We investigated whether tryptase released from mast cells activated by prostate stromal cells (PSC) reacted with Trichomonas vaginalis (Tv) promoted the proliferation of PSC through protease- activated receptor 2 (PAR2). Conditioned medium of PSC was prepared by stimulating them with Tv (Trichomonad-conditioned medium (TCM)), and mast cell-conditioned medium were prepared by incubating them with TCM (mast cell-TCM (M-TCM)). Mast cells incubated with TCM migrated more efficiently and produced more β-hexosaminidase and tryptase. M-TCM containing tryptase increased the proliferation of PSC, while inhibition of tryptase decreased proliferation. Expression of signalling molecules such as PAR2, p-ERK, COX-2, 15d-PGJ₂ and PPARγ, known to be involved in the tryptase-PAR2 pathway, increased in response to M-TCM, and blocking any of these signals decreased proliferation, indicating that tryptase-PAR2 signalling is involved in the proliferation of PSC. Inhibition of tryptase and PAR2 led to reduced expression of PAR2, p-ERK, COX-2, 15d-PGJ₂ and PPARγ, while inhibition of ERK or COX-2 reduced the expression of COX-2, 15d-PGJ₂ and PPARγ indicating that the tryptase-PAR2 pathway proceeds in the order p-ERK, COX-2, 15d-PGJ₂, and PPARγ. These results show that interaction between PSC stimulated with Tv and mast cells causes proliferation of PSC through the tryptase-PAR2 pathway.

中文翻译：

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前列腺基质细胞增殖中的肥大细胞类胰蛋白酶-PAR2通路与阴道毛滴虫反应

我们研究了从与阴道毛滴虫(Tv)反应的前列腺基质细胞 (PSC) 激活的肥大细胞释放的类胰蛋白酶是否通过蛋白酶激活受体 2 (PAR2) 促进 PSC 的增殖。PSC的条件培养基是通过用Tv刺激制备的（毛滴虫条件培养基（TCM）），肥大细胞条件培养基是通过用TCM（肥大细胞-TCM（M-TCM））培养制备的。与 TCM 一起培养的肥大细胞迁移效率更高，并产生更多的 β-氨基己糖苷酶和类胰蛋白酶。含有类胰蛋白酶的 M-TCM 增加了 PSC 的增殖，而抑制类胰蛋白酶则降低了增殖。PAR2、p-ERK、COX-2、15d-PGJ _{2等信号分子的表达}和已知参与类胰蛋白酶-PAR2途径的PPARγ响应M-TCM而增加，并且阻断任何这些信号会降低增殖，表明类胰蛋白酶-PAR2信号传导参与了PSC的增殖。类胰蛋白酶和 PAR2 的抑制导致 PAR2、p-ERK、COX-2、15d-PGJ ₂和 PPARγ 的表达降低，而 ERK 或 COX-2 的抑制降低了 COX-2、15d-PGJ ₂和 PPARγ 的表达，表明类胰蛋白酶-PAR2 途径以 p-ERK、COX-2、15d-PGJ ₂和 PPARγ 的顺序进行。这些结果表明，用 Tv 刺激的 PSC 和肥大细胞之间的相互作用导致 PSC 通过类胰蛋白酶-PAR2 途径增殖。