Macrophages are targets of retinoic acid signaling during the wound-healing process after thulium laser resection of the prostate
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Dian-Jun Yu1,4,*, Xing-Jie Wang2,*, Yun-Feng Shi1,5,*, Chen-Yi Jiang2, Rui-Zhe Zhao2, Yi-Ping Zhu2, Li Chen4, Yuan-Qing Yang4, Xiao-Wen Sun1,2,3 and Shu-Jie Xia1,2,3
1Department of Urology, Shanghai General Hospital of Nanjing Medical University, Shanghai 200080, China
2Department of Urology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China
3Institute of Urology, Shanghai Jiao Tong University, Shanghai 200080, China
4Department of Urology, Ningbo Medical Center Lihuili Eastern Hospital, Ningbo 315048, China
5Department of Urology, Wujin Hospital Affiliated Jiang Su University, Changzhou 213302, China
*These authors contributed equally to this work
Shu-Jie Xia, email: firstname.lastname@example.org
Xiao-Wen Sun, email: email@example.com
Yuan-Qing Yang, email: firstname.lastname@example.org
Keywords: benign prostatic hyperplasia, wound healing, retinoic acid, RARβ, macrophage
Received: March 13, 2017 Accepted: May 10, 2017 Published: May 26, 2017
BACKGROUND: The wound-healing process is very important for reducing complications after thulium laser resection of the prostate (TmLRP). The retinoic acid (RA) signaling pathway has been well studied in the wound-healing process of the skin and other organs. The goals of this study were to identify the role of RA signaling in the repair of the prostate after TmLRP and to investigate the molecular mechanism of this process.
RESULTS: Retinoic acid receptors (RARs) were present in the prostate, and their expression was increased after TmLRP. RARβ was expressed in the macrophages and may be related to the role of stromal cells in the wound-healing process. In vitro, RA enhanced the function of anti-inflammatory macrophages and promoted stromal cell activation and angiogenesis. Arg1 was also increased via RARβ after treatment with RA.
MATERIALS AND METHODS: The expression of RARs was analyzed in vivo by immunohistochemistry (IHC), real time qPCR, and western blot analysis. THP-1 cells were co-treated with or without RA and stimulating factor and then assessed by ELISA and qPCR. The supernatants from these cells were cultured with stromal cells and vascular endothelial cells, and the effects on these cells were analyzed.
CONCLUSIONS: We found that RA signaling was involved in the wound-healing process of the prostate after TmLRP. RA treated macrophages activated stromal cells and promoted angiogenesis. RARβ was the key isoform in this process.
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