Charles E. McCall, MD

Professor, Internal Medicine - Molecular Medicine, Microbiology and Immunology, and Infectious Diseases

Director, Wake Forest University Translational Sciences Institute

Email: chmccall@wfubmc.edu

Education:

Wake Forest University Medical School (then Bowman Gray School of Medicine), MD, 1961

Harvard Medical School, Boston City Hospital, Residency 1961-1963

Center for Disease Control, Epidemic Intelligence Officer 1963-1965

Harvard Medical School, Fellowship, Infectious Diseases 1966-68

The Royal Society of Medicine (London), Fellowship, 1973

Board Certification:

American Board of Internal Medicine, 1968

American Board of Internal Medicine - Infectious Disease, 1972

American Board of Internal Medicine - Allergy and Immunology, 1974

Research Interests:

Epigenetics and reprogramming of gene expression in severe systemic inflammation.

Current Research:

The general objective of our laboratories’ research is to investigate the epigenetics and bioenergetics of severe systemic inflammation (SSI), a highly destructive pathology. Our research uses human and animals models and cell culture, with application of biochemical and genetic tools. We focus on three distinct areas in the pathophysiology of SSI, which are not mutually exclusive: 1) Epigenetic silencing through the interplay of transcription factors, histone and DNA modifiers to condense chromatin to the state of heterochromatin; 2) differential expression and function of micro RNAs in SSI that independently regulate protein synthesis; 3) cellular bioenergetics of SSI as linked to mitochondria and autophagy. Our general hypothesis is that alterations and gene expression and cell energetic combine to regulate the SSI phenotypes. The laboratories are supported by NIH grants. 

Recent Publications:

Chen X, Yoza BK, El Gazzar M, Hu JYQ, Cousart SL, McCall CE. RelB sustains IkappaBalpha expression during endotoxin tolerance. Clin Vaccine Immunol 2009;16(1):104-110.

El Gazzar M, Yoza BK, Chen X, Garcia BA, Young NL, McCall CE. Chromatin-specific remodeling by HMGB1 and linker histone H1 silence Proinflammatory genes during endotoxin tolerance. Mol Cell Biol 2009;29(7):1959-1971.

Hoth JJ, Wells JD, Brownlee NA, Hiltbold EM, Meredith JW, McCall CE. Toll-like receptor 4-dependent responses to lung injury in a murine model of pulmonary contusion. Shock 2009;31(4):376-381.

El Gazzar M, Yoza BK, Chen X, Hu J, Hawkins G, McCall CE. G9a and HP1 couple histone and DNA methylation to TNFalpha transcription silencing during endotoxin tolerance. J Biol Chem. 2008 Sep 22. 2008;283(47):32198-208.

McCall CE, Yoza BK. Gene silencing in severe systemic inflammation. Am J Respir Crit Care Med. 175(8):763-7. 2007.

Yoza BK, Hu JY, Cousart SL, Forrest LM, McCall CE. Induction of RelB Participates in Endotoxin Tolerance. J Immunol. 2006 15;177(6):4080-5, 2006.

Chan C, Li L, McCall CE, Yoza BK Endotoxin Tolerance Disrupts Chromatin Remodeling and NFKB Transactivation of the IL-1 β promoter. J Immunol. 175: 461-8, 2005.

Publications:
For a listing of additional publications, refer to PubMed, a service provided by the National Library of Medicine