Natalie Briones
Anschutz Medical Campus
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Publication
Featured researches published by Natalie Briones.
American Journal of Pathology | 2011
Cory M. Yamashita; Lior Dolgonos; Rachel L. Zemans; Scott K. Young; Jennifer Robertson; Natalie Briones; Tomoko Suzuki; Megan Campbell; Jack Gauldie; Derek C. Radisky; David W. H. Riches; Guoying Yu; Naftali Kaminski; Christopher A. McCulloch; Gregory P. Downey
Idiopathic pulmonary fibrosis (IPF) may be triggered by epithelial injury that results in aberrant production of growth factors, cytokines, and proteinases, leading to proliferation of myofibroblasts, excess deposition of collagen, and destruction of the lung architecture. The precise mechanisms and key signaling mediators responsible for this aberrant repair process remain unclear. We assessed the importance of matrix metalloproteinase-3 (MMP-3) in the pathogenesis of IPF through i) determination of MMP-3 expression in patients with IPF, ii) in vivo experiments examining the relevance of MMP-3 in experimental models of fibrosis, and iii) in vitro experiments to elucidate possible mechanisms of action. Gene expression analysis, quantitative RT-PCR, and Western blot analysis of explanted human lungs revealed enhanced expression of MMP-3 in IPF, compared with control. Transient adenoviral vector-mediated expression of recombinant MMP-3 in rat lung resulted in accumulation of myofibroblasts and pulmonary fibrosis. Conversely, MMP-3-null mice were protected against bleomycin-induced pulmonary fibrosis. In vitro treatment of cultured lung epithelial cells with purified MMP-3 resulted in activation of the β-catenin signaling pathway, via cleavage of E-cadherin, and induction of epithelial-mesenchymal transition. These processes were inhibited in bleomycin-treated MMP-3-null mice, as assessed by cytosolic translocation of β-catenin and cyclin D1 expression. These observations support a novel role for MMP-3 in the pathogenesis of IPF, through activation of β-catenin signaling and induction of epithelial-mesenchymal transition.
American Journal of Pathology | 2014
Yael Aschner; Anthony P. Khalifah; Natalie Briones; Cory M. Yamashita; Lior Dolgonos; Scott K. Young; Megan Campbell; David W. H. Riches; Elizabeth F. Redente; William J. Janssen; Peter M. Henson; Jan Sap; Nathalie Vacaresse; Andras Kapus; Christopher A. McCulloch; Rachel L. Zemans; Gregory P. Downey
Fibrotic lung diseases represent a diverse group of progressive and often fatal disorders with limited treatment options. Although the pathogenesis of these conditions remains incompletely understood, receptor type protein tyrosine phosphatase α (PTP-α encoded by PTPRA) has emerged as a key regulator of fibroblast signaling. We previously reported that PTP-α regulates cellular responses to cytokines and growth factors through integrin-mediated signaling and that PTP-α promotes fibroblast expression of matrix metalloproteinase 3, a matrix-degrading proteinase linked to pulmonary fibrosis. Here, we sought to determine more directly the role of PTP-α in pulmonary fibrosis. Mice genetically deficient in PTP-α (Ptpra(-/-)) were protected from pulmonary fibrosis induced by intratracheal bleomycin, with minimal alterations in the early inflammatory response or production of TGF-β. Ptpra(-/-) mice were also protected from pulmonary fibrosis induced by adenoviral-mediated expression of active TGF-β1. In reciprocal bone marrow chimera experiments, the protective phenotype tracked with lung parenchymal cells but not bone marrow-derived cells. Because fibroblasts are key contributors to tissue fibrosis, we compared profibrotic responses in wild-type and Ptpra(-/-) mouse embryonic and lung fibroblasts. Ptpra(-/-) fibroblasts exhibited hyporesponsiveness to TGF-β, manifested by diminished expression of αSMA, EDA-fibronectin, collagen 1A, and CTGF. Ptpra(-/-) fibroblasts exhibited markedly attenuated TGF-β-induced Smad2/3 transcriptional activity. We conclude that PTP-α promotes profibrotic signaling pathways in fibroblasts through control of cellular responsiveness to TGF-β.
Immunity | 2006
Paula M. Oliver; Xiao Cao; George Scott Worthen; Peijun Shi; Natalie Briones; Megan K. L. MacLeod; Janice White; Patricia A. Kirby; John W. Kappler; Philippa Marrack; Baoli Yang
Archive | 2015
Ushma Savla; Lars E. Olson; Christopher M. Waters; Lynn M. Crosby; Charlean L. Luellen; Zhihong Zhang; Larry Tague; Scott E. Sinclair; M. Ridge; Micah R. Rogel; Pritin N. Soni; James R. Troken; Albert Sitikov; Humberto E. Trejo; F. Lau; Michael Kahn; Gregory P. Downey; Rachel L. Zemans; Yael Aschner; Natalie Briones; Scott K. Young
american thoracic society international conference | 2012
Rachel L. Zemans; Jazalle McClendon; Yael Aschner; Scott K. Young; Natalie Briones; Yoko Ito; Robert J. Mason; Gregory P. Downey
american thoracic society international conference | 2012
Yael Aschner; Anthony P. Khalifah; Natalie Briones; Scott K. Young; Rachel L. Zemans; Gregory P. Downey
american thoracic society international conference | 2011
Rachel L. Zemans; Natalie Briones; Jazalle McClendon; Gregory P. Downey
american thoracic society international conference | 2011
Rachel L. Zemans; Jazalle McClendon; Natalie Briones; Hong Wei Chu; Gregory P. Downey
american thoracic society international conference | 2011
Milene T. Saavedra; Nathan D. Pennock; Jerry A. Nick; Frank J. Accurso; Linda Sanders; Ickes B; Natalie Briones; David Wagner
american thoracic society international conference | 2011
Anthony P. Khalifah; Scott K. Young; Megan Campbell; Natalie Briones; Cory M. Yamashita; Gregory P. Downey