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Inhibition of MicroRNA-92a Improved Erectile Dysfunction in Streptozotocin-Induced Diabetic Rats via Suppressing
Zhe Tang1,2, Jingyu Song1,2, Zhe Yu1,2
1Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Purpose:
To determine whether microRNA could be a therapy target of erectile dysfunction (ED) and the underlying mechanisms.
Materials And Methods:
Eight-week-old fasting male SD rats were intraperitoneally injected with streptozotocin to construct diabetic rat models. Diabetic ED rats were treated with miRNA-92a inhibitor. The cavernous nerves were electrically stimulated to measure the intracavernous pressure and mean arterial pressure of rats in each group. After the detection, the penile cavernous tissues are properly stored for subsequent experiments. Rat aortic endothelial cells were used in in vitro studies.
Results:
The expression of miR-92a was significantly increased in the corpus cavernosum of Streptozocin (STZ)-induced diabetic rats and injection of miR-92a antagomir into the corpus cavernosum of diabetic rats significantly increased eNOS/NO/cGMP signaling pathway activities, cavernous endothelial cell proliferation, endothelial cell-cell junction protein expression and decreased the levels of oxidative stress. These changes restored erectile function in STZ-induced diabetic rats. Moreover, in vitro study demonstrated that the miR-92a expression increased significantly in endothelial cells treated with high glucose, inhibiting AMPK/eNOS and AMPK/Nrf2/HO-1 signaling pathways in rat aortic endothelial cells via targeting Prkaa2, causing endothelial dysfunction and overactive oxidative stress, miR-92a inhibitor can improve the above parameters.
Conclusions:
miRNA-92a inhibitor could exert an inhibition role on oxidative stress and endothelial dysfunction to improve diabetic ED effectively.
Insights
MicroRNA-92a inhibition effectively treats diabetic erectile dysfunction (ED) by reducing oxidative stress and improving endothelial function. This targeted therapy restores erectile function in diabetic rats, offering a promising new treatment avenue.
Area of Science:
- Endocrinology
- Molecular Biology
- Urology
Background:
- Diabetic erectile dysfunction (ED) is a complex condition with significant impact.
- MicroRNAs (miRNAs) are emerging as key regulators in various physiological and pathological processes.
- Understanding the role of specific miRNAs in diabetic complications is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate microRNA-92a (miR-92a) as a potential therapeutic target for diabetic ED.
- To elucidate the underlying molecular mechanisms by which miR-92a influences erectile function in diabetes.
Main Methods:
- Diabetic rat models were established using streptozotocin injection.
- Diabetic ED rats were treated with a miR-92a inhibitor (antagomir).
- Erectile function was assessed via intracavernous pressure measurements; in vitro studies used rat aortic endothelial cells.
Main Results:
- miR-92a expression was significantly elevated in the corpus cavernosum of diabetic rats.
- miR-92a inhibition restored erectile function by enhancing eNOS/NO/cGMP signaling, promoting endothelial cell proliferation, and reducing oxidative stress.
- In vitro, high glucose increased miR-92a, inhibiting AMPK/eNOS and AMPK/Nrf2/HO-1 pathways, leading to endothelial dysfunction and oxidative stress; miR-92a inhibition reversed these effects.
Conclusions:
- miRNA-92a inhibitor demonstrates significant potential in treating diabetic ED.
- Targeting miR-92a effectively mitigates oxidative stress and endothelial dysfunction associated with diabetic ED.
