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Mechanisms of tissue inhibitor of metalloproteinase 1 augmentation by IL-13 on TGF- β1–stimulated primary human fibroblasts  Xiuxia Zhou, PhD, Haizhen.

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Presentation on theme: "Mechanisms of tissue inhibitor of metalloproteinase 1 augmentation by IL-13 on TGF- β1–stimulated primary human fibroblasts  Xiuxia Zhou, PhD, Haizhen."— Presentation transcript:

1 Mechanisms of tissue inhibitor of metalloproteinase 1 augmentation by IL-13 on TGF- β1–stimulated primary human fibroblasts  Xiuxia Zhou, PhD, Haizhen Hu, BS, Mai-Lan N. Huynh, MD, Chakradhar Kotaru, MD, Silvana Balzar, MD, John B. Trudeau, BA, Sally E. Wenzel, MD  Journal of Allergy and Clinical Immunology  Volume 119, Issue 6, Pages (June 2007) DOI: /j.jaci Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

2 Fig 1 Phosphorylation of Smad-2 (A) and Smad-3 (B) was increased in the presence of TGF-β1 and IL-13+TGF-β1 at 1 and 6 hours. ∗P < .05 compared with media-treated cells. The addition of IL-13 augmented TGF-β1–induced Smad-2 and Smad-3 phosphorylation at 1 hour (P = .02 and .03, respectively; n = 4). Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci ) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

3 Fig 2 A, Phosphorylation of Smad-2 and Smad-3 was inhibited by DN–Smad-2 or DN–Smad-3 in the presence of TGF-β1 or IL-13+TGF-β1 (n = 3). B, Both DN–Smad-2 and DN–Smad-3 decreased TIMP-1 mRNA in the presence of TGF-β1 and IL-13+TGF-β1. ∗P < .05 compared with the absence of DN–Smad-2 or DN–Smad-3 (n = 3). Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci ) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

4 Fig 3 Both IL-13 and IL-13+TGF-β1 increased ERK phosphorylation at 0.25 hour (∗P < .05 vs same time media control). In addition, both IL-13 alone and IL-13+TGF-β1 activated ERK more strongly than TGF-β1 alone (P = .05 for IL-13 and P = .01 for IL-13+TGF-β1; n = 4). Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci ) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

5 Fig 4 A, U0126 inhibited ERK phosphorylation (n = 3). Both TIMP-1 mRNA (B) and protein (C) were inhibited by U0126 (10 μmol/L) in the presence of TGF-β1 and IL-13+TGF-β1 (P < .05 or .01). There was greater inhibition of TIMP-1 mRNA and protein in the presence of IL-13+TGF-β1 compared with TGF-β1 alone (P = .005 for mRNA [n = 4] and P = .03 for protein [n = 5]). Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci ) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

6 Fig 5 A, Akt phosphorylation was increased by U0126 (10 μmol/L; ∗P < .05, ∗∗P < .01; n = 3). B, ERK phosphorylation was increased by LY (10 and 25 μmol/L; ∗P < .05, ∗∗P < .01; n = 4). Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci ) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

7 Fig 6 A, U0126 moderately reduced IL-13+TGF-β1–induced Smad-2 phosphorylation. B, U0126 decreased IL-13+TGF-β1–induced Smad-3 phosphorylation (∗P < .05), to a greater degree than that observed for TGF-β1 (P = .02). TGF-β1–induced Smad-2 (C) and Smad-3 (D) phosphorylation was increased by LY (∗P < .05). LY (25 μmol/L) increased TGF-β1–induced Smad-2, -3 phosphorylation more than observed for IL-13+TGF-β1 (P = .02 and .01, respectively). Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci ) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

8 Fig 7 A schematic representation of the interaction between IL-13 and TGF-β1 signaling pathways regulating TIMP-1 expression in human airway fibroblasts. Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci ) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

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