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The effect of FGF7 on the ADAM17-EGFR-ERK1/2 signaling pathway in 16HBE cells. (A, B) Representative Western blots and densitometry for FGF7 and <t>p-FGFR2/FGFR2</t> under the following conditions: Control, CSE (5%), CSE + rFGF7, and CSE + rFGF7 with SB202190 (p38 inhibitor, 10 μM, 1 h pretreat), LY294002 (PI3K inhibitor, 10 μM, 1 h), or AG1478 (EGFR inhibitor, 10 μM, 1 h) (n=3 biological replicates). (C, D) Representative Western blots and densitometry for FGF7, ADAM17, p-p38/p38, and p-AKT/AKT under the following conditions: Control, CSE (5%), CSE + rFGF7, and CSE + rFGF7 with SB202190 (p38 inhibitor, 10 μM, 1 h pretreat), LY294002 (PI3K inhibitor, 10 μM, 1 h), or AG1478 (EGFR inhibitor, 10 μM, 1 h) (n=3 biological replicates). (E, F) Representative Western blots and densitometry for ADAM17, p-EGFR/EGFR, and p-ERK1/2/ERK1/2 under the following conditions: Control, CSE (5%), CSE + rFGF7, and CSE + rFGF7 with SB202190 (p38 inhibitor, 10 μM, 1 h pretreat), LY294002 (PI3K inhibitor, 10 μM, 1 h), or AG1478 (EGFR inhibitor, 10 μM, 1 h) (n=3 biological replicates). Compared to Control, * P < 0.05; Compared to CSE, # P < 0.05; Compared to CSE+FGF7, & P < 0.05.
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The effect of FGF7 on the ADAM17-EGFR-ERK1/2 signaling pathway in 16HBE cells. (A, B) Representative Western blots and densitometry for FGF7 and <t>p-FGFR2/FGFR2</t> under the following conditions: Control, CSE (5%), CSE + rFGF7, and CSE + rFGF7 with SB202190 (p38 inhibitor, 10 μM, 1 h pretreat), LY294002 (PI3K inhibitor, 10 μM, 1 h), or AG1478 (EGFR inhibitor, 10 μM, 1 h) (n=3 biological replicates). (C, D) Representative Western blots and densitometry for FGF7, ADAM17, p-p38/p38, and p-AKT/AKT under the following conditions: Control, CSE (5%), CSE + rFGF7, and CSE + rFGF7 with SB202190 (p38 inhibitor, 10 μM, 1 h pretreat), LY294002 (PI3K inhibitor, 10 μM, 1 h), or AG1478 (EGFR inhibitor, 10 μM, 1 h) (n=3 biological replicates). (E, F) Representative Western blots and densitometry for ADAM17, p-EGFR/EGFR, and p-ERK1/2/ERK1/2 under the following conditions: Control, CSE (5%), CSE + rFGF7, and CSE + rFGF7 with SB202190 (p38 inhibitor, 10 μM, 1 h pretreat), LY294002 (PI3K inhibitor, 10 μM, 1 h), or AG1478 (EGFR inhibitor, 10 μM, 1 h) (n=3 biological replicates). Compared to Control, * P < 0.05; Compared to CSE, # P < 0.05; Compared to CSE+FGF7, & P < 0.05.
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MedChemExpress selective fgfr2 inhibitor
(A) Relative expression levels of miR-671-5p after treatment with the si-circSmad4 ± TGF-β1 (n = 8–9 per group). (B) Relative <t>Fgfr2</t> mRNA expression levels after treatment with the si-circSmad4 ± TGF-β1 (n = 8–9 per group). p-values were determined using Tukey’s HSD test following one-way ANOVA. All data are presented as mean ± SEM. *p ≤ 0.05; **p ≤ 0.01; ****p ≤ 0.0001.
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(A) Relative miR-671-5p amount in NIH3T3 treated with TGF-β1 (n = 6 per group). (B) Relative mRNA levels of fibrosis-related genes ( Acta2, Col1a1, Col3a1, Ctgf ) under the indicated combinations of miR-671-5p mimic and TGF-β1 (n = 6 per group). (C) Collagen concentrations measured in the culture medium (Media collagen) and the matrix-associated fraction (Matrix collagen) transfected with miR-671-5p mimic in NIH3T3 cells (n = 8 per group). (D) Relative <t>Fgfr2</t> mRNA expression levels in NIH3T3 fibroblasts treated with TGF-β1 (n = 6 per group). (E) Effect of miR-671-5p mimic on TGF-β1-induced in Fgfr2 mRNA expression (n = 6 per group). (F) Effect of si-circSMAD4 on TGF-β1-induced increase in Fgfr2 mRNA expression (n = 6 per group). (G) Changes in the expression of Acta2, Col1a1, Ctgf, Fibronectin-1 ( Fn1 ) in NIH3T3 <t>cells</t> <t>under</t> <t>FGFR2-IN-1</t> and TGF-β1 treatments (n = 7 per group). p-values were determined using Tukey’s HSD test following one-way ANOVA. All data are presented as mean ± SEM. ns, not significant. *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001; ****p ≤ 0.0001.
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(A) Relative miR-671-5p amount in NIH3T3 treated with TGF-β1 (n = 6 per group). (B) Relative mRNA levels of fibrosis-related genes ( Acta2, Col1a1, Col3a1, Ctgf ) under the indicated combinations of miR-671-5p mimic and TGF-β1 (n = 6 per group). (C) Collagen concentrations measured in the culture medium (Media collagen) and the matrix-associated fraction (Matrix collagen) transfected with miR-671-5p mimic in NIH3T3 cells (n = 8 per group). (D) Relative <t>Fgfr2</t> mRNA expression levels in NIH3T3 fibroblasts treated with TGF-β1 (n = 6 per group). (E) Effect of miR-671-5p mimic on TGF-β1-induced in Fgfr2 mRNA expression (n = 6 per group). (F) Effect of si-circSMAD4 on TGF-β1-induced increase in Fgfr2 mRNA expression (n = 6 per group). (G) Changes in the expression of Acta2, Col1a1, Ctgf, Fibronectin-1 ( Fn1 ) in NIH3T3 <t>cells</t> <t>under</t> <t>FGFR2-IN-1</t> and TGF-β1 treatments (n = 7 per group). p-values were determined using Tukey’s HSD test following one-way ANOVA. All data are presented as mean ± SEM. ns, not significant. *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001; ****p ≤ 0.0001.
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The effect of FGF7 on the ADAM17-EGFR-ERK1/2 signaling pathway in 16HBE cells. (A, B) Representative Western blots and densitometry for FGF7 and p-FGFR2/FGFR2 under the following conditions: Control, CSE (5%), CSE + rFGF7, and CSE + rFGF7 with SB202190 (p38 inhibitor, 10 μM, 1 h pretreat), LY294002 (PI3K inhibitor, 10 μM, 1 h), or AG1478 (EGFR inhibitor, 10 μM, 1 h) (n=3 biological replicates). (C, D) Representative Western blots and densitometry for FGF7, ADAM17, p-p38/p38, and p-AKT/AKT under the following conditions: Control, CSE (5%), CSE + rFGF7, and CSE + rFGF7 with SB202190 (p38 inhibitor, 10 μM, 1 h pretreat), LY294002 (PI3K inhibitor, 10 μM, 1 h), or AG1478 (EGFR inhibitor, 10 μM, 1 h) (n=3 biological replicates). (E, F) Representative Western blots and densitometry for ADAM17, p-EGFR/EGFR, and p-ERK1/2/ERK1/2 under the following conditions: Control, CSE (5%), CSE + rFGF7, and CSE + rFGF7 with SB202190 (p38 inhibitor, 10 μM, 1 h pretreat), LY294002 (PI3K inhibitor, 10 μM, 1 h), or AG1478 (EGFR inhibitor, 10 μM, 1 h) (n=3 biological replicates). Compared to Control, * P < 0.05; Compared to CSE, # P < 0.05; Compared to CSE+FGF7, & P < 0.05.

