Loss of epithelial G q and G 11 signaling inhibits TGFβ production but promotes IL-33–mediated macrophage polarization and emphysema-Reference-Cited by-同舟云学术

Loss of epithelial G q and G 11 signaling inhibits TGFβ production but promotes IL-33–mediated macrophage polarization and emphysema

Published:2016-10-25 Issue:451 Volume:9 Page:
ISSN:1945-0877
Container-title:Science Signaling
language:en
Short-container-title:Sci. Signal.

Author:

John Alison E.¹,Wilson Michael R.²,Habgood Anthony¹,Porte Joanne¹,Tatler Amanda L.¹,Stavrou Anastasios¹,Miele Gino³,Jolly Lisa¹,Knox Alan J.¹,Takata Masao²,Offermanns Stefan⁴,Jenkins R. Gisli¹

Affiliation:

1. Division of Respiratory Medicine, University of Nottingham, Nottingham, U.K.

2. Department of Anaesthetics, Pain Medicine and Intensive Care, Imperial College, London, U.K.

3. Epistem Ltd., Manchester, U.K.

4. Department of Pharmacology, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.

Abstract

Signaling by G q/11 is required for optimal TGFβ activation in the lung to prevent inflammation.

Funder

Wellcome Trust

Medical Research Council Industry Collaboration Agreement

National Centre of the Replacement, Refinement, and Reduction of Animals in Research

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Cell Biology,Molecular Biology,Biochemistry

Reference54 articles.

1. G12/G13-mediated signalling in mammalian physiology and disease

2. Gαq signalling: The new and the old

3. Lysophosphatidic Acid Increases Proximal Tubule Cell Secretion of Profibrotic Cytokines PDGF-B and CTGF through LPA2- and Gαq-Mediated Rho and αvβ6 Integrin-Dependent Activation of TGF-β

4. Lysophosphatidic Acid Induces αvβ6 Integrin-Mediated TGF-β Activation via the LPA2 Receptor and the Small G Protein Gαq

5. Smad3 Null Mice Develop Airspace Enlargement and Are Resistant to TGF-β-Mediated Pulmonary Fibrosis

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