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A Syngeneic Murine Model of Endometriosis using Naturally Cycling Mice
Published on: November 24, 2020
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Enriched Environment Decelerates the Development of Endometriosis in Mouse
Bo Yin1, Hongyuan Jiang1, Xishi Liu2,3
1Shanghai OB/GYN Hospital, Fudan University, Shanghai, 200011, China.
Reproductive Sciences (Thousand Oaks, Calif.)
|April 23, 2020
Summary
An enriched environment (EE) significantly reduces endometriosis lesion weight and fibrogenesis in mice. This effect is linked to decreased adrenergic signaling and vascular endothelial growth factor, alongside enhanced autophagy and lower leptin levels.
Area of Science:
- Reproductive biology
- Neuroendocrinology
- Cellular biology
Background:
- Endometriosis is a chronic, painful condition affecting women of reproductive age.
- Current treatments for endometriosis have limitations and side effects.
- The role of environmental factors and neuroendocrine signaling in endometriosis progression is not fully understood.
Purpose of the Study:
- To investigate the impact of an enriched environment (EE) on endometriosis development in a mouse model.
- To explore the underlying mechanisms, including adrenergic signaling, autophagy, and leptin levels.
Main Methods:
- Balb/C mice were housed in standard (SE) or enriched environments (EE) before and after endometriosis induction.
- Lesion weight, pain sensitivity (hotplate latency), and immunohistochemistry for ADRB2, DRD2, VEGF, and LC3 were assessed.
- Plasma leptin levels were measured.
Main Results:
- EE significantly reduced endometriosis lesion weight by 40.8% compared to SE.
- EE decreased ADRB2 and VEGF expression and fibrogenesis in lesions.
- EE increased LC3 (autophagy marker) and DRD2 expression.
- EE led to reduced plasma leptin levels.
Conclusions:
- An enriched environment decelerates endometriosis development and fibrogenesis in mice.
- EE may exert its effects by modulating adrenergic signaling, vascular endothelial growth factor, autophagy, dopamine receptor D2, and leptin levels.
- EE also improved generalized hyperalgesia associated with endometriosis.
