American Journal of Obstetrics and Gynecology

1984

DOI: 10.1016/0002-9378(84)90240-0

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Transplantation of normal and ectopic human endometrial tissue into athymic nude mice

Nezaam M. Zamah

¹

,

Melvin G. Dodson

²

,

L. Clifton Stephens

³

et al.

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модели эндометриоза на грызунах2

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2002

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Cited by 89 publications

(53 citation statements)

References 9 publications

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“…35,41,42,64 Others have transplanted human endometrial xenografts in mice without attaching it to the abdominal wall. 36,65 Although this model mimics the adhesion of the lesions, we believe it is associated with other problems. For example, lesions may be missed because they often get stuck in the postsurgical adhesions that form.…”

Section: Discussionmentioning

confidence: 99%

A Novel Noninvasive Model of Endometriosis for Monitoring the Efficacy of Antiangiogenic Therapy

¹

,

²

,

Satchi‐Fainaro

³

et al. 2006

The American Journal of Pathology

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Endometriosis, the presence of ectopic endometrial tissue, is a common disease associated with high morbidity and socioeconomic problems. Angiogenesis, the formation of new blood vessels, plays an important role in the formation and growth of endometriotic lesions. We have created a novel, noninvasive model to monitor the growth of these lesions and the associated angiogenesis in vivo. First, we generated luciferase-expressing transgenic mice by inserting the human ubiquitin C promoter coupled to the firefly luciferase reporter. Injection of luciferin in these mice causes full-body bioluminescence, which can be detected using a lowlight CCD camera. Endometrial tissue from these transgenic mice was surgically implanted into nonluminescent recipients. Bioluminescence of lesions was noninvasively imaged after intravenous or intraperitoneal injection of luciferin. Transabdominal luminescence compared well with the location of the transgenic endometriotic lesions, and lesion size correlated with the intensity of luminescence. Systemic treatment with the angiogenesis inhibitors caplostatin and endostatin peptide mP-1 delayed and suppressed the onset and intensity of the luminescent signal. Caplostatin suppressed the growth of endometriotic lesions by 59% compared with controls. This novel, noninvasive model of endometriosis provides a means to study early angiogenesis in vivo and to monitor endometriotic growth and the efficacy of systemic antiangiogenic therapy.

“…35,41,42,64 Others have transplanted human endometrial xenografts in mice without attaching it to the abdominal wall. 36,65 Although this model mimics the adhesion of the lesions, we believe it is associated with other problems. For example, lesions may be missed because they often get stuck in the postsurgical adhesions that form.…”

Section: Discussionmentioning

confidence: 99%

A Novel Noninvasive Model of Endometriosis for Monitoring the Efficacy of Antiangiogenic Therapy

¹

,

²

,

Satchi‐Fainaro

³

et al. 2006

The American Journal of Pathology

View full text Add to dashboard Cite

Endometriosis, the presence of ectopic endometrial tissue, is a common disease associated with high morbidity and socioeconomic problems. Angiogenesis, the formation of new blood vessels, plays an important role in the formation and growth of endometriotic lesions. We have created a novel, noninvasive model to monitor the growth of these lesions and the associated angiogenesis in vivo. First, we generated luciferase-expressing transgenic mice by inserting the human ubiquitin C promoter coupled to the firefly luciferase reporter. Injection of luciferin in these mice causes full-body bioluminescence, which can be detected using a lowlight CCD camera. Endometrial tissue from these transgenic mice was surgically implanted into nonluminescent recipients. Bioluminescence of lesions was noninvasively imaged after intravenous or intraperitoneal injection of luciferin. Transabdominal luminescence compared well with the location of the transgenic endometriotic lesions, and lesion size correlated with the intensity of luminescence. Systemic treatment with the angiogenesis inhibitors caplostatin and endostatin peptide mP-1 delayed and suppressed the onset and intensity of the luminescent signal. Caplostatin suppressed the growth of endometriotic lesions by 59% compared with controls. This novel, noninvasive model of endometriosis provides a means to study early angiogenesis in vivo and to monitor endometriotic growth and the efficacy of systemic antiangiogenic therapy.

