Linear regression analysis of ultrasound follicular growth series: evidence for an abnormality of follicular growth in endometriosis patients

Doody, Michael C.; Gibbons, William E.; Buttram, Veasy C.

doi:10.1016/s0015-0282(16)59646-0

Cited by 72 publications

(30 citation statements)

References 6 publications

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“…3,12 Such anomalies, directly or indirectly, may account for impaired follicular growth, reduced dominant follicle size, fewer mature ovarian follicles, and decreased ovulation in women with endometriosis. 6,9,12,13 The process of ovulation is normally controlled through multiple temporal inputs, including protein and steroid hormones, metabolic signals, intrafollicular paracrine factors from the theca, mural, and cumulus granulosa cells and the oocyte. 14 Animal models replicating signs and symptoms of human disease have provided opportunities for in-depth characterization of mechanisms involved in the process of ovulation in women with endometriosis.…”

Section: Introductionmentioning

confidence: 99%

Elevated Peritoneal Fluid TNF-α Incites Ovarian Early Growth Response Factor 1 Expression and Downstream Protease Mediators: A Correlation With Ovulatory Dysfunction in Endometriosis

et al. 2013

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Endometriosis-associated infertility manifests itself via multiple, poorly understood mechanisms. Our goal was to characterize signaling pathways, between peritoneal endometriotic lesions and the ovary, leading to failed ovulation. Genome-wide microarray analysis comparing ovarian tissue from an in vivo endometriosis model in the rat (Endo) with controls (Sham) identified 22 differentially expressed genes, including transiently expressed early growth response factor 1 (Egr1). The Egr1 regulates gene requisites for ovulation. The Egr1 promoter is responsive to tumor necrosis factor-alpha (TNF-a) signaling. We hypothesized that altered expression of ovarian EGR1 is induced by elevated peritoneal fluid TNF-a which is upregulated by the presence of peritoneal endometriosis. Endo rats, compared to controls, had more peritoneal fluid TNF-a and quantitative, spatial differences in Egr1 mRNA and EGR1 protein localization in follicular compartments. Interactions between elevated peritoneal fluid TNF-a and overexpression of follicular Egr1/EGR1 expression may affect downstream protease pathways impeding ovulation in endometriosis. Preliminary studies identified similar patterns of EGR1 protein localization in human ovaries from women with endometriosis and compared to those without endometriosis.

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Section: Introductionmentioning

confidence: 99%

Elevated Peritoneal Fluid TNF-α Incites Ovarian Early Growth Response Factor 1 Expression and Downstream Protease Mediators: A Correlation With Ovulatory Dysfunction in Endometriosis

et al. 2013

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“…These include ovarian anomalies such as the reduced rates of follicular growth, functional capacity of the pre-ovulatory follicle and early luteal function [1, 12, 16, 17]. Gamete and embryo anomalies include reduced rates of fertilization and defects in embryo development [12, 18, 20, 21].…”

Section: Introductionmentioning

confidence: 99%

Reduced Fecundity in Female Rats with Surgically Induced Endometriosis and in Their Daughters: A Potential Role for Tissue Inhibitors of Metalloproteinase 11

Stilley

Woods-Marshall

Sutovsky³

et al. 2009

Biology of Reproduction

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The cause of reduced fecundity in women with endometriosis is unknown. Expression of matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) by both ectopic and eutopic endometrium reportedly play a role in the pathogenesis of endometriosis. We hypothesize that anomalous endometriotic TIMP protein synthesis, secretion, and localization also cause reproductive pathologies resulting in reduced fecundity. An established rat model for endometriosis (Endo) compared to non-endometriotic controls (Sham) was used to investigate reduced fecundity in endometriosis. Comparing Endo and Sham rats, Endo rats had altered ovarian dynamics including fewer ovarian follicles and corpora lutea (CL) with luteinized unruptured follicles. Further, in vivo anomalies in post-ovulatory oocyte structure and preimplantation embryo development including misaligned chromosomes, nuclear and cytoplasmic fragmentation and delayed or arrested cleavage as well as spontaneous abortions were found only in Endo rats. A causative role for TIMP-1 in these phenomena is supported by our findings that Endo rats have more TIMP-1 in their peritoneal fluid as detected by ELISA and more TIMP-1 immunolocalization in the theca of antral follicles as measured by computer-assisted morphometric analysis. These data suggest that in endometriosis, accumulation of TIMP-1 disrupts the normal MMP/TIMP enzymatic milieu in the peritoneal cavity and negatively impacts ovarian dynamics, oocyte quality and preimplantation embryo development, thereby decreasing fecundity. Most intriguingly, daughters from Endo rats which had no experimental interventions exhibited these same reproductive abnormalities. We predict that developmental exposure to endometriosis leads to permanent epigenetic changes in subsequent generations.

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“…Clear mechanisms causing the endometriosis-associated infertility have not been firmly established. Infertility in women with endometriosis may be associated with subtle, explicit or multifaceted abnormalities [1][2][3][4][5][6][7][8]. Anomalies have been identified in the ovary such as reduced rates of follicular growth, functional capacity of the preovulatory follicle, and early luteal function [1,2,4,5]; in gametes and embryos, including reduced rates of fertilization and defects in embryo development [1,6,[8][9][10]; and in endometrial function [7,11].…”

Section: Introductionmentioning

confidence: 99%

Proteasomes and Proteasome Activator 200 kDa (PA200) Accumulate on Chromatin in Response to Ionizing Radiation

Blickwedehl¹,

McEvoy²,

Wong³

et al. 2007

Radiation Research

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Linear regression analysis of ultrasound follicular growth series: evidence for an abnormality of follicular growth in endometriosis patients

Cited by 72 publications

References 6 publications

Elevated Peritoneal Fluid TNF-α Incites Ovarian Early Growth Response Factor 1 Expression and Downstream Protease Mediators: A Correlation With Ovulatory Dysfunction in Endometriosis

Elevated Peritoneal Fluid TNF-α Incites Ovarian Early Growth Response Factor 1 Expression and Downstream Protease Mediators: A Correlation With Ovulatory Dysfunction in Endometriosis

Reduced Fecundity in Female Rats with Surgically Induced Endometriosis and in Their Daughters: A Potential Role for Tissue Inhibitors of Metalloproteinase 11

Proteasomes and Proteasome Activator 200 kDa (PA200) Accumulate on Chromatin in Response to Ionizing Radiation

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