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This lecture was delivered by Prof. Akhilesh Kulkarni at Sree Chitra Thirunal Institute of Medical Sciences and Technology. This is part of Cancer Cytogenetic course. It includes: Mesothelium, Amniotic, Fragments, Endomaterial, Adhsion, Molecules, Metalloproteinases, Collagen, Matrix, Elastin
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Potent stimulator of MMP-3 in proliferative phase endometrium Progesterone exposure in vivo reduces the IL-
α^ stimulation of MMP-3 in
secretory phase tissueIL-1α^ stimulation of MMP-3 is restored in a dose-dependent manner with progesterone withdrawalCultured endometriotic cells obtained from a rat endo model express higher levels of MMP-3 mRNA than eutopic rat endometrial stromal cellswhen treated with progesteroneElevated and persistent MMP-3 expression by endometriotic stromal cells cultured in the presence of progesterone correlates with elevated levels of IL-1α^ mRNA detected in the endometriotic stromal cellsProduction of IL-
α^ by the endometriotic lesions - overcomes the progesterone-induced suppression of MMP-3 IL-1α^ - related mechanism promotes MMP-3 production by endometrioticcells even in the presence of progesterone
DyspareuniaChronic pelvic pain
Endometriomas and extra-ovarian endometriotic^ implants express high levels of aromatase
Cultured stromal cells derived from endometriotic implants andincubated with a CAMP analog display extraordinarily high levels ofaromatase Growth factors, cytokines - possible inducers of aromataseProstaglandin E
was identified as the most potent inducer 2 Estrogen - up-regulates prostaglandin E
formation 2
Stimulates cyclo-oxygenase type 2 enzyme in endometrial stromal cells Positive feedback loop for continuous local estrogen andprostaglandin E
production 2 Possible genetic defect in aromatase expression in endo
Androstenedione of adrenal and ovarian origins – premenopausalwomenAdrenal androstenedione in postmenopausal womenEstrone - weakly estrogenic Must be converted to estradiol 17 α-hydroxysteroid dehydrogenase (
α-HSD) type 1 is expressed
in endometriosis In contrast 17
α-HSD type 2 inactivates estradiol by catalyzing its conversion to estrone in eutopic endometrial glandular cells duringthe luteal phase Progesterone induces the activity of 17
α-HSD
Inactivation of estradiol to estrone one of the anti-estrogenicproperties of progesterone 17 α-HSD type 2 is absent from endometriotic glandular cells