Michael J. Thomas, PhD

Professor

Locations

Pharmacology and Toxicology

Contact Information

General Interests

Lipidomic Analysis of Lipoproteins

Education

Post doctoral Research Associate, Louisiana State University, 1978
Postdoctoral Research Associate, Michigan State University, 1976
PhD, Chemistry, University of California-Los Angeles, 1973
BS, Chemistry, Indiana University, 1969

Biography

Honors and Awards

Chemistry with Honors, Indiana University - 1969

Research Interests

Two areas of specialized interest are improving lipidomic analysis of lipoproteins and determining the three-dimensional structure apolipoprotein A-I in lipoproteins. We have developed chemical cross-linking methods employed with mass spectrometry to assess the conformation of apolipoprotein A-I in both the lipid-free and lipid bound forms. I am also interested in the application of mass spectrometry to biomedical and biochemical studies. We are constantly working to implement simple mass spectrometric procedures for performing experiments and quantifying the results.

Recombinant LCAT (Lecithin:Cholesterol Acyltransferase) Rescues Defective HDL (High-Density Lipoprotein)-Mediated Endothelial Protection in Acute Coronary Syndrome.

(Ossoli A, Simonelli S, Varrenti M, Morici N, Oliva F, Stucchi M, Gomaraschi M, Strazzella A, Arnaboldi L, Thomas MJ, Sorci-Thomas MG, Corsini A, Veglia F, Franceschini G, Karathanasis SK, Calabresi L.) Arterioscler Thromb Vasc Biol. 2019 May;39(5):915-924.
Interleukin-17 Drives Interstitial Entrapment of Tissue Lipoproteins in Experimental Psoriasis.

(Huang LH, Zinselmeyer BH, Chang CH, Saunders BT, Elvington A, Baba O, Broekelmann TJ, Qi L, Rueve JS, Swartz MA, Kim BS, Mecham RP, Wiig H, Thomas MJ, Sorci-Thomas MG, Randolph GJ.) Cell Metab. 2019 Feb 05;29(2):475-487.e7.
High-Density Lipoprotein Functionality as a New Pharmacological Target on Cardiovascular Disease: Unifying Mechanism That Explains High-Density Lipoprotein Protection Toward the Progression of Atherosclerosis.

(Favari E, Thomas MJ, Sorci-Thomas MG.) J Cardiovasc Pharmacol. 2018 06;71(6):325-331.
Deactivation of 12(S)-HETE through (ω-1)-hydroxylation and β-oxidation in alternatively activated macrophages.

(Kriska T, Thomas MJ, Falck JR, Campbell WB.) J Lipid Res. 2018 04;59(4):615-624.
Apolipoprotein AI prevents regulatory to follicular helper T cell switching during atherosclerosis.

(Gaddis DE, Padgett LE, Wu R, McSkimming C, Romines V, Taylor AM, McNamara CA, Kronenberg M, Crotty S, Thomas MJ, Sorci-Thomas MG, Hedrick CC.) Nat Commun. 2018 03 15;9(1):1095.
A consensus model of human apolipoprotein A-I in its monomeric and lipid-free state.

(Melchior JT, Walker RG, Cooke AL, Morris J, Castleberry M, Thompson TB, Jones MK, Song HD, Rye KA, Oda MN, Sorci-Thomas MG, Thomas MJ, Heinecke JW, Mei X, Atkinson D, Segrest JP, Lund-Katz S, Phillips MC, Davidson WS.) Nat Struct Mol Biol. 2017 Dec;24(12):1093-1099.
Anti-inflammatory liaisons: T regulatory cells and HDL.

(Sorci-Thomas MG, Thomas MJ.) J Lipid Res. 2017 08;58(8):1491-1492.
AIBP, NAXE, and Angiogenesis: What's in a Name?

(Sorci-Thomas MG, Thomas MJ.) Circ Res. 2017 05 26;120(11):1690-1691.
S1P in HDL promotes interaction between SR-BI and S1PR1 and activates S1PR1-mediated biological functions: calcium flux and S1PR1 internalization.

(Lee MH, Appleton KM, El-Shewy HM, Sorci-Thomas MG, Thomas MJ, Lopes-Virella MF, Luttrell LM, Hammad SM, Klein RL.) J Lipid Res. 2017 02;58(2):325-338.
The Role of Sialylated Glycans in Human Platelet Endothelial Cell Adhesion Molecule 1 (PECAM-1)-mediated Trans Homophilic Interactions and Endothelial Cell Barrier Function.

(Lertkiatmongkol P, Paddock C, Newman DK, Zhu J, Thomas MJ, Newman PJ.) J Biol Chem. 2016 Dec 09;291(50):26216-26225.
Lipid-Free Apolipoprotein A-I Reduces Progression of Atherosclerosis by Mobilizing Microdomain Cholesterol and Attenuating the Number of CD131 Expressing Cells: Monitoring Cholesterol Homeostasis Using the Cellular Ester to Total Cholesterol Ratio.

(Kaul S, Xu H, Zabalawi M, Maruko E, Fulp BE, Bluemn T, Brzoza-Lewis KL, Gerelus M, Weerasekera R, Kallinger R, James R, Zhang YS, Thomas MJ, Sorci-Thomas MG.) J Am Heart Assoc. 2016 11 07;5(11).
Nogo-B receptor deficiency increases liver X receptor alpha nuclear translocation and hepatic lipogenesis through an adenosine monophosphate-activated protein kinase alpha-dependent pathway.

(Hu W, Zhang W, Chen Y, Rana U, Teng RJ, Duan Y, Liu Z, Zhao B, Foeckler J, Weiler H, Kallinger RE, Thomas MJ, Zhang K, Han J, Miao QR.) Hepatology. 2016 11;64(5):1559-1576.

Michael J. Thomas, PhD