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. 2021 Dec 2;12:772941. doi: 10.3389/fimmu.2021.772941

Figure 2.

Figure 2

TRPV4 partakes in the elevated production of TSLP in dry skin conditions. (A) The production of TSLP in the murine keratinocytes was increased by SLIGRL (50 µM, a PAR2 agonist), carvacrol (100 µM, a TRPV3 agonist), and GSK101 (10 µM, a TRPV4 agonist). (B) A schematic illustration of the putative relationship between the elevated production of TSLP and proteins-of-interest (PAR2, TRPV3, and TRPV4) in dry skin conditions. (C) The transcriptional levels of Trpv4 increased in the keratinocytes of AEW-treated mice, whereas those of Par2 and Trpv3 remained unaltered (n = 3). (D) The activation of PAR2 expressed in HaCaT cells did not alter the production of TSLP. PAR2 was activated by 50 µM SLIGRL (n = 3) and inhibited by 10 µM FSLLRY (n = 3). (E) The activation of TRPV3 expressed in HaCaT cells did not alter the production of TSLP. TRPV3 was activated by 100 µM carvacrol (n = 3) and inhibited by 100 µM of 2-APB (n = 3). (F) The activation of TRPV4 expressed in HaCaT cells induced the production of TSLP. TRPV4 was activated by 10 µM GSK101 (n = 3) and inhibited by 100 µM HC067047 (HC067; n = 3). (G) The immunostaining of TRPV4 in the skin tissues of AEW-treated mice revealed that the fluorescence intensity was higher than that of the control (H; AU: arbitrary unit). The scale bar indicates 50 µm. (I) The production of TSLP significantly increased in the keratinocytes of Trpv4 +/+ mice following treatment with 10 µM GSK101. However, the levels of TSLP in the keratinocytes of Trpv4 -/- mice remained unaltered even after treatment with 10 µM GSK101. *p < 0.05, **p < 0.01, ***p < 0.001, n.s. not significant.