Quantitative expression of apoptosis-regulating genes in endometrium from women with and without endometriosis

Braun, Donald P.; Ding, Jane; Shaheen, Fehr; Willey, James C.; Rana, Nasir; Dmowski, W. Paul

doi:10.1016/j.fertnstert.2006.06.026

Cited by 57 publications

(48 citation statements)

References 19 publications

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“…The heritable traits of endometriosis have previously been reported, with a 5-7-fold increased risk of endometriosis development in first-degree relatives (6) There are numerous recognized endometriosis susceptibility genes, which are associated with steroid hormone action, immune response, oxidative stress, glucose homeostasis, vascular and tissue remodeling, and apoptosis (7,8). Endometriosis is characterized by the abnormal survival and growth of endometrial tissue in the abdominal organs (1), which are resistant to apoptosis (8,9). Among the critical factors affecting apoptosis in endometriosis, it has been proposed that survivinl may inhibit apoptosis (10).…”

Section: Introductionmentioning

confidence: 99%

Polymorphic variants in vitamin D signaling pathway genes and the risk of endometriosis-associated infertility

Szczepańska

Mostowska

Wirstlein

et al. 2015

Molecular Medicine Reports

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Abstract. It has recently been reported that vitamin D blood plasma levels are associated with reduced risk of endometriosis. The present study aimed to investigate whether the vitamin D binding protein (GC), vitamin D receptor (VDR), and retinoid X receptor (RXR) gene variants may be genetic risk factors for endometriosis-associated infertility. The subjects consisted of 154 women with endometriosis-associated infertility and 347 controls. Using polymerase chain reaction restriction fragment length polymorphism and high resolution melt techniques, the GC rs1155563, rs2298849 and rs7041; RXRA rs10881578, rs10776909 and rs749759; VDR BsmI rs1544410; and FokI rs2228570 single nucleotide polymorphisms (SNPs) were investigated in the patients with endometriosis and the healthy controls. The results indicated that no significant differences were observed between the genotype and allele frequencies of all experimental SNPs in the vitamin D signaling pathway genes in women with endometriosis-associated infertility and controls. However, a significant association was present between the A-T haplotype, consisting of VDR rs1544410 and rs222857 minor alleles, and endometriosis-associated infertility [OR=1.659 (1.122-2.453), P=0.011]. The results of the present study suggested that VDR gene variants act as genetic risk factors for endometriosis-associated infertility.

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Section: Introductionmentioning

confidence: 99%

Polymorphic variants in vitamin D signaling pathway genes and the risk of endometriosis-associated infertility

Szczepańska

Mostowska

Wirstlein

et al. 2015

Molecular Medicine Reports

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show abstract

“…Furthermore, there are several recognized endometriosis susceptibility genes, which are associated with steroid hormone action, immune response, oxidative stress, glucose homeostasis, vascular and tissue remodeling, and apoptosis [45,46].…”

Section: Vitamin D and Endometriosismentioning

confidence: 99%

Vitamin D and Female Reproduction

Elhusseini¹,

Lizneva²,

Gavrilova-Jordan³

et al. 2017

A Critical Evaluation of Vitamin D - Basic Overview

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Vitamin D deficiency has an impact on the reproduction of more than 40% of reproductive age women globally. Fibroids are more common among African-American females owing to their decreased milk consumption and reduced absorption of ultraviolet rays, supporting the relation between vitamin D deficiency and fibroid development. Vitamin D has an inhibitory effect on leiomyoma cells by suppression of proliferation cell nuclear antigen (PCNA), BCL-2, BCL-w, CDK1, and catechol-Omethyltransferase (COMT) protein levels. A growing evidence support the relationship between vitamin D deficiency and endometriosis through overexpression of vitamin D recseptor (VDR) and α-hydroxylase enzyme, however, it is still unclear if the endometriosis patients could benefit from vitamin D supplementation. Effect of vitamin D supplementation on the metabolic outcomes of polycystic ovary (PCO) has been studied and reveled that it is negatively correlated with fasting glucose, fasting insulin, triglycerides, C-reactive protein, free androgen index, and Dehydroepiandrosterone (DHEAS) and positively associated with quantitative insulin sensitivity check index (QUICKI), high density lipoprotein cholesterol (HDL-C), and sexual hormone binding globulin (SHBG), whereas its impact on the ovarian function is still unclear. Vitamin D deficiency may worse the obstetrical outcomes, including preeclampsia, gestational diabetes, low birth weight, increased cesarean section rate, neonatal asthma, seizures, and preterm labor. The relationship between serum levels of 25-hydroxy-vitamin D (25(OH) D) and pregnancy rates in ART is still debatable, with the need to conduct more clinical trials toward it. The in vitro antiproliferative and prodifferentiative effect of vitamin D might find a role in control of hyperplastic overactive bladder. Several studies support that vitamin D deficiency constitutes a risk factor for development of many types of cancer such as breast, ovarian, and colorectal.

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“…Marked cell proliferation has been attributed to a change in the expression levels of proteins such as B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X proteins (Bcl-XL, Bcl-XS). A number of other genes are associated with apoptosis in endometriosis, including defender against cell death-1, P53, survivin, caspase-1, calpain, proliferating cell nuclear antigen and PGE 2 synthesis genes (31,(33)(34)(35). PGE 2 promotes cell survival through the EP2/EP4 receptor-dependent activation of ERK1/2, Akt, NF-κB, and β-catenin signaling pathways, suppressing proapoptotic proteins (Bax and Bad) and enhancing antiapoptotic proteins (Bcl-2/Bcl-XL) (33).…”

Section: Antiapoptosismentioning

confidence: 99%

Pathogenesis of endometriosis: The role of initial infection and subsequent sterile inflammation (Review)

Kobayashi

Higashiura

Shinmoto

et al. 2013

Molecular Medicine Reports

111

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Abstract. Endometriosis is a common type of chronic inflammatory disease with an immunological background. In this review, we aimed to explore the contemporary literature on the infection and sterile inflammation that support the pathogenesis of endometriosis. This article reviews the English-language literature on inflammatory, environmental, immunological and oxidative factors associated with endometriosis in an effort to identify factors that cause a predisposition to endometriosis. Intrauterine microbes may be critical for the initiation of endometriosis; the initial activation of pathogen recognition receptors by microbial stimuli results in the activation of proinflammatory pathways and innate immunity. In addition to their response to various exogenous pathogen-associated molecular patterns, Toll-like receptors (TLRs) also recognize a wide range of endogenous danger-associated molecular patterns (DAMPs). The increased expression levels of DAMPs may be involved in the subsequent process of nuclear transcription factor-κB-dependent sterile inflammation. Oxidative stress, secondary to the influx of iron during retrograde menstruation, is involved in the progression of endometriosis. DAMP-mediated danger signals and oxidative stress are bidirectional during sterile inflammation (danger signal spiral). This review supports the hypothesis that there are at least two distinct phases of endometriosis development: The initial wave of TLR activation in modulating innate immune responses would be followed by the second big wave of sterile inflammation.

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Quantitative expression of apoptosis-regulating genes in endometrium from women with and without endometriosis

Cited by 57 publications

References 19 publications

Polymorphic variants in vitamin D signaling pathway genes and the risk of endometriosis-associated infertility

Polymorphic variants in vitamin D signaling pathway genes and the risk of endometriosis-associated infertility

Vitamin D and Female Reproduction

Pathogenesis of endometriosis: The role of initial infection and subsequent sterile inflammation (Review)

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