Marc Peters-Golden, M.D.

Professor of Internal Medicine, Division of Pulmonary and Critical Care Medicine
Accepting Students

Biography

Dr. Marc Peters-Golden is a physician-scientist and Professor of Internal Medicine in the Division of Pulmonary and Critical Care Medicine. He was the Division's Fellowship Program Director from 1996-2011 and currently serves as Associate Program Director for Research Training. He has also served as Associate Director of the Division's T32 NIH Postdoctoral Research Training Grant.

He joined the faculty at UM in 1984 after completing his M.D. at Duke University School of Medicine, his residency in Internal Medicine at Tufts-New England Medical Center, and his clinical and research training in Pulmonary Diseases at Johns Hopkins University.

He is an elected member of the American Society for Clinical Investigation and the Association of American Physicians. He is a recipient of the American Thoracic Society's Recognition Award for Scientific Achievement.

Research Interests

My research centers on the molecular and cellular biology of lung injury, inflammation, immunity, repair, and fibrosis. Using normal cells, cells from diseased patients, and animal models of disease, we study the biology of lung macrophages and other immune cells, epithelial cells, and fibroblasts. We are particularly interested in receptors, mediators, cell signaling, and transcriptional programs that control cell fate and function. Ongoing projects include: 1) the role of extracellular vesicles as vectors for cell-cell communication in the lung; 2) mechanisms controlling alveolar macrophage proliferation; 3) the role of macrophages in allergic inflammation; 4) transcriptional programs in fibroblasts that govern proliferation, collagen synthesis, and myofibroblast differentiation. Our ultimate goal is to gain novel insights into lung homeostasis and disease pathogenesis, and to identify new strategies for therapeutic targeting. Mentoring is an important focus of mine, and my laboratory consists of a highly interactive and collaborative group of M.D. and Ph.D. trainees from around the world.

Research Opportunities for Rotating Students

1. Extracellular vesicles as vectors of cell-cell communication in the lung.
We have recently shown that alveolar macrophages secrete suppressors of cytokine signaling (SOCS) in extracellular vesicles, which can be taken up by epithelial cells to inhibit cytokine-induced JAK-STAT inflammatory signaling (Bourdonnay E, J Exp Med 2015;212(5):729-42). Secretion by alveolar macrophages and uptake by epithelial cells are both regulated processes, and can be altered in inflammatory conditions. A variety of rotation projects are available to participate in ongoing studies to address the many questions about this phenomenon that remain unanswered.

2. Molecular regulation of lung fibroblast activation.
Fibrotic tissue responses affect virtually all organs and are important causes of morbidity and mortality. Pulmonary fibrosis is a devastating disease. Fibroblasts are the key effector cells of fibrogenesis. We have longstanding research interests in understanding pathways controlling the fibroblast activation phenotype (proliferation, differentiation to myofibroblasts, extracellular matrix deposition and survival), its dysregulation in pulmonary fibrosis, and how it might be reprogrammed. Rotation projects are available to participate in studies of transcriptional regulation of fibroblast programs, expression of endogenous anti-fibrotic molecules, and therapeutic development and testing.

3. Novel insights in asthma pathogenesis.
We have studied various aspects of allergic asthma pathogenesis and airway remodeling due to chronic allergen challenge. A current focus of interest is understanding how alveolar macrophages restrain the development of allergic asthmatic inflammation, including the potential roles of secreted SOCS and prostaglandin E2, and how SOCS secretion is dysregulated in allergic asthma.Rotation projects in these areas may be available.

Publications

http://www.ncbi.nlm.nih.gov/pubmed/?term=peters-golden

Medeiros AI, Serezani CH, Lee SP, Peters-Golden M. Efferocytosis impairs pulmonary macrophage and lung antibacterial function via PGE2/EP2 signaling. J Exp Med 2009 206:61-8.

Kim SH, Serezani CH, Okunishi K, Zaslona Z, Aronoff DM, Peters-Golden M. Distinct protein kinase A anchoring proteins direct prostaglandin E2 modulation of Toll-like receptor signaling in alveolar macrophages. J Biol Chem. 2011;286:8875-83.

