Identification of transferrin receptor in cervical and endometrial tissues

Mizuuchi, Hidemitsu; Kudo, Ryuichi; Tamura, H.; Tsukahara, Kunihiko; Tsumura, Noritoshi; Kumai, Kentoku; Sato, Kenichiro

doi:10.1016/s0090-8258(88)80007-6

Cited by 10 publications

(2 citation statements)

References 8 publications

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“…Transferrin may then be assimilated by ectopic endometrial cells. Indeed, endometrial cells express transferrin receptor (50), and in vitro studies have shown that endometrial stromal and epithelial cells are able to incorporate transferrin and metabolize it into ferritin (51).…”

Section: Iron Metabolism In the Pelvic Cavitymentioning

confidence: 99%

Peritoneal endometriosis is an inflammatory disease

Donnez¹

2012

Front Biosci

103

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Introduction 2.1. Peritoneal fluid and environment in peritoneal endometriosis 2.2. Oxidative stress and peritoneal endometriosis 3. Involvement of iron in the pathogenesis of peritoneal endometriosis 3.1. Iron overload in the peritoneal cavity of endometriosis patients 3.2. Origin of iron in the pelvic cavity 3.3. Iron metabolism in the pelvic cavity 3.4. Effect of iron overload on endometriosis development 3.5. Iron chelators as endometriosis treatment 4. Involvement of nuclear factor-kappa B in the pathogenesis of peritoneal endometriosis 4.1. The nuclear factor-kappa B signaling system 4.2. Nuclear factor-kappa B activation and endometriosis 4.3. Effect of nuclear factor-kappa B activation on endometriosis development 4.4. Nuclear factor-kappa B inhibitors as endometriosis treatment 5. Involvement of prostaglandins in the pathogenesis of peritoneal endometriosis 5.1. Eicosanoid biosynthesis 5.2. Prostaglandin receptors 5.3. Prostaglandin biosynthesis in endometriosis 5.4. Effect of prostaglandins on endometriosis development 5.5. Targeting prostaglandin biosynthesis as endometriosis treatment 6. Summary and perspectives 7. Acknowledgments 8. References

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Section: Iron Metabolism In the Pelvic Cavitymentioning

confidence: 99%

Peritoneal endometriosis is an inflammatory disease

Donnez¹

2012

Front Biosci

103

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“…Cellular metabolism of hemoglobin and heme releases iron, which is then incorporated into ferritin in macrophages or returned to the iron transporter transferrin in peritoneal fluid. Transferrin may subsequently be incorporated by ectopic endometrial cells (24) and metabolized into ferritin (19), a soluble and nontoxic form (25). However, iron conglomerates have also been observed in peritoneal macrophages and endometriotic lesions in case of endometriosis (11).…”

Section: Peritoneal Iron Metabolismmentioning

confidence: 99%

Involvement of Iron, Nuclear Factor-Kappa B (NF-κB) and Prostaglandins in the Pathogenesis of Peritoneal Endometriosis-Associated Inflammation: A Review

Lousse

Defrère

Ramos

et al. 2009

Journal of Endometriosis

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Peritoneal endometriosis is a chronic pelvic inflammatory disease, characterized by increased numbers of peritoneal macrophages and their secreted products such as cytokines, growth and angiogenic factors in peritoneal fluid. Inflammation plays a major role in pain and infertility associated with endometriosis, but is also extensively involved in the molecular and cellular processes that lead to peritoneal endometriotic lesion development. Several inflammatory mediators have therefore been studied in the context of endometriosis over the last few years. The aim of this review is to focus on three that have been clearly implicated in the pathogenesis of endometriosis and may be linked: peritoneal iron metabolism, nuclear factor-kappa B (NF-κB) activation, and prostaglandin biosynthesis. Peritoneal iron overload has been conclusively demonstrated in endometriosis patients and may induce oxidative stress in the peritoneal cavity. Oxidative stress and proinflammatory cytokines are well known to be potent activators of the NF-κB pathway, which has recently been implicated in peritoneal endometriosis. Induced NF-κB activation leads to expression of numerous proinflammatory genes such as cytokines, which may provide positive feedback to the pathway, self-perpetuating the inflammatory response. Other important NF-κB-regulated molecules are prostaglandin biosynthesis enzymes, and cyclooxygenase-2 (COX-2) in particular. Increased concentrations of prostaglandins have been evidenced in the peritoneal fluid of endometriosis patients and COX-2 inhibitors have proved to be effective in ‘in vitro’ and ‘in vivo’ experimental models. In the light of available data collected from patient biopsies, as well as ‘in vitro’ and ‘in vivo’ studies, the respective implication and potential molecular association of iron, NF-κB and prostaglandins in the pathogenesis of endometriosis are discussed. The key role of peritoneal macrophages is emphasized and potential therapeutic targets are examined.

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