“…However, endometriosis occurs spontaneously only in primates, which are too costly for experimental use 22 . Consequently, experimental models have been surgically produced in small animals such as rabbits, rats and mice [23][24][25][26][27][28] …”

Section: Introduction Introduction Introduction Introduction Introducmentioning

confidence: 99%

Desenvolvimento de modelo experimental de endometriose em ratas

¹

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²

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³

et al. 2009

Rev. Col. Bras. Cir.

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OBJETIVO: Desenvolver um modelo de endometriose experimental em ratas. MÉTODOS: Foram utilizadas 30 ratas adultas da linhagem Wistar. A técnica cirúrgica consistiu em laparotomia mediana com identificação do útero bicorno e ressecção de um segmento de 2 cm do corno uterino direito. Um retalho de 0,25 cm² foi retirado dessa estrutura e suturado na parede abdominal com a face endometrial voltada para a cavidade peritoneal. As ratas foram divididas aleatoriamente em dois grupos de acordo com o tempo para a reoperação: grupo 1 (n=15), reoperado em 30 dias, e grupo 2 (n=15), em 60 dias. No momento da segunda laparotomia os implantes foram avaliados macroscopicamente, ressecados e encaminhados para análise microscópica com coloração hematoxilina-eosina e imunohistoquímica (HEMA, AE1 e AE2). RESULTADOS: Os implantes se desenvolveram em 83,3 % do Grupo 1 e 71,4% no Grupo 2. Não houve diferença estatisticamente significativa entre o peso dos animals dos dois grupos. Também não houve diferença estatisticamente significativa no tamanho da área das lesões induzidas: no Grupo 1 a média foi 0,37 cm² e no Grupo 2, de 0,25 cm². Segundo a classificação histológica semi-quantitativa de Keenan (de acordo com a preservação da camada epitelial de endométrio), o Grupo 1 teve média de 1,9 e o Grupo 2, de 2,4. CONCLUSÃO: A técnica utilizada para o desenvolvimento de endometriose em ratas foi satisfatória.

“…Although various models have been developed in mice to study endometrial adhesion to the peritoneal lining, most investigators used fresh endometrial fragments (6,(8)(9)(10) or organ cultures (11,12). Until now, the use of dispersed cells was not successful (13,14) and hormonal environment was never taken into account.…”

mentioning

confidence: 99%

Role of endocrine status and cell type in adhesion of human endometrial cells to the peritoneum in nude mice

¹

,

²

,

³

et al. 2002

Fertility and Sterility

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Objective: To investigate the role of different cellular types (epithelial and stromal endometrial cells and peritoneal cells) in the ectopic implantation of endometrium and to evaluate the importance of endocrine environment on the adhesion of endometrial cells to the peritoneum.Design: Experimental prospective study.Setting: University hospital, department of cell biology. Animal(s):One hundred one nude mice. Intervention(s):Monolayer culture of human epithelial and stromal endometrial cells obtained from patients undergoing hysterectomy or laparoscopy for benign disease. Intraperitoneal injection of cells into nude mice.Main Outcome Measure(s): Two weeks after cell injection, adhesion of endometrial cells was evaluated by histological and immunohistochemical examination. Result(s):Mixed cultures of stromal and epithelial cells, but not purified epithelial or stromal cells alone, adhered to the mouse peritoneum and led to endometriotic-like nodules. Pretreatment of cells with estrogen alone or with estrogen and progestin resulted in a higher percentage of animals developing endometriotic-like nodules, whereas treatment with progestin alone did not affect endometriotic implantation. Conclusion(s):Our data indicate that the success of endometrial cell implantation is dependent on the cooperativeness between stromal and epithelial endometrial cells, as well as on the endocrine environment of endometrial cells, but not that of recipient animals. The results emphasize the role of both endometrial cell types for ectopic implantation.

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