Philip Sannes, PhD
Professor, Cell Biology
Ph.D.: The Ohio State University
Post-doctoral Training: Medical University of South Carolina, Division of Pathobiology
Biological BarriersResearch has mainly been focused on the mechanisms which regulate repair and renewal of epithelial surfaces in the pulmonary alveolus. This has included how extracellular matrix (ECM), especially their sulfated components, influence cellular responses to growth factors and alter specific gene expression leading to proliferation and ending with differentiation or transition. Recent studies have examined specific signaling pathways that intersect and control cell fate decisions in adult lung. These processes are understood to be key in determining whether epithelial injury effectively resolves, or results in irreversible fibrosis. Influenced by results obtained through a recent RO3 mechanism focused on a cohort of idiopathic pulmonary fibrosis (IPF) patients obtained from the Lung Tissue Research Consortium and the NIH, we continue to expand on our historical interests in normal alveolar epithelial turnover to more translational application of specific biologic principals to lung pathology, and specifically fibrosis. These include specific cell-cell and cell-ECM interactions as they control the initiation and perpetuation of fibrogenesis in lung diseases like IPF.
Our work has focused on the mechanisms that influence the activities of a key cell in the adult pulmonary alveolus - the type II (AT2) epithelial cell – that plays a crucial role in repair processes following injury. In addition to producing surfactant, it acts as a facultative stem cell with the capacity to renew itself as well as serve as the precursor for AT1 cells, which cover over 90% of the alveolar surface area. We’ve developed data suggesting that the interaction of alveolar epithelial cells with specific components of the extracellular matrix (ECM) directly affects their ability to proliferate, to synthesize effector molecules vital to the repair process (such as cytokines and additional ECM components), and to effectively differentiate into type I (AT1) cells.
- Expression of WNT5A in Idiopathic Pulmonary Fibrosis and Its Control by TGF-β and WNT7B in Human Lung FibroblastsNewman, D.R., Sills, W.S., Hanrahan, K., Ziegler, A., Tidd, K.M., Cook, E., Sannes, P.L. | J Histochem Cytochem 2016. 64(2) 99–111.
- Heparin inhibits LPS-induced COX-2 Expression in H292 CellsYi, N. Y., Newman, D.R., Morales Johansson, H, Zhang, H., and P.L. Sannes | Experimental Lung Research 2015 Nov;41(9):499-513.
- (2014) MARCKS-dependent mucin clearance and lipid metabolism in ependymal cells is required for maintenance of forebrain homeostasis during agingMuthusamy, N., L. Sommerville, A. Moeser, D. Stumpo, P. Sannes, K. Adler, P. Blackshear, J. Weimer, H.T. Ghashghaei | Aging Cell Oct; 14(5):764-73.
- Whole-Genome Analysis of Temporal Gene Expression during Early Transdifferentiation of Human Lung Alveolar Epithelial Type 2 Cells In VitroJohansson H.M., D.R. Newman, and P.L. Sannes | PLoS ONE 2014; 9(4): e93413.
- Expression of Fibroblast Growth Factor-9 in Normal Human Lung and Idiopathic Pulmonary FibrosisCoffey, E, D.R. Newman, P.L. Sannes | J. Histochem. Cytochem. 2013; 61(9):671-679. *Featured on cover, J. Histochem. Cytochem September, 2013*
- Over-expression of Human Endosulfatase-1 Exacerbates Cadmium-induced Injury to Transformed Human Lung Cells In VitroZhang, H., D. R. Newman, J. C. Bonner, P. L. Sannes | Tox. & Appl. Pharm. 2012 Nov 15;265(1):27-42.
- Wnt7B in fibroblastic foci of idiopathic pulmonary fibrosisMeuten, T, A. Hickey, K. Franklin, B. Grossi, J. Tobias, H. Zhang, D.R. Newman, S. Jennings, M. Correa, P. L. Sannes | Resp. Res. 2012; 28;13(1):62.
- HSulf-1 Inhibits ERK and AKT Signaling and Decreases Cell Viability in vitro in Human Lung Epithelial CellsZhang, H., D. R. Newman, P. L. Sannes | Respir Res. 2012. 13(1):69.
- (2011) Heterotaxin: A TGF-β Signaling Inhibitor Identified in a Multi-Phenotype Profiling Screen in Xenopus EmbryosDush, M.K., A.L. McIver, M.A. Parr, D.D. Young, J. Fisher, D.R. Newman, P.L. Sannes, M.L. Hauck, A. Deiters, N. Nascone-Yoder | Chem.Biol. 2011.18:252-263.
NC State College of Veterinary Medicine Researcher Finding Cellular Causes of Lung-Hardening DiseaseIdiopathic Pulmonary Fibrosis, or IPF, is an incurable lung disease that, over time, turns healthy lung tissue into inflexible scar tissue – hardening the lungs and eventually causing respiratory distress and death. Currently, there is no cure. Phil Sannes, a professor of cell biology in the Department of Molecular Biomedical Sciences in the NC State
NC State Researcher Tracks Cellular Mechanisms that Lead to Pulmonary Fibrosis
The following originally appeared in Results, a publication of NC State University’s Research, Innovation and Economic Development Program. As a marathon runner, Dr. Phil Sannes knows the value of strong, healthy lungs. As a professor in the Department of Molecular Biomedical Sciences in the College of Veterinary Medicine and a researcher with the Center for Comparative Medicine and