Journal: Frontiers in Immunology

Article Title: FGF7 mitigates airway inflammation and epithelial injury in cigarette smoke-induced COPD model

doi: 10.3389/fimmu.2026.1815550

Figure Lengend Snippet: The effect of FGF7 on the ADAM17-EGFR-ERK1/2 signaling pathway in 16HBE cells. (A, B) Representative Western blots and densitometry for FGF7 and p-FGFR2/FGFR2 under the following conditions: Control, CSE (5%), CSE + rFGF7, and CSE + rFGF7 with SB202190 (p38 inhibitor, 10 μM, 1 h pretreat), LY294002 (PI3K inhibitor, 10 μM, 1 h), or AG1478 (EGFR inhibitor, 10 μM, 1 h) (n=3 biological replicates). (C, D) Representative Western blots and densitometry for FGF7, ADAM17, p-p38/p38, and p-AKT/AKT under the following conditions: Control, CSE (5%), CSE + rFGF7, and CSE + rFGF7 with SB202190 (p38 inhibitor, 10 μM, 1 h pretreat), LY294002 (PI3K inhibitor, 10 μM, 1 h), or AG1478 (EGFR inhibitor, 10 μM, 1 h) (n=3 biological replicates). (E, F) Representative Western blots and densitometry for ADAM17, p-EGFR/EGFR, and p-ERK1/2/ERK1/2 under the following conditions: Control, CSE (5%), CSE + rFGF7, and CSE + rFGF7 with SB202190 (p38 inhibitor, 10 μM, 1 h pretreat), LY294002 (PI3K inhibitor, 10 μM, 1 h), or AG1478 (EGFR inhibitor, 10 μM, 1 h) (n=3 biological replicates). Compared to Control, * P < 0.05; Compared to CSE, # P < 0.05; Compared to CSE+FGF7, & P < 0.05.

