Clay B. Marsh, MD

Professor
Sr Assoc VP for Health Sciences Research
Vice Dean of Research for the College of Medicine
Executive director of the Center for Personalized Health Care

201 Davis Heart and Lung Research Institute
473 West 12th Avenue
Columbus, OH 43210
Phone: (614) 293-9309

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 Sr Assoc VP for Health Sciences Research, Vice Dean of Research for the College of Medicine, and Executive Director of the Center for Personalized Health Care.

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 past Chair of the Scientific Committee of the Sarnoff Foundation for Cardiovascular Sciences and past 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

My laboratory focuses on the mechanisms underlying human health and disease. As part of our approach, we have projects ranging from biomarker discovery using microRNA molecules to define genetic pathways and proteins important in tissue environments including breast cancer, lung cancer, lung fibrosis, and melanoma; cell biology studying the growth factors macrophage colony-stimulating factor (M-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) and mononuclear phagocytes in tissue environments including breast cancer, melanoma; stress pathways and human disease; and systems biology approaches to defining what networks underlie health.

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. We are also interested in the mechanisms of repair and remodeling related to mononuclear phagocytes in the lung and in wound repair. Translationally, we are interested in lung fibrosis and lung injury. In addition, because of the important role of these cells in inflammation, we have been involved with studies in emphysema, breast cancer and transplant vascular disease. In the area of breast cancer, 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 have also started a program in translational research focusing on defining the underlying genetics and environment effects on health and disease to develop the tools for predictive and personalized health care. We are adapting systems biology approaches to solving complicated phenotype questions for patients.

My laboratory is divided into five modules:

1)    Systems Biology and genetics

2)    Signaling and cell survival/differentiation

3)    Lung repair and remodeling

4)    Angiogenesis in breast cancer and melanoma

5)    Stress and depression in human health, aging and disease

6)    Translational Research in pulmonary fibrosis and breast cancer

My goal is to help people in my laboratory grow and become independent scientists/investigators. In addition, I hope that we uncover some of the basic mechanisms underlying mononuclear phagocyte-induced inflammation and translate these findings to novel approaches to patients with 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).

18. Opalek JM, Ali NA, Lobb JM, Hunter MG, Marsh CB.  Alveolar Macrophages Lack CCR2 Expression and do not Migrate to CCL2. Journal of Inflammation. 4(1):19, 2007.

19. Bringardner BD, Baran CP, Eubank TD, Marsh CB. The role of inflammation in the pathogenesis of idiopathic pulmonary fibrosis. Antioxid Redox Signal. 2008 Feb;10(2):287-302.

20. Hunter M, Wang Y, Eubank T, Baran C, Nana-Sinkam P, Marsh C. Survival of monocytes and macrophages and their role in health and disease. Invited review; Frontiers in Bioscience 2008, in press.
 
21. Crawford, M., Brawner, E., Batte, K., Yu, L., Hunter, MG, Otterson, GA, Nuovo, G., Marsh, CB, Nana-Sinkam, SP.MicroRNA-126 inhibits invasion in non-small cell lung carcinoma cell lines. Biochem Biophys Res Commun. 2008 Sep 5;373(4):607-12.
 
22. Nana-Sinkam, S.P., Hunter, M.G., Nuovo, G.J., Schmittgen, T.D., Gelinas, R., Galas, D., Marsh, C.B., Integrating the microRNome into the study of lung disease, American Journal of Respiratory and Critical Care Medicine, 2008, in press

23. Piper-Hunter M, Ismail N, Zhang X, Aguda BD, Lee EJ, Yu L, Xiao T, Schafer J, Lee M-L T, Schmittgen TD, Nana-Sinkam SP, Jarjoura D , Marsh CB. "Detection of microRNA Expression in Human Peripheral Blood Microvesicles." PLos One 2008, in press

24. Aguda B, Kim Y, Piper-Hunter M, Friedman A, Marsh CB. MicroRNA Regulation of a Cancer Network: Consequences of the Feedback Loops Involving miR-17-92, E2F, and Myc, PNAS 2008, in press.

Marsh Lab 2008-2009