Yesterday’s blog was about the new research grants that are now available thanks to the wonderful organization, The Coalition for Pulmonary Fibrosis (CPF).
I thought you, dear reader, may be interested in the specific research that has previously been funded through CPF and the American Thoracic Society (ATS).
Here it is thanks to CPF who e-mailed this information to me!
Past CPF/ATS Partnership Awards, through 2008, were granted to:
• Sonye K. Danoff, M.D., Ph.D., of Johns Hopkins University: 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, M.D., assistant professor at Harvard Medical School in the Pulmonary and Critical Care Division and at Massachusetts General Hospital. His study was: (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, Ph.D., of the Center for Lung Research at Vanderbilt University Medical Center: 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, Ph.D., of the Davis Heart and Lung Research Institute at Ohio State University who studied whether the loss of the expression of miR-17-92 (microRNA) cluster contributes to the pathogenesis of pulmonary fibrosis.
Grants Awarded by the CPF/PFF/ATS partnership beginning 2009 were:
• Steven Huang MD., lecturer, University of Michigan Medical School: His study is 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, M.D., PhD,, of Yale University’s Division of Pulmonary and Critical Care Medicine:, His study is 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.
• Zhou, Beiyun Ph.D., assistant professor of medicine, of the University of South California’s Division of Pulmonary & Critical Care: The study is 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.
• Simonian, Philip M.D, assistant professor of pulmonary sciences & critical care –at the University of Colorado Denver: His study is 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.