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Increasing sodium concentration upregulates Ccl20 expression in KCs through the <t>JNK/p38–SGK1</t> pathway. ( a ) qPCR analysis of selected chemokines, cytokines, and Sgk1 in KCs (n = 5 for each group). (b) Immunoblot analysis of <t>p38,</t> <t>phosphorylated</t> p38, JNK, and phosphorylated JNK in KCs for different time (0 min, 30 min, 60 min), and tubulin was used as control. The relative densitometry of all bands (arbitrary unit) was normalized to the level of 0 min (n = 3 for each group). (c) qPCR analysis of Ccl20 and Sgk1 RNA expression in KCs treated with pharmacological inhibitors (n = 3 for each group). Data are shown as mean ± SEM. For a, P -values were determined by 2-tailed Student’s t -test. For c, P -values were determined by 1-way ANOVA. ∗∗ P < .01, ∗∗∗ P < .01, and ∗∗∗∗ P < .0001. KC, keratinocyte; min, minute.
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Increasing sodium concentration upregulates Ccl20 expression in KCs through the <t>JNK/p38–SGK1</t> pathway. ( a ) qPCR analysis of selected chemokines, cytokines, and Sgk1 in KCs (n = 5 for each group). (b) Immunoblot analysis of <t>p38,</t> <t>phosphorylated</t> p38, JNK, and phosphorylated JNK in KCs for different time (0 min, 30 min, 60 min), and tubulin was used as control. The relative densitometry of all bands (arbitrary unit) was normalized to the level of 0 min (n = 3 for each group). (c) qPCR analysis of Ccl20 and Sgk1 RNA expression in KCs treated with pharmacological inhibitors (n = 3 for each group). Data are shown as mean ± SEM. For a, P -values were determined by 2-tailed Student’s t -test. For c, P -values were determined by 1-way ANOVA. ∗∗ P < .01, ∗∗∗ P < .01, and ∗∗∗∗ P < .0001. KC, keratinocyte; min, minute.
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Increasing sodium concentration upregulates Ccl20 expression in KCs through the JNK/p38–SGK1 pathway. ( a ) qPCR analysis of selected chemokines, cytokines, and Sgk1 in KCs (n = 5 for each group). (b) Immunoblot analysis of p38, phosphorylated p38, JNK, and phosphorylated JNK in KCs for different time (0 min, 30 min, 60 min), and tubulin was used as control. The relative densitometry of all bands (arbitrary unit) was normalized to the level of 0 min (n = 3 for each group). (c) qPCR analysis of Ccl20 and Sgk1 RNA expression in KCs treated with pharmacological inhibitors (n = 3 for each group). Data are shown as mean ± SEM. For a, P -values were determined by 2-tailed Student’s t -test. For c, P -values were determined by 1-way ANOVA. ∗∗ P < .01, ∗∗∗ P < .01, and ∗∗∗∗ P < .0001. KC, keratinocyte; min, minute.

Journal: JID Innovations

Article Title: High-salt diet aggravates skin inflammation of psoriasis-like mouse model with CCL20‒CCR6 axis further activation

doi: 10.1016/j.xjidi.2026.100451

Figure Lengend Snippet: Increasing sodium concentration upregulates Ccl20 expression in KCs through the JNK/p38–SGK1 pathway. ( a ) qPCR analysis of selected chemokines, cytokines, and Sgk1 in KCs (n = 5 for each group). (b) Immunoblot analysis of p38, phosphorylated p38, JNK, and phosphorylated JNK in KCs for different time (0 min, 30 min, 60 min), and tubulin was used as control. The relative densitometry of all bands (arbitrary unit) was normalized to the level of 0 min (n = 3 for each group). (c) qPCR analysis of Ccl20 and Sgk1 RNA expression in KCs treated with pharmacological inhibitors (n = 3 for each group). Data are shown as mean ± SEM. For a, P -values were determined by 2-tailed Student’s t -test. For c, P -values were determined by 1-way ANOVA. ∗∗ P < .01, ∗∗∗ P < .01, and ∗∗∗∗ P < .0001. KC, keratinocyte; min, minute.

Article Snippet: JNK Rabbit mAb (Cell Signaling Technology, catalog number 5292), phosphorylated JNK Rabbit mAb (Cell Signaling Technology, catalog number 4668), p38 Rabbit mAb (Cell Signaling Technology, catalog number 8690), phosphorylated p38 Rabbit mAb (Cell Signaling Technology, catalog number 4511), mouse anti-Alpha Tubulin mAb (Proteintech, catalog number HRP-66031) were used as primary antibodies, and goat antirabbit antibody (Abcam, catalog number ab6721) was used as secondary antibody.

Techniques: Concentration Assay, Expressing, Western Blot, Control, RNA Expression