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The major experimental problem is the following: The statement made in our manuscript (page 690, last sentence of first paragraph) that GSK1016790Awas applied in a concentration of 50 nM for 45 s in all subsequent experiments was incorrect. As highlighted in Fig. 1, the TRPV4 currents elicited by GSK1016790A depended on the concentration of the drug and its time of application. Therefore, it is critically important to use the same GSK1016790A concentrations and application times, when comparing GSK1016790A activated TRPV4 currents from different experimental groups. This is why we decided to use a 45 s application time and 50 nM GSK1016790A as standard protocol to estimate TRPV4 currents. However, a detailed re-analysis of the digital raw data from the experiments shown in Figs. 4 to 9 revealed that application times erroneously were quite variable ranging from about 10 s to 60 s. Moreover, we realized that on average application times were relatively short in experimental groups with low TRPV4 currents and long in experimental groups with high TRPV4 currents. In the light of this bias we have to conclude that the different TRPV4 currents observed in the various experimental groups in Figs. 4 to 9 were most likely due to differences in GSK1016790A application times. Furthermore, in recent control experiments we could not reproduce the finding shown in Fig. 3e + f that pre-incubating oocytes with BAPTA-AM reliably abolished the activation of endogenous calcium-activated chloride channels. We also realized that heterologous expression of human PAR2 in oocytes was highly variable and functionally difficult to distinguish from the endogenous Xenopus laevis PAR2-like receptor.

pflügers archiv für die gesamte physiologie des menschen und der tiere/pflügers archiv

Erratum to: Sensitisation of TRPV4 by PAR2 is independent of intracellular calcium signalling and can be mediated by the biased agonist neutrophil elastase