Article Snippet: Antibodies used included β-actin (1:1000, 100166-MM10, Sino Biological); KGF (1:800-1:1000, ab131162, abcam); ADAM17 (1:800-1:1000, ab2051, abcam); p38 (1:1500-1:2500, ab170099, abcam); p-p38 (1:800-1:1000, ab47363, abcam); AKT (1:1000-1:1200, 4691S, CST); p-AKT (1:800-1:1000, ab192623, abcam); EGFR (1:1000, ab32077, abcam); p-EGFR (1:600-1:1000, 3777S, CST); ERK1/2 (1:1000, ab184699, abcam); p-ERK1/2 (1:800-1:1000, 9101S, CST); FGFR2 (1:1000, A19051, Abclonal); p-FGFR2 (1:500, PFGFR2-240AP, Thermo).

Techniques: Western Blot, Control

(A) Relative expression levels of miR-671-5p after treatment with the si-circSmad4 ± TGF-β1 (n = 8–9 per group). (B) Relative Fgfr2 mRNA expression levels after treatment with the si-circSmad4 ± TGF-β1 (n = 8–9 per group). p-values were determined using Tukey’s HSD test following one-way ANOVA. All data are presented as mean ± SEM. *p ≤ 0.05; **p ≤ 0.01; ****p ≤ 0.0001.

Journal: The Korean Journal of Physiology & Pharmacology : Official Journal of the Korean Physiological Society and the Korean Society of Pharmacology

Article Title: Circular RNA circSmad4 controls pulmonary fibrosis

doi: 10.4196/kjpp.25.123

Figure Lengend Snippet: (A) Relative expression levels of miR-671-5p after treatment with the si-circSmad4 ± TGF-β1 (n = 8–9 per group). (B) Relative Fgfr2 mRNA expression levels after treatment with the si-circSmad4 ± TGF-β1 (n = 8–9 per group). p-values were determined using Tukey’s HSD test following one-way ANOVA. All data are presented as mean ± SEM. *p ≤ 0.05; **p ≤ 0.01; ****p ≤ 0.0001.

Article Snippet: FGFR2-IN-1 (HY-145230; MedChemExpress) was used as a selective FGFR2 inhibitor and dissolved in dimethyl sulfoxide to the desired concentrations.

Techniques: Expressing

(A) Relative miR-671-5p amount in NIH3T3 treated with TGF-β1 (n = 6 per group). (B) Relative mRNA levels of fibrosis-related genes ( Acta2, Col1a1, Col3a1, Ctgf ) under the indicated combinations of miR-671-5p mimic and TGF-β1 (n = 6 per group). (C) Collagen concentrations measured in the culture medium (Media collagen) and the matrix-associated fraction (Matrix collagen) transfected with miR-671-5p mimic in NIH3T3 cells (n = 8 per group). (D) Relative Fgfr2 mRNA expression levels in NIH3T3 fibroblasts treated with TGF-β1 (n = 6 per group). (E) Effect of miR-671-5p mimic on TGF-β1-induced in Fgfr2 mRNA expression (n = 6 per group). (F) Effect of si-circSMAD4 on TGF-β1-induced increase in Fgfr2 mRNA expression (n = 6 per group). (G) Changes in the expression of Acta2, Col1a1, Ctgf, Fibronectin-1 ( Fn1 ) in NIH3T3 cells under FGFR2-IN-1 and TGF-β1 treatments (n = 7 per group). p-values were determined using Tukey’s HSD test following one-way ANOVA. All data are presented as mean ± SEM. ns, not significant. *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001; ****p ≤ 0.0001.

