PTGS1 Regulates Macrophage Polarization Through PPARγ Nuclear Translocation to Affect Oxidative Stress Injury in Chronic Prostatitis.
4 affiliations
- 1Department of Urology, The First Affiliated Hospital of Anhui Medical University, Hefei, China.
- 2Department of Urology, The First Affiliated Hospital of Anhui Medical University, Institute of Urology, and Anhui Province Key Laboratory of Urological and Andrological Diseases Research and Medical Transformation, Hefei, China.
- 3Department of Urology, Anhui Provincial Children's Hospital/Children's Hospital of Fudan University (Affiliated Anhui Branch), Hefei, China.
- 4Department of Urology, East City Campus of First Affiliated Hospital of Anhui Medical University, Hefei, China.
Abstract
Chronic Prostatitis/Chronic Pelvic Pain Syndrome (CP/CPPS) is a condition marked by persistent inflammation of the prostate, whose underlying mechanisms remain poorly defined. This study aimed to investigate the role of prostaglandin-endoperoxide synthase 1 (PTGS1) in macrophages and in a mouse model of experimental autoimmune prostatitis (EAP). Using multiple experimental methods, we found that PTGS1 was induced during IL-4-mediated M2 macrophage polarization, whereas PTGS1 silencing further enhanced M2 polarization. Mechanistically, PTGS1 functioned as a feedback regulatory checkpoint by interacting with PPARγ in the cytoplasm and restraining its nuclear translocation; PTGS1 silencing released this constraint, enhanced PPARγ nuclear accumulation, and promoted M2 macrophage polarization. In EAP mice, PTGS1 knockdown alleviated disease progression and reduced oxidative stress injury, accompanied by increased M2 macrophage polarization and reduced iNOS-positive pro-inflammatory macrophage accumulation. Furthermore, PTGS1 silencing diminished the PTGS1-PPARγ interaction, thereby enhancing PPARγ nuclear translocation and strengthening the M2 polarization program. In summary, our findings show that PTGS1 knockdown attenuates F4/80⁺/iNOS⁺ pro-inflammatory macrophage accumulation, mitigates prostatic inflammation and oxidative stress, and offers a potential immunomodulatory strategy for CP/CPPS.
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BibTeX
@article{song2026ptgs1,
title = {{PTGS1 Regulates Macrophage Polarization Through PPARγ Nuclear Translocation to Affect Oxidative Stress Injury in Chronic Prostatitis.}},
author = {Jian Song and Weiyi Li and Shanchuan Han and Weijie Song and Chaozhao Liang and Yi Liu and Kaiping Zhang and Xianguo Chen},
journal = {Journal of cellular and molecular medicine},
year = {2026},
month = oct,
doi = {10.1111/jcmm.71397},
url = {https://europepmc.org/article/MED/42961190},
note = {CC BY},
}
RIS
TY - JOUR
TI - PTGS1 Regulates Macrophage Polarization Through PPARγ Nuclear Translocation to Affect Oxidative Stress Injury in Chronic Prostatitis.
AU - Jian Song
AU - Weiyi Li
AU - Shanchuan Han
AU - Weijie Song
AU - Chaozhao Liang
AU - Yi Liu
AU - Kaiping Zhang
AU - Xianguo Chen
PY - 2026
DA - 2026/10/30
JO - Journal of cellular and molecular medicine
DO - 10.1111/jcmm.71397
UR - https://europepmc.org/article/MED/42961190
AB - Chronic Prostatitis/Chronic Pelvic Pain Syndrome (CP/CPPS) is a condition marked by persistent inflammation of the prostate, whose underlying mechanisms remain poorly defined. This study aimed to investigate the role of prostaglandin-endoperoxide synthase 1 (PTGS1) in macrophages and in a mouse model of experimental autoimmune prostatitis (EAP). Using multiple experimental methods, we found that PTGS1 was induced during IL-4-mediated M2 macrophage polarization, whereas PTGS1 silencing further enhanced M2 polarization. Mechanistically, PTGS1 functioned as a feedback regulatory checkpoint by interacting with PPARγ in the cytoplasm and restraining its nuclear translocation; PTGS1 silencing released this constraint, enhanced PPARγ nuclear accumulation, and promoted M2 macrophage polarization. In EAP mice, PTGS1 knockdown alleviated disease progression and reduced oxidative stress injury, accompanied by increased M2 macrophage polarization and reduced iNOS-positive pro-inflammatory macrophage accumulation. Furthermore, PTGS1 silencing diminished the PTGS1-PPARγ interaction, thereby enhancing PPARγ nuclear translocation and strengthening the M2 polarization program. In summary, our findings show that PTGS1 knockdown attenuates F4/80⁺/iNOS⁺ pro-inflammatory macrophage accumulation, mitigates prostatic inflammation and oxidative stress, and offers a potential immunomodulatory strategy for CP/CPPS.
SN - 1582-1838
SN - 1582-4934
ER -