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Clay B. Marsh, MD Professor Director-Pulmonary, Allergy, Critical Care & Sleep Medicine 201 Davis Heart and Lung Research Institute 473 West 12th Avenue
Columbus, OH 43210
Phone: (614) 247-7707 Clinical Interest
Pulmonary Fibrosis Research Interests
MicroRNA Regulation of Gene Transcription in the Lung;
Role of Stress and Depression in Advanced Lung Disease
NetWellness
Dr. Marsh is a NetWellness expert in pulmonary fibrosis and lung and respiratory diseases. NetWellness is an unbiased, non-profit consumer health information service delivered on the Web through the collaborative efforts of the University of Cincinnati, The Ohio State University, and Case Western Reserve University. Since 1995, NetWellness’ mission has been to provide the highest quality health information and education to meet the growing trend of the public to use the Internet for medical and health information. Health care professionals, including physicians, nurses, dietitians, pharmacists, dentists, genetic counselors, optometrists, psychologists, psychiatrists, physical therapists, speech and hearing therapists, occupational therapists, athletic trainers, and social workers answer consumer questions and provide current health information.
Dr. Marsh is a Professor of Medicine and Director of the Division of Pulmonary, Allergy, Critical Care & Sleep Medicine (Department of Internal Medicine), Director of the Center for Critical Care, Deputy Director, Davis Heart and Lung Research Institute for Lung Research and Vice Chair for Research in the Department of Internal Medicine.
Dr. Marsh did his undergraduate training in Biology and completed medical school at West Virginia University. He matriculated to Ohio State University in 1985 and completed his training in Internal Medicine in 1988. In 1988-89 he spent a year in the research laboratory of Dr. Mark Wewers in Pulmonary Critical Care Medicine and then served as Chief Medical Resident for the Department of Internal Medicine from 1989-1990. Following this year, he completed his fellowship in Pulmonary and Critical Care Medicine in 1992 and elected to spend an additional 3 years in the laboratory. In 1995, he became an Assistant Professor of Medicine in the Division of Pulmonary and Critical Care Medicine. In 1998, he was promoted to the rank of Associate Professor of Medicine, and promoted to Professor of Medicine in 2004. He was appointed Associate Director for Educational and Research Initiatives for the DHLRI in 2000 and was also appointed Vice Chair for Research, Department of Internal Medicine, 2000. He is cross-appointed as Professor in Molecular Virology, Immunology and Medical Genetics; OSU Biochemistry Program; Veterinary Biosciences; Pathology; Integrated Biomedical Graduate Program; and Molecular and Cellular Developmental Biology.
In 1988, Dr. Marsh was named Outstanding Teacher in the Internal Medicine training program and was also the recipient of a Medical School Teaching Award. In 1992, he received the James Warren Research Award as the outstanding research fellow in the Department. In 1997-98 he was named the Teacher of the Year by the Department of Internal Medicine. In 1999 and 2005, he was recognized by the Landacre medical student research society as an honorary member for contributions to medical science. Dr. Marsh is a member of the American Society of Clinical Investigation; The American Thoracic Society; the American Association for the Advancement of Science; The American Association of Immunologists; and The International Cytokine Society. He is also a member of AOA. He is also immediate past Chair of the Scientific Committee of the Sarnoff Foundation for Cardiovascular Sciences and is the Chair of the Board of Directors for this organization in 2007-2008. He is also the leader of the signature program in Critical Care Medicine and Director of the Cornerstone research program in Inflammation, Immune Repair and Fibrosis in the Davis HLRI. Interest and Subspecialty Our laboratory focuses on the role of the growth factor macrophage colony-stimulating factor (M-CSF) and mononuclear phagocytes in health and disease. We are interested in understanding the native signaling pathways and proteins responsible for mononuclear phagocyte survival and differentiation and apply this information to understand how this is dysregulated in diseases, including lung disease, heart disease and cancer. We are also interested in the mechanisms of repair, remodeling and angiogenesis related to mononuclear phagocytes in pulmonary fibrosis. Translationally, we are interested in lung fibrosis, emphysema, and cancer. In addition, because of the important role of these cells in inflammation, we have been involved with studies in coronary artery disease and transplant vascular disease. Lastly, we found an important role for mononuclear phagocytes in the regulation of VEGF production and biological activity and are interested in how this may apply to cancer growth and spread. We are also dedicated to growing translational research and personalized/predictive health care in the areas of critical care, respiratory disease, trauma, burn and wound healing and explore the influence of Stress/Depression on driving advanced lung and critical care disease. Our laboratory is divided into five modules related to monocyte/macrophage biology: 1) Signaling and cell survival/differentiation
2) Lung repair, remodeling and fibrosis
3) Angiogenesis
4) The role of stress/depression in lung disease and cancer
5) MicroRNA in lung and critical care disease My goal is to help people in our program grow and become independent scientists/investigators. We hope to uncover basic mechanisms underlying mononuclear phagocyte-induced inflammation using a phenotype-based patient-centered approach and translate these findings to novel approaches to identifying, classifying, treating and preventing disease.
