CPF and PFF to partner with ATS to fund pulmonary fibrosis research

Mar 21 2013

The Coalition for Pulmonary Fibrosis (CPF), the Pulmonary Fibrosis Foundation (PFF), and the American Thoracic Society (ATS)-the world's leading professional organization for pulmonary, critical care and sleep medicine-today announced that the CPF and the PFF will again partner with the ATS to fund pulmonary fibrosis (PF) research. This is the seventh partnership grant between the three organizations.

"We are pleased to once again participate in the partnership grants with the ATS and the CPF. The Pulmonary Fibrosis Foundation feels that supporting these types of early stage grants can (and has) led to both an improved understanding of the pathophysiology of pulmonary fibrosis and to the development of more effective therapies. We applaud the leadership of the ATS in fostering these types of collaborations," said Daniel M. Rose, MD, Chairman and CEO of the PFF.

"We are honored to again join with ATS and the PFF to support critical research in pulmonary fibrosis," said Mishka Michon, Chief Executive Officer of the CPF. "The CPF is proud to be supporting these research efforts in an economic time of uncertainty regarding federal funding. It is an opportunity for the private sector to fill the gap and demonstrate our continued commitment to finding treatments and a cure for this devastating disease."

The patient organizations will each commit $20,000 per year to co-fund a two-year research grant to be awarded in 2013. The ATS will provide partial funding and management of the grant.

"We cannot advance in the area of pulmonary fibrosis treatment without sophisticated research. The research funded by these grants has helped advance our understanding of pulmonary fibrosis," said Jesse Roman, MD, member of the ATS Scientific Advisory Committee, Chair of PFF Research Advisory Committee, and Chair of Medicine at the University of Louisville. "This important work may lead to new approaches to the treatment of this devastating disease."

Including the 2013 grant, the CPF and the PFF have together supported $1.22 million of research for PF in partnership with the ATS.

"The three way partnership ATS grant provided important support to my research program, allowing significant advancement in the understanding that Semaphorin 7a and alternatively activated macrophages might play in the progression of fibrotic lung disease in IPF. It is our hope that one day these novel findings might translate into new therapies for all patients with pulmonary fibrosis," said Erica Herzog M.D, PhD, Yale University's Division of Pulmonary and Critical Care Medicine and recipient of a joint grant for her research.

CPF/ATS Partnership Awards through 2011 were granted to:

• Sonye K. Danoff, MD, PhD, of Johns Hopkins University, for her study "VEGF: Marker or Mediator of Lung Injury in Pulmonary Fibrosis?" Her research is currently testing the hypothesis that locally elevated levels of vascular endothelial growth factor (VEGF) in the lungs of patients with autoimmune pulmonary fibrosis contribute to disease progression.

   

• Andrew Tager, MD, assistant professor at Harvard Medical School in the Pulmonary and Critical Care Division and at Massachusetts General Hospital, for his study "(LPA) and its Receptor LPA1." His study is investigating the role of lysophosphatidic acid (LPA) and its cognate receptor LPA1 in lung injury and fibroproliferation following bleomycin treatment.

   

• Harikrishna Tanjore, PhD, of the Center for Lung Research at Vanderbilt University Medical Center, for his study "Contribution of EMT to Pulmonary Fibrosis." The study's purpose was to determine the extent to which epithelial to mesenchymal transition (EMT) contributes to lung fibrosis and to investigate the role of TGFβ in EMT in the lungs.

   

• Melissa Hunter Piper, PhD, of the Davis Heart and Lung Research Institute at Ohio State University, for her study "MicroRNA Regulation in Idiopathic Pulmonary Fibrosis (IPF)." The study's purpose was to determine whether the loss of the expression of miR-17~92 (microRNA) cluster contributes to the pathogenesis of pulmonary fibrosis. PFF/ATS Partnership Awards through 2012 were granted to:

   

• Anne Holland, PhD, of La Trobe University, for her study "Where Does Pulmonary Rehabilitation Fit in the Management of Pulmonary Fibrosis?" This study will provide patients and doctors with certainty regarding the role and timing of pulmonary rehabilitation in IPF, ensuring best possible outcomes in quality of life and community functioning.

   

• Anthony Shum, MD of the University of California, San Francisco, for his study "Defining the Molecular Basis of Interstitial Lung Disease in Rheumatoid Arthritis." Dr. Shum will take advantage of an exciting new technology called exome sequencing to identify the genes that trigger ILD in rheumatoid arthritis patients. Awarded by the CPF/PFF/ATS Partnership beginning 2009 were:

   
• Steven Huang, MD, lecturer, University of Michigan Medical School, for his study "The Regulation and Pattern of the DNA Methylome in Pulmonary Fibrosis." The study involves hypermethylation of DNA, an epigenetic process recognized to be important in many diseases though understudied in IPF and genes that may be hypermethylated, and to profile the DNA methylome of fibrotic lung fibroblasts. Also, his study addresses how prostaglandin E2, an antifibrotic lipid mediator, may be able to regulate DNA methylation machinery.

   

• Erica Herzog, MD, PhD, of Yale University's Division of Pulmonary and Critical Care Medicine, for her study "Semaphorin 7a and Alternative Macrophage Activation in Idiopathic Pulmonary Fibrosis." The research seeks to determine the mechanism through which semaphorin 7a promotes the appearance of M2s and collagen deposition in a mouse model of pulmonary fibrosis and to determine the mechanism through which semaphorin 7a affects the differentiation and activation of M2s obtained from patients with IPF.

   

• Beiyun Zhou, PhD, assistant professor of medicine, of the University of South California's Division of Pulmonary & Critical Care, for her study "Endoplasmic Reticulum (ER) Stress Induces Epithelial-Mesenchymal Transition (EMT) in Alveolar Idiopathic Pulmonary Fibrosis." The researcher is investigating the hypothesis that ER stress induces EMT in epithelial cells thereby contributing directly to fibrosis. Understanding the mechanisms whereby ER stress contributes directly to fibroblast accumulation in IPF should provide new insights into the causes of pulmonary fibrosis that may in turn offer novel therapeutic strategies for this otherwise fatal disease.

   

• Philip Simonian, MD, assistant professor of Pulmonary Sciences & Critical Care at the University of Colorado Denver, for his study "Protection from Inflammation-Induced Pulmonary Fibrosis by IL-22." The focus of the research is to determine the mechanism by which IL-22 protects against lung fibrosis so that better therapies can be developed that protect patients from the development of pulmonary fibrosis.

   

• Jia Guo, MD, MS, of the University of Rochester for his study "Fibrocyte Differentiation is Regulated by Yin Yang 1 in Pulmonary Fibrosis." His research team has discovered that a protein called yin yang 1 (YY1) regulates the activity of genes involved in promoting the scarring process and can regulate the production and accumulation of myofibroblasts in lung scarring. The ultimate goal of the research is to develop therapies to interfere with the functions of YY1 as a novel treatment for idiopathic pulmonary fibrosis and other lung scarring diseases.

   

• Yan Sanders, MD, MS, of the University of Alabama at Birmingham for her study "Epigenetic Regulation of Caveolin-1 by TGF-beta Mediated Signal Pathway in Lung Fibroblasts." Completion of this study will establish epigenetic regulation as one important factor in the pathogenesis of IPF, which may lead to new therapies to reverse this deadly disease.

   

Source: American Thoracic Society