Aberrant Adherence of Peritoneal Macrophages in Endometriosis

Sharpe-Timms, Kathy L.; Zimmer, Randy L; Ricke, Emily A.; Horowitz, Gary M.

doi:10.1016/s0015-0282(00)00780-9

Cited by 3 publications

(1 citation statement)

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“…62 Adherence, the first step in the phagocytic process, is decreased when endometriotic haptoglobin is bound to peritoneal macrophages, while paradoxically IL-6 production is upregulated in these same haptoglobin-bound macrophages. 62 Endometriotic haptoglobin can also increase proliferation of endothelial cells and elicits neovascularization (Sharpe-Timms, unpublished data). Hence, differential expression of haptoglobin by eutopic endometrium from women with endometriosis may explain why although most women have retrograde menstruation, only some develop this disease.…”

Section: Protein Production and Gene Expressionmentioning

confidence: 99%

Endometrial Anomalies in Women with Endometriosis

Sharpe-Timms

2001

Annals of the New York Academy of Sciences

170

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Endometriotic lesions are defined by extrauterine growth of endometrial glands and stroma. Retrograde menstruation with subsequent attachment, invasion, and neovascularization are believed to give rise to the endometriotic lesions. As most women exhibit some degree of retrograde menstruation, some other unidentified factor(s) must render certain women susceptible to attachment and growth of ectopic endometrial tissue. A variety of theories have been proposed to account for this susceptibility, including genetic predisposition, aberrant immunological response, and an altered peritoneal environment. Ectopic endometriotic lesions are histologically similar to their putative eutopic precursors, yet significant biochemical differences exist between these two tissues. Less information is available regarding differences between eutopic endometrium from women with or without endometriosis. This report describes anomalies in structure, proliferation, immune components, adhesion molecules, proteolytic enzymes and inhibitors, steroid and cytokine production and responsiveness, and gene expression and protein production that have been identified in eutopic endometrium from women with endometriosis.

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Section: Protein Production and Gene Expressionmentioning

confidence: 99%

Endometrial Anomalies in Women with Endometriosis

Sharpe-Timms

2001

Annals of the New York Academy of Sciences

170

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Differential expression and localization of de-novo synthesized endometriotic haptoglobin in endometrium and endometriotic lesions

et al. 2000

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Endometriosis protein-I (ENDO-I) mRNA expression and protein localization were evaluated using in-situ hybridization and immunohistochemistry in endometriotic lesions and eutopic endometrium from women with endometriosis, and in eutopic endometrium from women without endometriosis (controls). When present, ENDO-I mRNA and protein were observed in the functionalis zone of endometrial stroma and the stroma of endometriotic lesions. Expression and localization differences were scored and statistically analysed. During the secretory stage, ENDO-I mRNA expression by endometriotic lesions and eutopic endometrium from women with disease was significantly greater than ENDO-I mRNA expression by proliferative stage eutopic endometrium from women with disease or eutopic endometrium from controls, regardless of cycle stage (P < 0.001). More ENDO-I protein was localized in endometriotic lesions and eutopic endometrium from women with disease than in eutopic endometrium from controls, regardless of cycle stage (P < 0.001). Differential expression and localization of ENDO-I may help develop minimally invasive diagnostic strategies for endometriosis. Further, as ENDO-I shares nucleotide sequence and amino acid sequence with hepatic haptoglobin-which in certain disease states is immunosuppressive and angiogenic-differences in ENDO-I expression and localization in the peritoneal cavity may contribute to the pathogenesis of endometriosis and/or facilitate development of unprecedented diagnostic or therapeutic approaches for management of this enigmatic disease.

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Using Rats as a Research Model for the Study of Endometriosis

Sharpe-Timms

2002

Annals of the New York Academy of Sciences

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Although there are disadvantages of extrapolating data across species, the rat model may be used to study events involved in the pathogenesis and pathophysiologies of endometriosis or novel therapeutic approaches for this disorder that are not accessible in humans. Rat endometriotic tissues are similar to human lesions in vivo, and rat endometriotic tissues and cells perform in a similar manner as human endometriotic tissues and cells in organ explant culture and isolated cell culture. The rat model permits studies of mechanisms and regulators in a controlled manner free from confounding influences such as individual patient variation and environmental influences. The primary method used for induction of endometriosis in rats has been autotransplantation of uterine squares (implants) into the peritoneal cavity. Beyond mere growth of endometrium in ectopic locations, rats with endometriosis display similar symptoms, including a reduction in fertility and fecundity, and the endometriotic implants react similarly to therapeutics as those of humans with the disease. Similar alterations in gene expression and protein production have been observed in endometriotic tissues from rats and humans that may, in part, be causative agents involved in the pathogenesis or pathophysiologies of endometriosis.

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Aberrant Adherence of Peritoneal Macrophages in Endometriosis

Cited by 3 publications

References 0 publications

Endometrial Anomalies in Women with Endometriosis

Endometrial Anomalies in Women with Endometriosis

Differential expression and localization of de-novo synthesized endometriotic haptoglobin in endometrium and endometriotic lesions

Using Rats as a Research Model for the Study of Endometriosis

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