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. 2022 Jun 30;27(13):4205. doi: 10.3390/molecules27134205

Figure 2.

Figure 2

Role of the JAK/STAT3 pathway in IL-4-induced PER2 expression. (A) HaCaT cells were treated with 20 ng/mL IL-4 for different periods (0–60 min). Whole-cell lysates were prepared, and immunoblotting was performed using phosphorylation-specific or total protein antibodies. GAPDH was used as an internal control. Uncropped blots are shown in Figure S2. (B) HaCaT cells were treated with 20 ng/mL IL-4 for 24 h in the absence or presence of 40 μM AG490 and 6.2 μM pyridone 6. GAPDH was used as an internal control. Relative band intensities were measured using ImageJ. *** p < 0.001 compared to IL-4 alone-treated group (n = 3) by Sidak’s multiple comparisons test. (C,D) HaCaT cells expressing scrambled (shCT) or STAT3 shRNA (shSTAT3) were treated with (+) or without (−) 20 ng/mL IL-4 for 15 min (C) or 24 h (D). The protein levels of p-STAT3 (Tyr705) and total STAT3 (C) and PER2 (D) were measured by immunoblotting. GAPDH was used as an internal control. JAK, Janus kinase; STAT3, signal transducer and activator of transcription 3.