Journal: The Korean Journal of Physiology & Pharmacology : Official Journal of the Korean Physiological Society and the Korean Society of Pharmacology

Article Title: Circular RNA circSmad4 controls pulmonary fibrosis

doi: 10.4196/kjpp.25.123

Figure Lengend Snippet: (A) Relative miR-671-5p amount in NIH3T3 treated with TGF-β1 (n = 6 per group). (B) Relative mRNA levels of fibrosis-related genes ( Acta2, Col1a1, Col3a1, Ctgf ) under the indicated combinations of miR-671-5p mimic and TGF-β1 (n = 6 per group). (C) Collagen concentrations measured in the culture medium (Media collagen) and the matrix-associated fraction (Matrix collagen) transfected with miR-671-5p mimic in NIH3T3 cells (n = 8 per group). (D) Relative Fgfr2 mRNA expression levels in NIH3T3 fibroblasts treated with TGF-β1 (n = 6 per group). (E) Effect of miR-671-5p mimic on TGF-β1-induced in Fgfr2 mRNA expression (n = 6 per group). (F) Effect of si-circSMAD4 on TGF-β1-induced increase in Fgfr2 mRNA expression (n = 6 per group). (G) Changes in the expression of Acta2, Col1a1, Ctgf, Fibronectin-1 ( Fn1 ) in NIH3T3 cells under FGFR2-IN-1 and TGF-β1 treatments (n = 7 per group). p-values were determined using Tukey’s HSD test following one-way ANOVA. All data are presented as mean ± SEM. ns, not significant. *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001; ****p ≤ 0.0001.

Article Snippet: FGFR2-IN-1 (HY-145230; MedChemExpress) was used as a selective FGFR2 inhibitor and dissolved in dimethyl sulfoxide to the desired concentrations.

Techniques: Transfection, Expressing

(A) Relative miR-671-5p amount in NIH3T3 treated with TGF-β1 (n = 6 per group). (B) Relative mRNA levels of fibrosis-related genes ( Acta2, Col1a1, Col3a1, Ctgf ) under the indicated combinations of miR-671-5p mimic and TGF-β1 (n = 6 per group). (C) Collagen concentrations measured in the culture medium (Media collagen) and the matrix-associated fraction (Matrix collagen) transfected with miR-671-5p mimic in NIH3T3 cells (n = 8 per group). (D) Relative Fgfr2 mRNA expression levels in NIH3T3 fibroblasts treated with TGF-β1 (n = 6 per group). (E) Effect of miR-671-5p mimic on TGF-β1-induced in Fgfr2 mRNA expression (n = 6 per group). (F) Effect of si-circSMAD4 on TGF-β1-induced increase in Fgfr2 mRNA expression (n = 6 per group). (G) Changes in the expression of Acta2, Col1a1, Ctgf, Fibronectin-1 ( Fn1 ) in NIH3T3 cells under FGFR2-IN-1 and TGF-β1 treatments (n = 7 per group). p-values were determined using Tukey’s HSD test following one-way ANOVA. All data are presented as mean ± SEM. ns, not significant. *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001; ****p ≤ 0.0001.

Journal: The Korean Journal of Physiology & Pharmacology : Official Journal of the Korean Physiological Society and the Korean Society of Pharmacology

Article Title: Circular RNA circSmad4 controls pulmonary fibrosis

doi: 10.4196/kjpp.25.123

Figure Lengend Snippet: (A) Relative miR-671-5p amount in NIH3T3 treated with TGF-β1 (n = 6 per group). (B) Relative mRNA levels of fibrosis-related genes ( Acta2, Col1a1, Col3a1, Ctgf ) under the indicated combinations of miR-671-5p mimic and TGF-β1 (n = 6 per group). (C) Collagen concentrations measured in the culture medium (Media collagen) and the matrix-associated fraction (Matrix collagen) transfected with miR-671-5p mimic in NIH3T3 cells (n = 8 per group). (D) Relative Fgfr2 mRNA expression levels in NIH3T3 fibroblasts treated with TGF-β1 (n = 6 per group). (E) Effect of miR-671-5p mimic on TGF-β1-induced in Fgfr2 mRNA expression (n = 6 per group). (F) Effect of si-circSMAD4 on TGF-β1-induced increase in Fgfr2 mRNA expression (n = 6 per group). (G) Changes in the expression of Acta2, Col1a1, Ctgf, Fibronectin-1 ( Fn1 ) in NIH3T3 cells under FGFR2-IN-1 and TGF-β1 treatments (n = 7 per group). p-values were determined using Tukey’s HSD test following one-way ANOVA. All data are presented as mean ± SEM. ns, not significant. *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001; ****p ≤ 0.0001.

Article Snippet: FGFR2-IN-1 (HY-145230; MedChemExpress) was used as a selective FGFR2 inhibitor and dissolved in dimethyl sulfoxide to the desired concentrations.

Techniques: Transfection, Expressing