抄録
Growing evidence has been accumulated that myofibroblasts may play a pivotal role in inflammatory and neoplastic processes in the gastrointestinal tract, especially via release of an important inflammatory mediator, prostaglandin E2. Part of the release has been shown to be dependent on Ca2+, but what source contributes thereto remains entirely unclear. In this study, we explored the potential role of transient receptor potential (TRP) proteins for this process by evaluating their expression profile and function in the human colonic myofibroblast cell line CCD-18Co. RT-PCR amplification with specific primers detected the expression of seven TRP isoforms in CCD-18Co cells, including TRPC1, TRPC5, TRPC6, TRPV2, TRPV4, TRPM3 and TRPM7. Activators so far known for these TRP isoforms such as OAG, hypoosmolarity, 2-APB and sphinganine evoked elevation of the intracellular Ca2+ concentration ([Ca2+]i). Whole-cell current recording confirmed that all these activators could activate non-selective cationic currents, although their magnitudes and pattern of activation were highly variable. The observed I-V relationship and pharmacological sensitivity suggest that at least five out of the seven TRP isoforms, i.e. TRPC6, TRPV2, TRPV4, TRPM3 and TRPM7, are functional. In addition, one of well-established inflammatory cytokines in the gut, TNFα, was also able to evoke [Ca2+]i rise and a concomitant nonselective cationic current with properties reminiscent of TRPC or TRPV subfamily members. [J Physiol Sci. 2007;57 Suppl:S219]
