RESUMO
BACKGROUND: Endometriosis is a debilitating disease that affects women of reproductive age and may lead to impaired fertility. Cell attachment, invasion of the underlying tissue, and vascular ingrowth are important processes in endometrial lesion development. However, the degree of cellular exchange between host peritoneum and endometrial tissue is unclear. METHODS: An experimental endometriosis model was employed whereby uterine horn fragments from wild-type mice were implanted into genetically identical eGFP (enhanced green fluorescent protein) host mice and vice versa. Hormone sensitivity of the ectopic lesions was assessed and cellular exchange determined histologically. RESULTS: White cyst-like lesions developed from implanted fibrin-rich fragments by day 7. Lesions consisted of a well-developed stroma with glandular and luminal epithelium. Both ovariectomy and treatment with a GnRH agonist, leuprorelin, resulted in the suppression of ectopic lesion growth, whereas estradiol treatment increased the size of the ectopic lesion (4 mice per group on day 14). Ingrowth and outgrowth of blood vessels was apparent as well as the exchange of cells between host peritoneum and lesion. CONCLUSION: These findings support the proposal that there is a close cellular interplay between host peritoneum and ectopic tissue and the suitability of this mouse model to study these interactions.
Assuntos
Modelos Animais de Doenças , Endometriose/fisiopatologia , Animais , Adesão Celular , Endometriose/metabolismo , Endometriose/patologia , Células Epiteliais/patologia , Estradiol/administração & dosagem , Feminino , Proteínas de Fluorescência Verde/genética , Leuprolida/administração & dosagem , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , OvariectomiaRESUMO
BACKGROUND: Peritoneal adhesions are fibrous bands of tissue connecting normally separated organs and frequently involve the fat-laden greater omentum. Remodelling of fibrin-rich exudate under reduced fibrinolytic conditions is thought to initiate adhesion formation following surgery. It is unclear whether adhesions that involve the omentum develop in a similar manner. To improve understanding of omental adhesion formation, adipose tissue distribution, cell proliferation and procollagen type I gene expression were investigated in a murine surgical model and in established omental adhesions from patients undergoing abdominal surgery. METHODS: Experimental murine omental adhesions and human omental adhesions were analysed for signs of tissue remodelling using histology, immunohistochemistry and in situ hybridization. RESULTS: Murine omental tissue showed intense inflammation and reduced adipose tissue 3-7 days after surgery, but increased cellularity and collagen production. Adipose tissue remodelling was reversible with increased adipose tissue and decreased cell proliferation and procollagen type I gene expression, shown by proliferating cell nuclear antigen immunolocalization and in situ hybridization respectively. Human omental adhesions were heterogeneous, with varying amounts of fibrotic and adipose-rich regions, although most displayed proliferating and collagen-producing cells. CONCLUSION: Omental adhesions are not static scar tissue as traditionally thought, but undergo active adipose tissue remodelling over-time.