Oral contraceptives treatment suppresses proliferation and enhances apoptosis of eutopic endometrial tissue from patients with endometriosis.

Meresman, Gabriela Fabiana; Auge, L.; Barañao, Rosa Inés; Lombardi, Eduardo; Tesone, Marta; Sueldo, Carlos

doi:10.1016/s0015-0282(01)02157-4

Cited by 4 publications

(4 citation statements)

References 27 publications

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“…Several reports have demonstrated that VEGF not only induces angiogenesis, but also works as a survival factor for tumour and endothelial cells, protecting them from apoptosis (Liu et al, 2000;Harmey and Bouchier-Hayes, 2002). We recently reported on the increased survival capability of the eutopic endometrium from patients with endometriosis, possibly regulated by an elevated expression of Bcl-2, as well as on the impact of short-term oral contraceptives in reversing this effect (Meresman et al, 2000(Meresman et al, , 2002.…”

Section: Introductionmentioning

confidence: 89%

Effect of GnRH analogues on apoptosis and release of interleukin-1 and vascular endothelial growth factor in endometrial cell cultures from patients with endometriosis

Meresman

Bilotas²,

Lombardi³

et al. 2003

Human Reproduction

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Section: Introductionmentioning

confidence: 89%

Effect of GnRH analogues on apoptosis and release of interleukin-1 and vascular endothelial growth factor in endometrial cell cultures from patients with endometriosis

Meresman

Bilotas²,

Lombardi³

et al. 2003

Human Reproduction

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“…149,150 Combination oral contraceptives significantly diminish cell proliferation and induce apoptosis of eutopic endometrial tissue from patients with endometriosis. 151 These agents induce Bax expression in the eutopic endometrium from women with endometriosis, whereas they reduce Bcl-2 expression in these tissues. 151 Cell proliferation was significantly reduced in the epithelium and stroma of both the eutopic and the ectopic endometrium after treatment with the levonorgestrel-releasing intrauterine system.…”

Section: Apoptosis-inducing Properties Of Current Medical Treatment For Endometriosismentioning

confidence: 99%

“…151 These agents induce Bax expression in the eutopic endometrium from women with endometriosis, whereas they reduce Bcl-2 expression in these tissues. 151 Cell proliferation was significantly reduced in the epithelium and stroma of both the eutopic and the ectopic endometrium after treatment with the levonorgestrel-releasing intrauterine system. 148 The use of levonorgestrel-releasing intrauterine system induces Fas expression in the epithelial cells of the ectopic and eutopic endometrium.…”

Section: Apoptosis-inducing Properties Of Current Medical Treatment For Endometriosismentioning

confidence: 99%

Aberrant Expression of Apoptosis-Related Molecules in Endometriosis: A Possible Mechanism Underlying the Pathogenesis of Endometriosis

et al. 2011

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Endometriosis, a disease affecting 3% to 10% of women of reproductive age, is characterized by the ectopic growth of endometrial tissue under the influence of estrogen. It is also becoming recognized as a condition in which ectopic endometrial cells exhibit abnormal proliferative and apoptotic regulation in response to appropriate stimuli. Apoptosis plays a critical role in maintaining tissue homeostasis and represents a normal function to eliminate excess or dysfunctional cells. Accumulated evidence suggests that, in healthy women, endometrial cells expelled during menstruation do not survive in ectopic locations because of programmed cell death, while decreased apoptosis may lead to the ectopic survival and implantation of these cells, resulting in the development of endometriosis. Both the inability of endometrial cells to transmit a "death" signal and the ability of endometrial cells to avoid cell death have been associated with increased expression of antiapoptotic factors and decreased expression of preapoptotic factors. Further investigations may elucidate the role of apoptosis-associated molecules in the pathogenesis of endometriosis. Medical treatment with apoptosis-inducing agents may be novel and promising therapeutic strategy for endometriosis.

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“…One investigation suggested that oral contraceptives suppress proliferation and enhance programmed cell death (apoptosis) in endometrial tissue, perhaps providing a mechanistic clue to the action of these drugs. 21…”

Section: Oral Contraceptives (Combination Estrogen-progestogen)mentioning

confidence: 99%

Medical Therapy of Endometriosis

Olive

2003

Semin Reprod Med

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The medical treatment of endometriosis is a critical aspect of the therapeutic approach to this disease. Past methods have been based upon systemic hormonal alterations, resulting in suppression of this estrogen-responsive disorder. Treatments such as danazol, progestogens, oral contraceptives, GnRH-agonists, and gestrinone achieve their effects upon endometriosis via this method. However, with a growing understanding of the pathogenesis of this disease, more precise molecular targets for treatment have been identified. Thus, a series of newer agents are under development and hold the potential of greater efficacy and flexibility than traditional treatments. This review analyzes the available and experimental medical treatments of endometriosis, their utility in the treatment of pain and infertility, and their role in the future.

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Oral contraceptives treatment suppresses proliferation and enhances apoptosis of eutopic endometrial tissue from patients with endometriosis.

Cited by 4 publications

References 27 publications

Effect of GnRH analogues on apoptosis and release of interleukin-1 and vascular endothelial growth factor in endometrial cell cultures from patients with endometriosis

Effect of GnRH analogues on apoptosis and release of interleukin-1 and vascular endothelial growth factor in endometrial cell cultures from patients with endometriosis

Aberrant Expression of Apoptosis-Related Molecules in Endometriosis: A Possible Mechanism Underlying the Pathogenesis of Endometriosis

Medical Therapy of Endometriosis

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