Serezani CH, Lewis C, Jancar S, Peters-Golden M. Leukotriene B4 amplifies NF-κB activation in mouse macrophages by reducing SOCS1 inhibition of MyD88 expression. J Clin Invest. 2011;121:671-82.

Zaslona Z, Serezani CH, Okunishi K, Aronoff DM, Peters-Golden M. Prostaglandin E2 restrains macrophage maturation via E prostanoid receptor 2/protein kinase A signaling. Blood. 2012;119:2358-67.

Serezani CH, Kane S, Collins L, Morato-Marques M, Osterholzer JJ, Peters-Golden M. Macrophage Dectin-1 Expression Is Controlled by Leukotriene B4 via a GM-CSF/PU.1 Axis. J Immunol. 2012;189:906-15.

Zasłona Z, Okunishi K, Bourdonnay E, Domingo-Gonzalez R, Moore BB, Lukacs NW, Aronoff DM, Peters-Golden M. Prostaglandin E2 suppresses allergic sensitization and lung inflammation by targeting the E prostanoid 2 receptor on T cells. J Allergy Clin Immunol. 2014; 133(2):379-387.

Penke LRK, Huang SK, White ES, Peters-Golden M. Prostaglandin E2 inhibits ɑ-smooth muscle actin transcription during myofibroblast differentiation via distinct mechanisms of modulation of serum response factor and myocardin-related transcription factor-A. J Biol Chem. 2014; 289(24):17151-17162

DeGraaf AJ, Zaslona Z, Bourdonnay E, Peters-Golden M. Prostaglandin E2 reduces Toll-like receptor 4 expression in alveolar macrophages by inhibition of translation. Am J Respir
Cell Mol Biol. 2014; 51(2); 242-50

Zasłona Z, Przybranowski S, Wilke C, van Rooijen N, Moore BB, Peters-Golden M. Resident alveolar macrophages suppress while recruited monocytes promote allergic lung
inflammation in murine models of asthma. J Immunol. 2014;193(8):4245-53.

Bourdonnay E, Zaslona Z, Penke LRK, Speth JM, Schneider DJ, Przybranowski S, Swanson JA, Freeman CM, Mancuso P, Curtis J, Peters-Golden M. Transcellular delivery
of SOCS proteins from macrophages to epithelial cells blunts inflammatory signaling. J Exp Med 2015;212(5):729-42. [article accompanied by an “Insights” commentary]

Wettlaufer SH, Scott JP, McEachin RC, Peters-Golden M, Huang SK. Myofibroblast dedifferentiation by PGE2 is characterized by reversal of the global transcriptome. Am J Respir Cell Mol Biol 2016; 54(1):114-27.

Speth JM, Bourdonnay E, Penke LRK, Mancuso P, Moore BB, Weinberg JB, Peters-Golden M. Alveolar epithelial cell-derived prostaglandin E2 serves as a request signal for macrophage secretion of suppressor of cytokine signaling 3 during innate inflammation. J Immunol 2016; 196(12):5112-20.

Wettlaufer SH, Scott JP, McEachin RC, Peters-Golden M, Huang SK. Myofibroblast dedifferentiation by PGE2 is characterized by reversal of the global transcriptome. Am J Respir Cell Mol Biol 2016; 54(1):114-27.

Speth JM, Bourdonnay E, Penke LRK, Mancuso P, Moore BB, Weinberg JB, Peters-Golden M. Alveolar epithelial cell-derived prostaglandin E2 serves as a request signal for macrophage secretion of suppressor of cytokine signaling 3 during innate inflammation. J Immunol 2016; 196(12):5112-20. 

Wettlaufer SH, Penke LR, Okunishi K, Peters-Golden M. Distinct PKA regulatory subunits mediate PGE2 inhibition of TGF-1-stimulated collagen I translation and myofibroblast differentiation. Am J Physiol Lung [accepted]