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   Jayme Borensztajn, MD, PhD
   Professor of Pathology
   Director, Clinical Chemistry Laboratory        
   Tarry 7-751
   303 E. Chicago Avenue  
   Chicago, IL  60611

   jbb@northwestern.edu  

Phone:  (312) 503-8590
Fax:  (312) 503-8240  

Clinical Pathology
Chemistry  

Medical School

Faculdade Nacional de Medicina (Brazil)

Site of Residency

University of Chicago Medical Center   /  University of Oxford (PhD; Biochemistry)


Research Interests

Atherosclerosis - the main cause of cardiovascular disease - is now understood to result from a chronic inflammation of large arterial blood vessels superimposed upon by hyperlipidemias, as well as other risk factors. PPAR - a transcription factor belonging to a sub-family of nuclear hormone receptors – functions in regulating the expression of multiple genes involved in metabolic and inflammatory processes. Using mice as the experimental model, the aim of our research is to determine whether pharmacological activation of PPAR in arterial cells, and the resulting expression of anti-inflammatory genes, can prevent, retard or reverse the development of atherosclerotic lesions.

Selected Publications

Homanics GE, de Silva HV, Osada J, Zhang SH, Wong H, Borensztajn J, Maeda N. Mild dyslipidemia in mice following targeted inactivation of the hepatic lipase gene. J. Biol. Chem. 270: 2974-2980, 1995.

Crawford SE,. Borensztajn J. Plasma clearance and liver uptake of chylomicron remnants generated by hepatic lipase lipolysis: evidence for a lactoferrin-sensitive and apoprotein E-independent pathway. J. Lipid Res. 40: 797-805, 1999.

Fu T, Borensztajn J. Macrophage uptake of low-density lipoprotein bound to aggregated C-reactive protein: possible mechanism of foam-cell formation in atherosclerotic lesions. Biochem. J. 366: 195-201, 2002

Fu T, Kashireddy P, Borensztajn J. The PPAR alpha agonist ciprofibrate aggravates the hypercholesterolemia and accelerates the development of atherosclerosis of mice lacking apolipoprotein E. Biochem. J. 373, 941-947, 2003.

Fu T, Kozarsky KF, Borensztajn J. Overexpression of SR-BI by adenoviral vector reverses the fibrateinduced hypercholesterolemia of apolipoprotein E-deficient mice. J. Biol. Chem. 278, 52559-52563, 2003.

Fu T, Mukhopadhyay D, Davidson NO, Borensztajn J. The peroxisome proliferator-activated receptor a (PPAR a) agonist ciprofibrate inhibits apolipoprotein B mRNA editing in low density lipoprotein receptor-deficient mice: effects on plasma lipoproteins and the development of atherosclerotic lesions. J Biol Chem 279:28662-28669, 2004.

Fu T, Borensztajn J. Simvastatin causes the formation of cholesterol-rich remnants in mice lacking apoE. Biochem Biophys Res Commun 341:1172-1176, 2006

Rinella ME, Elias MS, Smolak RR, Fu T, Borensztajn J, Green RM.. Mechanisms of steatohepatitis in mice fed a lipogenic methionine choline deficient (MCD) diet. J. Lipid Res. 49: 1068-1076, 2008.


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View more Publications by Jayme Borensztajn, MD, PhD
listed in the National Library of Medicine (PubMed)
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