Mast cell tryptase-PAR2 pathway in proliferation of prostatic stromal cells reacted with Trichomonas vaginalis

초록

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 beta-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-PGJ(2) and PPAR gamma, 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-PGJ(2) and PPAR gamma, while inhibition of ERK or COX-2 reduced the expression of COX-2, 15d-PGJ(2) and PPAR gamma indicating that the tryptase-PAR2 pathway proceeds in the order p-ERK, COX-2, 15d-PGJ(2), and PPAR gamma. These results show that interaction between PSC stimulated with Tv and mast cells causes proliferation of PSC through the tryptase-PAR2 pathway.

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