• 5385 Citations
  • 40 h-Index
1989 …2023
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Personal profile

Research interests

Dr. Thomas Ma’s research focus for more than 25 years has been to delineate the role of defective intestinal epithelial tight junction (TJ) barrier in the pathogenesis of inflammatory bowel disease (IBD).

Long-term goals of the Ma Laboratory have been:

  • to delineate the intracellular processes that regulate the intestinal epithelial TJ barrier under normal physiological conditions;
  • to elucidate the pathogenic mechanism involved in dysregulation of intestinal TJ barrier in IBD; and
  • to discover novel therapeutic agents to enhance the intestinal TJ barrier during disease states.

Ongoing research efforts have resulted in a number of important scientific advancements that have impacted the current understanding of the intestinal TJ barrier regulation in health and in disease states.

The laboratory has extensive expertise delineating the intracellular and molecular mechanisms of intestinal TJ barrier regulation in in-vitro (cell-culture) and in-vivo (live mouse intestinal permeability studies) models, using cutting-edge cell biology and molecular approaches. Dr. Ma’s research has been continuously funded since 1990 by VA and NIH grants to study the mechanisms that regulate the intestinal TJ barrier and intestinal inflammation.

In addition to his own work, Dr. Ma has chaired several NIH and Veterans Affairs study sections and panels. He also serves or has served on the editorial board or as a reviewer for more than 25 journals.

Clinical interests

Consistent with his research interests, Dr. Thomas Ma’s clinical expertise is in the management of inflammatory bowel disease. He has been involved in number of clinical trials and investigator-initiated clinical studies related to defects in the intestinal barrier in inflammatory bowel disease, necrotizing enterocolitis and alcoholic hepatitis.

Teaching and educational interests

Dr. Thomas Ma has mentored undergraduate students, graduate students, medical students, postdoctoral research fellows, gastroenterology fellows and junior faculty throughout his career. He has moderated and/or organized educational symposia at the institutional, regional and national levels.

Professional information

Diplomate, American Board of Internal Medicine, 1988

Member, American Gastroenterological Association, 1988 to present

Diplomate, American Board of Gastroenterology, 1991, 2001 and 2013

Member, American Association for the Advancement of Science, 1994 to present

Fellow, American College of Gastroenterology, 1999 to present

Fellow, American College of Physicians – American Society of Internal Medicine, 2003 to present

Member, American Physiological Society, 2005 to present

Education/Academic qualification

Gastroenterology, Fellowship, University of California Irvine School of Medicine

… → 1990

Postdoctoral Research Fellowship, University of California Irvine School of Medicine

… → 1990

Internal Medicine, Residency, Robert Wood Johnson Medical School

… → 1987

Medicinal Chemistry, PhD, Virginia Commonwealth University

… → 1985

MD, The Medical College of Virginia

… → 1983

Biology/General Science, BS, Fordham University

… → 1978

External positions

Editor in Chief, World Journal of Gastrointestinal Pathophysiology

20112020

Fingerprint Dive into the research topics where Thomas Ma is active. These topic labels come from the works of this person. Together they form a unique fingerprint.

  • 5 Similar Profiles
Tight Junctions Medicine & Life Sciences
Permeability Medicine & Life Sciences
Myosin-Light-Chain Kinase Medicine & Life Sciences
Occludin Medicine & Life Sciences
Epithelial Cells Medicine & Life Sciences
Monolayers Chemical Compounds
Interleukin-1 Medicine & Life Sciences
Caco-2 Cells Medicine & Life Sciences

Network Recent external collaboration on country level. Dive into details by clicking on the dots.

Projects 1989 2023

Tight Junctions
Probiotics
Bacteria
Permeability
Liver
Tight Junctions
Inflammation
Inflammatory Bowel Diseases
Myosin-Light-Chain Kinase
Animal Models
Tight Junctions
Lipopolysaccharides
Permeability
Myosin-Light-Chain Kinase
Toll-Like Receptor 4

Autophagy and Crohn's Disease

Ma, T. & Deretic, V.

National Institutes of Health

9/26/098/31/12

Project: Research project

Autophagy
Crohn Disease
Mucosal Immunity
Inflammatory Bowel Diseases
Genes

Research Output 1989 2019

  • 5385 Citations
  • 40 h-Index
  • 85 Article
  • 3 Chapter
  • 3 Letter
  • 3 Review article

Intestinal epithelial tight junction barrier regulation by autophagy-related protein ATG6/beclin 1

Wong, M., Ganapathy, A. S., Suchanec, E., Laidler, L., Ma, T. & Nighot, P., May 1 2019, In : American Journal of Physiology - Cell Physiology. 316, 5, p. C753-C765

Research output: Contribution to journalArticle

Tight Junctions
Occludin
Autophagy
Caco-2 Cells
Endocytosis

Investigating intestinal permeability and gut microbiota roles in acute coronary syndrome patients

Alhmoud, T., Kumar, A., Lo, C. C., Al-Sadi, R., Clegg, S., Alomari, I., Zmeili, T., Gleasne, C. D., Mcmurry, K., Dichosa, A. E. K., Vuyisich, M., Chain, P. S. G., Mishra, S. & Ma, T., Aug 1 2019, In : Human Microbiome Journal. 13, 100059.

Research output: Contribution to journalArticle

Open Access
Acute Coronary Syndrome
Permeability
Proteobacteria
Lipopolysaccharides
Dysbiosis
3 Citations (Scopus)

Lipopolysaccharide-Induced Increase in Intestinal Permeability Is Mediated by TAK-1 Activation of IKK and MLCK/MYLK Gene

Nighot, M., Rawat, M., Al-Sadi, R., Castillo, E. F., Nighot, P. & Ma, T., Apr 1 2019, In : American Journal of Pathology. 189, 4, p. 797-812 16 p.

Research output: Contribution to journalArticle

Myosin-Light-Chain Kinase
Tight Junctions
Lipopolysaccharides
Permeability
Genes
1 Citation (Scopus)

MMP-9-induced increase in intestinal epithelial tight permeability is mediated by p38 kinase signaling pathway activation of MLCK gene

Al-Sadi, R., Youssef, M., Rawat, M., Guo, S., Dokladny, K., Haque, M., Watterson, M. D. & Ma, T. Y., Feb 2019, In : American Journal of Physiology - Gastrointestinal and Liver Physiology. 316, 2, p. G278-G290

Research output: Contribution to journalArticle

Myosin-Light-Chain Kinase
MAP Kinase Signaling System
Matrix Metalloproteinase 9
Permeability
Tight Junctions
9 Citations (Scopus)

Expression of programmed death-ligand 1 by human colonic CD90+ stromal cells differs between ulcerative colitis and Crohn's disease and determines their capacity to suppress Th1 cells

Beswick, E. J., Grim, C., Singh, A., Aguirre, J. E., Tafoya, M., Qiu, S., Rogler, G., McKee, R., Samedi, V., Ma, T. Y., Reyes, V. E., Powell, D. W. & Pinchuk, I. V., May 30 2018, In : Frontiers in immunology. 9, MAY, 1125.

Research output: Contribution to journalArticle

Th1 Cells
Stromal Cells
Ulcerative Colitis
Crohn Disease
Fibroblasts