In a previous report to the Society we presented data concerning Ca²⁺ handling and influx mechanisms in human cultured airway smooth muscle (ASM), and proposed that the latter was likely to be via one or more transient receptor potential (TRP) channels (McVicker et al., 2001). TRP channels were first discovered in mutated trp photoreceptors of Drosophila, and the mammalian TRP homologues have recently been unified into three subfamilies (TRPC, TRPM, and TRPV). The TRP-canonical (TRPC) subfamily (formally short-TRPs or STRPs) is most closely related to Drosophila TRP proteins. Comparatively little information is available concerning the expression of TRPC in human ASM, therefore in this study we compared the expression of message for all known human TRPC channels and alternative splice variants between several human secondary cell lines (HeLa, HEK-293, A549, JURKAT and MOLT-4) and primary cultured human ASM. ASM cells were cultured from tissue derived from 6 patients undergoing surgery, and passages 4-6 were used for experiments. This study was approved by the Guy’s and St Thomas’ Hospitals’ Research Ethics Committee and informed consent was obtained from donors. RNA was isolated from the cells and reverse transcribed to cDNA. The cDNA was used for RT-PCR (24-40 cycles) with the specific primers designed against the different trpc genes. RT-PCR revealed that message for TRPC1 (including short alternative splice variant) and TRPC3 were expressed in all secondary cell lines and ASM, except TRPC3 in A549. Conversely, message for TRPC4α, β, ε, η and ζ were only expressed in HeLa, HEK-293, and ASM. TRPC5 was found mainly in ASM and JURKAT cells and at very low levels (requiring 40 cycles) in HeLa, HEK-293 and MOLT-4. Message for TRPC6 full, and the alternative splice variant δ_316-431 were expressed in HeLa, ASM, and A549 cells alone. No message for TRPC4 γ, TRPC6δ_377-431 and TRPC7 was detected in any of the human cell lines or ASM. The results give a general profile of trpc expression in the different human cell lines, which can now be used to determine their suitability for expression, over-expression or knock down studies for the role of specific TRPC proteins in Ca2+ influx pathways.