James M May, M.D.

Official Affiliation: Molecular Physiology and Biophysics

Profile

Dr. May's laboratory is involved in three major areas involving antioxidant vitamins and micronutrients: the function of vitamin C in atherosclerosis; study of the role of vitamin C in protection against the oxidant stress of Alzheimer's disease, and study of the antioxidant interactions of selenium and vitamins C and E.

Dr. May's research interests invove the antioxidant effects of vitamins C and E in a variety of cell and animal models. His laboratory has long been active in the study of how vitamin C is taken up, maintained in a reduced form, and how it protects cells against oxidant stress. In the last several years, the effort has targeted the early stages of atherosclerosis, especially related to endothelial dysfunction and the ability of the vitamin to enhance release and function of nitric oxide. More recently, efforts have turned to testing whether the vitamin also plays a role in inhibiting the atherosclerotic process in other cells, including macrophages and vascular smooth muscle cells. The central hypothesis in this work is that the vitamin C transporter is crucial for maintaining high intracellular concentrations of this vitamin. Other functions of vitamin C besides those related to antioxidant mechanisms are also explored, including its role in cell proliferation, differentiation, and collagen formation.

Alzheimer's disease is associated with oxidant stress, and vitamin C has been implicated in clinical studies in protecting against this stress and in slowing progression of the disease. Studies are underway to assess the role of the vitamin in beta-amyloid secretion and action by cultured neuronal cells, and to asses whether dietary manipulation with vitamin C in normal mice and mice unable to synthesize the vitamin can slow the progression of the behavioral changes seen in animals transgenic for amyloid precursor protein and presenilin 1. Both of these proteins are implicated in many patients with Alzheimer's disease.

Selenium is a co-factor for several enzymes with antioxidant function, including glutathione peroxidase and thioredoxin reductase. Dr. May's laboratory showed that the latter enzyme can reduce the oxidized forms of vitamin C back to the reduced form. The ability of this selenoenzyme to recycle vitamin C may provide a missing link between the known ability of vitamin E or selenium to mitigate a deficiency in the other. In cultured cells and in guinea pigs (which can be made deficient in all three factors), studies are underway of the interactions between these factors with regard to cellular metabolism and lipid peroxidation. The approaches used in these studies include HPLC assays of antioxidants, enzyme assays, and assays of lipid peroxidation.

Publications

The following timeline graph is generated from all co-authored publications.

Featured publications are shown below:

  1. Macrophage IKKα Deficiency Suppresses Akt Phosphorylation, Reduces Cell Survival, and Decreases Early Atherosclerosis. Babaev VR, Ding L, Zhang Y, May JM, Lin PC, Fazio S, Linton MF (2016) Arterioscler Thromb Vasc Biol 36(4): 598-607
    › Primary publication · 26848161 (PubMed) · PMC4808396 (PubMed Central)
  2. Recreating blood-brain barrier physiology and structure on chip: A novel neurovascular microfluidic bioreactor. Brown JA, Pensabene V, Markov DA, Allwardt V, Neely MD, Shi M, Britt CM, Hoilett OS, Yang Q, Brewer BM, Samson PC, McCawley LJ, May JM, Webb DJ, Li D, Bowman AB, Reiserer RS, Wikswo JP (2015) Biomicrofluidics 9(5): 054124
    › Primary publication · 26576206 (PubMed) · PMC4627929 (PubMed Central)
  3. Ascorbate reverses high glucose- and RAGE-induced leak of the endothelial permeability barrier. Meredith ME, Qu ZC, May JM (2014) Biochem Biophys Res Commun 445(1): 30-5
    › Primary publication · 24472555 (PubMed) · PMC3955275 (PubMed Central)
  4. Regulation of embryonic neurotransmitter and tyrosine hydroxylase protein levels by ascorbic acid. Meredith ME, May JM (2013) Brain Res : 7-14
    › Primary publication · 24095796 (PubMed) · PMC3849618 (PubMed Central)
  5. Role of vitamin C in the function of the vascular endothelium. May JM, Harrison FE (2013) Antioxid Redox Signal 19(17): 2068-83
    › Primary publication · 23581713 (PubMed) · PMC3869438 (PubMed Central)
  6. Combined vitamin C and E deficiency induces motor defects in gulo(-/-)/SVCT2(+/-) mice. Pierce MR, Diasio DL, Rodrigues LM, Harrison FE, May JM (2013) Nutr Neurosci 16(4): 160-73
    › Primary publication · 23321552 (PubMed) · PMC3869026 (PubMed Central)
  7. Behavioral and monoamine changes following severe vitamin C deficiency. Ward MS, Lamb J, May JM, Harrison FE (2013) J Neurochem 124(3): 363-75
    › Primary publication · 23106783 (PubMed) · PMC3540126 (PubMed Central)

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615-936-1665 (p)
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Keywords & MeSH Terms

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Key: MeSH Term Keyword

Androstenedione Antioxidants Arsenicals Cell Line, Tumor Cell Membrane Central Nervous System Diseases Cytochalasin B Dietary Supplements Erythrocyte Membrane Glucose-6-Phosphate Glucosephosphates Glucose Transporter Type 2 Glucose Transporter Type 4 Glucose Trasport Glycine Hexokinase Hydroxylamine Insulin Action Intracellular Membranes Lipoxygenase Nerve Tissue Proteins Neurites Nitric Oxide Synthase Type III Osmolar Concentration Oxidants Oxidant Stress Palmitic Acid Protective Agents Selecum Severity of Illness Index Spermine Survival Analysis Thermolysin Thiazoles Thiocyanates TOR Serine-Threonine Kinases Vitamin C Vitamin E