Retinoic acid action is altered within endometrium of baboons affected with endometriosis
Lab / animal
OA: closed
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⤵ 3 in-corpus citations
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Endometriosis induction in baboons decreased STRA6 and CRABP2 expression over time while FABP5 remained stable, confirming altered retinoic acid action contributes to disease progression.
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Abstract
Objective: Using a baboon model, we determined the changing expression of Retinoic Acid (RA) target genes during the menstrual cycle and during disease progression. This change could explain the cellular response and changes characteristic of endometriosis. In previous studies, we established that endometriosis affects the CRABP2:FABP5 ratio in an in vitro environment, shifting toward apoptosis and differentiation with higher CRABP2, and anti-apoptosis with higher levels of FABP5. Intervention(s): Endometriosis was induced in female baboons with intraperitoneal inoculation of menstrual endometrium ( n = 2–4). Tissue was harvested via endometrectomy during different stages of the menstrual cycle as well at 3, 6, and 12 month timepoints after inoculation with endometriosis. Main outcome measure(s): Real time PCR was used to quantify STRA6 (a gene responsible for retinol uptake), CRABP2 (a gene necessary for apoptotic and anti-apoptotic estrogenic RA effects), and FABP5 (a gene that mediates the anti-apoptotic actions of RA). Results: STRA6 and CRABP2 expression were highest in the proliferative phase and lowest in the late secretory phase. FABP5 expression remained stable throughout the 12 months following the induction of the disease, whereas STRA6 and CRABP2 continued to decrease during the same period. Conclusions: Our study confirms that a shift in the CRABP2:FABP5 ratio has similar in vivo effects as it does in vitro: changing RA expression with disease induction and progression. As CRABP2 may be important in determining cell fate in the endometrium, gene expression changes could contribute to the anti-apoptotic behavior of affected cells. As expression changes more during progression, earlier rather than later treatment becomes more critical in reducing the rate of disease progression.
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References (27)
- Altered retinoid signaling compromises decidualization in human endometriotic stromal cells via openalex
- Altered retinoid uptake and action contributes to cell survival in endometriosis via openalex
- A modified baboon model for endometriosis via openalex
- Changes in eutopic endometrial gene expression during the progression of experimental endometriosis in the baboon, Papio anubis via openalex
- Clinical practice. Endometriosis via openalex
- Decreased Notch pathway signaling in the endometrium of women with endometriosis impairs decidualization via openalex
- Effect of endometriosis on in vitro fertilization via openalex
- Endometriosis expresses a molecular pattern consistent with decreased retinoid uptake, metabolism and action via openalex
- Endometriosis is associated with progesterone resistance in the baboon (Papio anubis) oviduct: evidence based on the localization of oviductal glycoprotein 1 (OVGP1) via openalex
- Endometriosis-related pelvic pain following laparoscopic surgical treatment via openalex
- Epidemiology of endometriosis: an assessment of risk factors via openalex
- Estrogen receptor-beta, estrogen receptor-alpha, and progesterone resistance in endometriosis via openalex
- Gene expression analysis of endometrium reveals progesterone resistance and candidate susceptibility genes in women with endometriosis via openalex
- Heritability of endometriosis via openalex
- Prostaglandin E2 via steroidogenic factor-1 coordinately regulates transcription of steroidogenic genes necessary for estrogen synthesis in endometriosis via openalex
- Retinoic acid suppresses growth of lesions, inhibits peritoneal cytokine secretion, and promotes macrophage differentiation in an immunocompetent mouse model of endometriosis via openalex
- Role of estrogen receptor-β in endometriosis via openalex
- Steroid receptor and aromatase expression in baboon endometriotic lesions via openalex
- W2107037828 via openalex
- W2102841529 via openalex
- W2079488315 via openalex
- W2137799669 via openalex
- W1495595158 via openalex
- W2043214272 via openalex
- W2157560598 via openalex
- W2010311608 via openalex
- W1999132350 via openalex
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