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Figure S1. Effect of hypoxia on urotensin II (U II) in cardiac fibroblasts. A, Representative Western blots for U II in fibroblast treated with different degree of hypoxia. B, Quantitative analysis of U II protein levels. The values from treated fibroblasts have been normalized to values in control cells. (n=4 per group). **P<0.05 vs. control. *P<0.001 vs. control.

Figure S2. Hydrogen peroxide (H2O2) induces U II protein expression in cardiac fibroblasts. A, Representative Western blots for U II in fibroblast treated with ROS stimulant. B, Quantitative analysis of U II protein levels. The values from treated fibroblasts have been normalized to values in control cells. (n=4 per group). *P<0.001 vs. control.

Figure S3. Effect of hypoxia on angiotensin II receptor (Ang II R) in cardiac fibroblasts. A, Representative Western blots for Ang II receptor in fibroblast treated with different degree of hypoxia. B, Quantitative analysis of Ang II receptor protein levels. The values from treated fibroblasts have been normalized to values in control cells. (n=4 per group). **P<0.001 vs. control.

Figure S4. Effect of hypoxia on c-jun in cardiac fibroblasts. A, Representative Western blots for c-jun in fibroblast treated with different degree of hypoxia. B, Quantitative analysis of c-jun protein levels. The values from treated fibroblasts have been normalized to values in control cells. (n=4 per group). **P<0.001 vs. control. *P<0.05 vs. control.

Figure S5. U II siRNA attenuates U II protein expression induced by hypoxia. A, Representative Western blots for U II in fibroblast treated with 2.5% oxygen with or without siRNA. B, Quantitative analysis of U II protein levels. The values from treated fibroblasts have been normalized to values in control cells. (n=4 per group).

Figure S6. Hypoxia increases collagen I labeling in cardiac fibroblasts. Immunohistochemical stain of cultured cardiac fibroblasts was performed after hypoxia with or without inhibitor or siRNA treatment. Labeling of collagen I (arrow) decreased after treatment with N-acetylcysteine (NAC), JNK pathway inhibitor (SP), and U II siRNA induced by hypoxia.

Figure S7. U II modulates cardiac fibroblast protein synthesis. *P<0.01 vs. control. +P<0.01 vs. hypoxia. (n=4 per group).

Figure S8. Knockdown of Ang II by Ang II antibody significantly attenuated the collagen I protein expression induced by hypoxia.

Figure S9. Urotensin II expression is increased in atrial tissue with atrial fibrillation. Confocal microscopic image for U II (arrow) labeling in atrial tissue from control patients (A, normal atrial function with sinus rhythm) and from patients with atrial fibrillation (B). Left panel, vimentin staining. Mid-Panel, U II staining. Right panel, merged staining for vimentin and U II.

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