Endothelial nitric oxide synthase gene Glu298Asp polymorphism is associated with advanced stage endometriosis

Kim, Hoon; Ku, Seung Yup; Kim, Sung Hoon; Lee, Gyoung Hoon; Choi, Young Min; Kim, Jong Mee; Lee, Taek Hoo; Moon, Shin Yong

doi:10.1093/humrep/dep212

Cited by 19 publications

(26 citation statements)

References 26 publications

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“…Furthermore, studies of single nucleotide polymorphism s reveal that GSTT1 (glutathione-S-transferase) null deletion [36] and eNOS [20] are associated with moderate risk of endometriosis. In addition, endometriosis-related infertility is associated with glutathione peroxidase activity [29].…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, high levels of serum and follicular NO in patients with endometriosis were associated with poor embryo quality and pregnancy outcome in assisted reproduction technology cycles [22]. Other previous studies have indentified the association of a polymorphism of endothelial NOS with advanced stage endometriosis [20]. Overall, increased microenviromental NO (in follicular fluid, tubal secretions, and endometrial tissue) might contribute to the pathologic effects of endometriosis on the development potential of embryos.…”

Section: Introductionmentioning

confidence: 89%

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Nitric oxide modulates mitochondrial activity and apoptosis through protein S-nitrosylation for preimplantation embryo development

Lee¹,

Lee²,

Huang³

et al. 2013

J Assist Reprod Genet

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Purpose Previous studies reported that patients with endometriosis had excess nitric oxide (NO) in the reproductive tract and poor embryo development in IVF cycles. This study aims to elucidate the effects of NO on early embryo development. Methods Zygotes from superovulated B6CBF1 mice were cultured to blastocysts in a variety of media. Sodium nitroprusside (SNP) and N G -nitro-L-arginine (LNA) were added to the culture medium as a NO donor and a NO synthase inhibitor, respectively. The localization and fluorescence intensity of S-nitrosylated (SNO) proteins within 2-cell stage embryos were analyzed with confocal microscopy. Apoptosis and ATP production in the blastocysts were measured. Result(s) Subsequent to NO exposure, the SNO proteins mainly colocalized with the mitochondria and endoplasmic reticulum and the intensity of SNO proteins increased. The addition of a quanylate cyclase inhibitor and a cyclic GMP mimic agent induced nonsignificant changes in SNO proteins, whereas addition of a superoxide scavenger or a reduced form of glutathione rescued the embryos from the effects of NO. However, superoxide scavenger supplementation resulted in decreased blastocyst ATP production. Conclusion(s) Elevated NO exerts deleterious effects on embryo development, possibly through protein S-nitrosylation in the mitochondria and endoplasmic reticulum. Including glutathione as a component in the culture medium might counteract this effect.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 89%

Nitric oxide modulates mitochondrial activity and apoptosis through protein S-nitrosylation for preimplantation embryo development

Lee¹,

Lee²,

Huang³

et al. 2013

J Assist Reprod Genet

View full text Add to dashboard Cite

show abstract

“…NOS3 may modulate angiogenesis and influence individual susceptibility to endometriosis, and it is widely accepted that angiogenesis plays an essential role in the growth and survival of endometriotic lesions. Moreover, NOS3 has also been reported to be associated with advanced stage endometriosis in a Korean population [33, 34]. Previous studies have shown altered levels of the CALD1 gene (encoding the protein caldesmon) in endometriosis and that precursor protein of caldesmon is a possible predictor of endometrial dysregulation in patients with endometriosis [35, 36].…”

Section: Discussionmentioning

confidence: 99%

Peptidomic Analysis of Endometrial Tissue from Patients with Ovarian Endometriosis

Xue

et al. 2018

Cell Physiol Biochem

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Background/Aims: Ovarian endometriosis (OvE) is ovarian cyst that is lined with endometrial tissue. They are found in 17–44% of women with endometriosis. Their clinical manifestations include pelvic pain, dysmenorrhea, dyspareunia, and infertility. Although the incidence of OvE has increased yearly, the exact pathogenesis of OvE is still unclear. We used peptidomics, an emerging branch of proteomics, to identify differentially expressed peptides in order to determine the possible roles of these peptides in the pathogenesis of OvE. Methods: The ectopic and eutopic endometria of OvE were used to extract peptides with 10-kDa molecular weight cutoff filters, and the peptide precursor proteins were then identified with PEAKS software, followed by quantification with the TMT labeling method and subsequent analysis by liquid chromatography-tandem mass spectrometry. Gene ontology (GO) analysis, pathway analysis, SMART, and SABLE were used to study the possible functions of these peptide according to their precursor proteins’ function. The effects of peptides derived from VCAM-1 (PDFV) on endometrial stromal cell (ESC) migration and invasion were examined with wound healing assays and Transwell assays and the expression of E-cadherin was detected by western blotting. Results: A total of 491 peptides were identified with abundant differences between the two groups of samples (p < 0.05, and absolute fold change ≥ 2). SMART and SABLE database showed that 42 of the 491 peptides were located in the conserved structural domains of their protein precursors and contained secondary structure and, among them, 2 peptides’ precursor proteins were associated with the cell proliferation. Additionally, 5 peptides’ precursor proteins were associated with endometriosis. Our study confirmed that PDFV promoted ESC migration and invasion and reduced E-cadherin expression (p < 0.05). Conclusion: PDFV and its precursor protein VCAM-1 may be involved in the process of OvE formation by reducing the expression of E-cadherin. The peptidomics analysis provides new insight for future studies of the mechanisms of OvE development.

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“…Retinopathy of prematurity is associated with all three polymorphisms (Rusai et al 2008;Yanamandra et al 2010), whereas the coding polymorphism affects endometriosis (Kim et al 2009a), and the promoter polymorphism affects idiopathic osteonecrosis of the femoral head (Glueck et al 2007).…”

Section: Nitric Oxide Synthase (Nos3/enos)mentioning

confidence: 99%

Common Polymorphisms in Angiogenesis

Rogers

D’Amato

2011

Cold Spring Harbor Perspectives in Medicine

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Endothelial nitric oxide synthase gene Glu298Asp polymorphism is associated with advanced stage endometriosis

Abstract: These findings suggest that the T allele, encoding aspartic acid, of the Glu298Asp polymorphism of the NOS3 may be associated with advanced stage endometriosis in the Korean population.

Cited by 19 publications

References 26 publications

Nitric oxide modulates mitochondrial activity and apoptosis through protein S-nitrosylation for preimplantation embryo development

Nitric oxide modulates mitochondrial activity and apoptosis through protein S-nitrosylation for preimplantation embryo development

Peptidomic Analysis of Endometrial Tissue from Patients with Ovarian Endometriosis

Common Polymorphisms in Angiogenesis

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