Richard Austin

, PhD

Professor
Pathology and Molecular Medicine

Division: Molecular Medicine

Henderson General Hospital
Hamilton, Ontario
905-527-2299 ext. 42628 (lab 43557)
raustin@thrombosis.hhscr.org

Education and Professional Standing

• PhD, Medical Sciences, McMaster University, 1991
• MSc, Medical Sciences, McMaster University, 1986
• BSc Hons. Biology, 1984

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Interests

The major focus of my research is on various aspects of the molecular biology of vascular disease and thrombosis. Other interests include the role of endoplasmic reticulum stress in human disease.

Specific studies include:

• Investigation of the mechanisms responsible for homocysteine-induced atherosclerosis and thrombosis.
• Examining the regulation of cell-surface tissue factor activity.
• Identifying the cellular role of dystrophin isoforms.

A wide range of molecular biological techniques are used including, RNA and DNA isolation and purification, agarose and polyacrylamide gel electrophoresis, Northern and Western blotting, polymerase chain reaction, eukaryotic and prokaryotic protein expression systems, mRNA differential display, and screening of cDNA microarrays.

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Selected Publications

• Lawrence de Koning AB, Werstuck GH, Zhou J, Austin RC. Hyperhomocysteinemia and its role in the development of atherosclerosis. Clin Biochem. 2003 Sep;36(6):431-41.
• Watson LM, Chan AKC, Berry L, Li J, Sood SK, Dickhout JG, Xu L, Werstuck GH, Bajzar L, Austin RC. (2003) Overexpression of the 78-kDa glucose-regulated protein/immunoglobulin binding protein (GRP78/BiP) inhibits tissue factor-dependent thrombin generation. J Biol Chem 278:17438-17447.
• Hossain GS, vanThienen JV, Werstuck G, Zhou J, Sood SK, Dickhout JG, de Koning ABL, Tang D, Wu D, Falk E, Poddar R, Jacobsen DW, Zhang K, Kaufman RJ, Austin RC. (2003) TDAG51 is induced by homocysteine, promotes detachment-mediated programmed cell death and is associated with the development of atherosclerosis in hyperhomocysteinemia. J Biol Chem. 2003 Aug 8;278(32):30317-27.
• Werstuck GH, Lentz SR, Dayal S, Hossain GS, Sood SK, Shi YY, Zhou J, Maeda N, Krisans SK, Malinow MR, Austin RC. (2001) Homocysteine-induced endoplasmic reticulum stress causes dysregulation of the cholesterol and fatty acid biosynthetic pathways. J Clin Invest 107:1263-1273.
• Zhou J, Moller J, Danielsen CC, Bentzon J, Ravn HB, Austin RC, Falk E. (2001) Dietary supplementation with methionine and homocysteine promotes atherosclerosis but not plaque rupture in ApoE-deficient mice. Arterioscler Thromb Vasc Biol 21:1470-1476.
• Outinen PA, Sood SK, Pfeifer SI, Pamidi S, Podor TJ, Li J, Weitz JI, Austin RC. (1999) Homocysteine-induced endoplasmic reticulum stress and growth arrest leads to specific changes in gene expression in human vascular endothelial cells. Blood 94:959-967.