Publications
1. Tridandapani S, Wardrop R, Baran C, Wang Y, Opalek, JM, Caligiuri MA, Marsh CB. TFG-?1 Suppresses Myeloid Fc??Receptor Function by Regulating the Expression and Function of the Common ?-Subunit. 2003. Journal of Immunology 170: 4572-4577. 2. Eubank T, Galloway M, Montague CM, Waldman WJ, Marsh CB. M-CSF induces vascular endothelial growth factor production and angiogenic activity from human monocytes. 2003. The Journal of Immunology 171:2637-2643. 3. Baran CP, Tridandapani S, Helgason CD, Humphries RK, Krystal G, Marsh CB. The Inositol 5’-Phosphatase SHIP-1 and the Src Kinase Lyn Negatively Regulate Macrophage Colony-stimulating Factor-Induced Akt Activity. 2003. Journal of Biological Chemistry Oct 3; 278 (40):38628-38636. 4. Jin M, Opalek J, Marsh C, and Wu H. Proteome Comparison of Alveolar Macrophages with Monocytes Reveals Distinct Protein Characteristics. 2004. American Journal of Respiratory and Molecular Cell Biology. May 6 (Epub ahead of print). Sep;31(3):322-9. 5. Baran C, Graham MM, Tridandapani S, Marsh CB, The role of ROS and RNS in monocyte survival, Current Pharmaceutical Design 2004. 10:855-866. 6. Wang Y, Tridandapani S, Marsh CB. SHIP2 is Recruited to the Cell Membrane upon M-CSF Stimulation and Regulates M-CSF-Induced Signaling 2004. The Journal of Immunology, Dec 1;173(11):6820-30. 7. Eubank TD, Roberts R, Galloway M, Wang Y, Cohn DE, Marsh CB. GM-CSF induces expression of soluble VEGF receptor-1 from human monocytes and inhibits angiogenesis in mice. 2004. Immunity, Dec;21(6):831-42. 8. Wu HM, Jin M, Marsh CB. Towards functional proteomics of alveolar macrophages. 2005. American Journal of Physiology: Lung Cellular and Molecular Physiology. 2005. Apr;288(4):L585-95. 9. Jing A, Maturu A, Johnson W, Wang Y, Marsh CB and Tridandapani S. The Inositol Phosphatase SHIP-2 Downregulates Fc?R-Mediated Phagocytosis in Murine Macrophages Independently of SHIP-1. 2005. Blood September 22, 2005. 10. Ai J, Maturu A, Johnson W, Wang Y, Marsh CB, Tridandapani S. The inositol phosphatase SHIP-2 down-regulates Fc?R-mediated phagocytosis in murine macrophages independently of SHIP-1. Blood. 2006 Jan 15;107(2):813-20. 11. Bhatt N, Baran CP, Magro C, Allen JN, Marsh CB. Promising pharmacologic innovations in treating pulmonary fibrosis. Current Opinions in Pharmacology. 2006. Jun;6(3):284-92. 12. Magro C, Waldman J, Opalek J, Allen J, Marsh CB. Idiopathic pulmonary fibrosis: is it really a forme fruste of limited autoimmune disease related to anti-endothelial cell antibodies? A hypothesis. Human Immunology 2006, 67(4-5):284-97. 13. Montague CR, Hunter MG, Gavrilin MA, Philllips GS, Goldschmidt-Clermont PJ, Marsh CB. Activation of estrogen receptor-? reduces aortic smooth muscle cell differentiation. Circualtion Research. 2006, 1:99(5):477-84. 14. Wang Y, Ziegler MM, Lam GK, Hunter MG, Eubank TD, Khramtsov VV, Tridandapani S, Marsh CB. The Role of the NADPH Oxidase Complex, p38 MAPK, and Akt in Regulating Human Monocyte/Macrophage Survival. American Journal of Respiratory Cell and Molecular Biology. 2006, Jan;36(1):68-77. Epub 2006 Aug 24. 15. Jin M, Diaz PT, Bourgeois T, Eng C, Marsh CB, Wu H. Two-dimensional gel proteome reference map of blood monocytes. Proteome Science. 2006 Sep 1;4:16. 16. Yang EV, Sood AK, Chen M, Li Y, Eubank TD, Marsh CB, Jewell S, Flavahan NA, Morrison C, Yeh PE, Lemeshow S, Glaser R. Norepinephrine up-regulates the expression of vascular endothelial growth factor, matrix metalloproteinase (MMP)-2, and MMP-9 in nasopharyngeal carcinoma tumor cells. Cancer Research. 2006 Nov 1;66(21):10357-64. 17. Baran CP, Opalek JM, McMaken S, Newland CA, O’Brien Jr JM, Hunter MG, Bringardner BD, Monick MM, Brigstock DR, Stromberg PC, Hunninghake GW and Marsh CB. Important roles for M-CSF, CCL2 and mononuclear phagocytes in the pathogenesis of pulmonary fiborsis. Am J Respir Crit Care Med. 2007 Apr 12 (Epub ahead of print).
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