1 ± 9.0 vs. 10.1 ± 6.5). E2Day 3 (AUC = 0.76, 95%CI: 0.71–0.82), E2FoldChange (AUC = 0.71, 95%CI: 0.65–0.77), AFC (AUC = 0.75, 95%CI: 0.70–0.81), and number of ova collected (AUC = 0.85, 95%CI: 0.81–0.89) were predictive for OHSS. All variables were predictive for culdocentesis intervention (E2Day 3: AUC = 0.63, 95%CI: 0.55–0.70; E2FoldChange: AUC = 0.63, 95%CI: 0.55–0.71; AFC: AUC = 0.74, 95%CI: 0.68–0.80; number of ova collected: AUC = 0.80, 95%CI: 0.75–0.85). Conclusions Day 3 E2 levels and number of ova collected predict patients who could develop OHSS and may require culdocentesis.

scholarly journals FBXW7 regulates endothelial barrier function by suppression of the cholesterol synthesis pathway and prenylation of RhoB

2019 ◽  
Vol 30 (5) ◽  
pp. 607-621 ◽  
Author(s):  
Manon C. A. Pronk ◽  
Jisca Majolée ◽  
Anke Loregger ◽  
Jan S. M. van Bezu ◽  
Noam Zelcer ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Barrier Function ◽  
Rho Gtpases ◽  
Umbilical Vein ◽  
Cholesterol Biosynthesis ◽  
Endothelial Barrier ◽  
Biosynthesis Pathway ◽  
Endothelial Barrier Function ◽  
Cholesterol Biosynthesis Pathway

Rho GTPases control both the actin cytoskeleton and adherens junction stability and are recognized as essential regulators of endothelial barrier function. They act as molecular switches and are primarily regulated by the exchange of GDP and GTP. However, posttranslational modifications such as phosphorylation, prenylation, and ubiquitination can additionally alter their localization, stability, and activity. F-box proteins are involved in the recognition of substrate proteins predestined for ubiquitination and subsequent degradation. Given the importance of ubiquitination, we studied the effect of the loss of 62 members of the F-box protein family on endothelial barrier function in human umbilical vein endothelial cells. Endothelial barrier function was quantified by electrical cell impedance sensing and macromolecule passage assay. Our RNA interference–based screen identified FBXW7 as a key regulator of endothelial barrier function. Mechanistically, loss of FBXW7 induced the accumulation of the RhoB GTPase in endothelial cells, resulting in their increased contractility and permeability. FBXW7 knockdown induced activation of the cholesterol biosynthesis pathway and changed the prenylation of RhoB. This effect was reversed by farnesyl transferase inhibitors and by the addition of geranylgeranyl pyrophosphate. In summary, this study identifies FBXW7 as a novel regulator of endothelial barrier function in vitro. Loss of FBXW7 indirectly modulates RhoB activity via alteration of the cholesterol biosynthesis pathway and, consequently, of the prenylation status and activity of RhoB, resulting in increased contractility and disruption of the endothelial barrier.

scholarly journals A Mutation in the Follicle-Stimulating Hormone Receptor as a Cause of Familial Spontaneous Ovarian Hyperstimulation Syndrome

2004 ◽  
Vol 89 (4) ◽  
pp. 1255-1258 ◽  
Author(s):  
Lucia Montanelli ◽  
Anne Delbaere ◽  
Costantino Di Carlo ◽  
Carmine Nappi ◽  
Guillaume Smits ◽  
...  
Keyword(s):  
In Vitro Fertilization ◽  
Ovarian Hyperstimulation Syndrome ◽  
Follicle Stimulating Hormone ◽  
High Sensitivity ◽  
Ovarian Hyperstimulation ◽  
Satisfactory Explanation ◽  
Vitro Fertilization ◽  
Increased Sensitivity ◽  
Stimulation Of

Abstract Ovarian hyperstimulation syndrome (OHSS) occurs mainly after excessive stimulation of the ovaries by exogenous gonadotropins administrated in the context of in vitro fertilization procedures (iatrogenic OHSS). Recently, spontaneous and recurrent occurrence of the disease (spontaneous OHSS) was shown in two families to be caused by mutations affecting the follitropin receptor (FSHr). The two mutant FSHr (T449I, D567N) harbor aminoacid substitutions in the serpentine portion of the receptor and display abnormally high sensitivity to the pregnancy hormone hCG, thus providing a satisfactory explanation to the phenotype. In addition, mutant D567N showed also increased sensitivity to thyrotopin (TSH) and displayed increase in basal (ligand-independent) activity. In this report, we describe a new familial case of recurrent OHSS. The affected women were heterozygous for a different mutation involving codon 449, where an alanine was substituted for threonine. Similar to D567N, the T449A FSHr mutant shows an increase of its sensitivity to both hCG and TSH, together with an increase in basal activity. Together with the two previous studies, this report shows that inappropriate stimulation of the FSHr by hCG is a cause of spontaneous OHSS.

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