التفاصيل البيبلوغرافية
| العنوان: |
Broad and diverse roles of sphingosine-1-phosphate/sphingosine-1-phosphate receptors in the prostate |
| المؤلفون: |
Daoquan Liu, Jianmin Liu, Yan Li, Lu Du, Qingqiong Cao, Liang Yang, Yongying Zhou, Ping Chen, Yuming Guo, Guang Zeng, Michael E. DiSanto, Weidong Hu, Xinhua Zhang |
| المصدر: |
iScience, Vol 27, Iss 12, Pp 111290- (2024) |
| بيانات النشر: |
Elsevier, 2024. |
| سنة النشر: |
2024 |
| المجموعة: |
LCC:Science |
| مصطلحات موضوعية: |
natural sciences, biological sciences, biochemistry, physiology, pathophysiology, Science |
| الوصف: |
Summary: Benign prostatic hyperplasia (BPH) is a common condition in aging males, but its underlying pathogenesis remains unclear. Sphingosine-1-phosphate (S1P) and its receptors (S1PRs) play important roles in various diseases, while less studied in prostate. Current study attempts to clarify the expression and functional activities of S1P/S1PRs in the prostate. We discovered that S1P/S1PRs were richly expressed in the prostate, with S1PR1/2/3 localized in the epithelial/stromal compartments, while S1PR4/5 were less expressed. In vitro, S1P/S1PR1/S1PR3 promoted cell proliferation via AKT and ERK1/2 pathways, S1P/S1PR2/S1PR3 enhanced contraction of WPMY-1 cells and human prostate via RhoA/ROCK pathway, while S1P/S1PR1/S1PR2/S1PR3 alleviated the inflammation response via STAT3 pathway. In vivo, S1P and S1PR1/3 agonists (SEW2871, CYM5541) led to prostate enlargement in rats, while S1PR1/3 antagonists (W-146, TY-52156) suppressed testosterone-induced BPH. Overall, this study suggests that S1P/S1PRs play a critical role in the development of BPH and may be a promising therapeutic target for BPH treatment. |
| نوع الوثيقة: |
article |
| وصف الملف: |
electronic resource |
| اللغة: |
English |
| تدمد: |
2589-0042 |
| Relation: |
http://www.sciencedirect.com/science/article/pii/S258900422402515X; https://doaj.org/toc/2589-0042 |
| DOI: |
10.1016/j.isci.2024.111290 |
| URL الوصول: |
https://doaj.org/article/bc00a08646ce41a1bbf0cd9413b9e7bc |
| رقم الانضمام: |
edsdoj.bc00a08646ce41a1bbf0cd9413b9e7bc |
| قاعدة البيانات: |
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