Petra Haberzettl, Ph.D.
Assistant Professor of Medicine
Email: Email Dr. Haberzettl
Extensive epidemiological and experimental evidence indicates that obesity is a strong and robust risk factor for the development of type 2 diabetes (T2D) and cardiovascular disease (CVD). Numerous studies have also reported strong associations between ambient air particulate matter (PM) and an increased CVD and T2D risk. However, the mechanism(s) by which obesity and exposure to environmental air pollutants increase the risk of T2D and CVD remain unknown. A common feature underlying these pathological states is a damaged endothelium. Endothelial health is maintained with the participation of endothelial progenitor cells (EPCs). The presence of CVD risk factors has been shown to decrease not only the circulating levels of EPCs, but their ability to stimulate tissue repair, as well. The number of circulating EPCs is decreased in patients with T2D. Furthermore, our previous work demonstrates that exposures to environmental air pollutions decrease the number of circulating EPCs and impair vascular VEGF signaling. Therefore, our ongoing research examines the effects of exposures to fine particulate matter (PM2.5) and volatile (e.g. acrolein) air pollutions as well as obesity on EPC levels and function, endothelial health and vascular resistance to insulin and VEGF to investigate changes leading to the progression of the vascular complications and the metabolic syndrome. Results of these studies will not only advance our understanding of the mechanisms by which environmental air pollutions and obesity affect vascular health, but could also lead to the development of new diagnostic and therapeutic strategies for the treatment and management of CVDs and T2D.
Selected Publications:
- Haberzettl P, Lee J, Duggineni D, McCracken J, Bolanowski D, O'Toole TE, Bhatnagar A, Conklin DJ. Exposure to ambient air fine particulate matter prevents VEGF-induced mobilization of endothelial progenitor cells from the bone marrow. Environ Health Perspect. 2012 Jun;120(6):848-56. Epub 2012 Mar 14.
- Vladykovskaya E, Sithu SD, Haberzettl P, Wickramasinghe NS, Merchant ML, Hill BG, McCracken J, Agarwal A, Dougherty S, Gordon SA, Schuschke DA, Barski OA, O'Toole T, D'Souza SE, Bhatnagar A, Srivastava S. Lipid peroxidation product 4-hydroxy-trans-2-nonenal causes endothelial activation by inducing endoplasmic reticulum stress. J Biol Chem. 2012 Mar 30;287(14):11398-409. Epub 2012 Jan 6.
- Ismahil MA, Hamid T, Haberzettl P, Gu Y, Chandrasekar B, Srivastava S, Bhatnagar A, Prabhu SD. Chronic oral exposure to the aldehyde pollutant acrolein induces dilated cardiomyopathy. Am J Physiol Heart Circ Physiol. 2011 Nov;301(5):H2050-60. Epub 2011 Sep 9.
- Wheat LA,* Haberzettl P, Hellmann J, Baba SP, Bertke M, Lee J, McCracken J, O’Toole TE, Bhatnagar A, Conklin DJ. Acrolein inhalation prevents VEGF-induced mobilization of Flk-1+/Sca-1+ cells in mice. Arterioscler Thromb Vasc Biol. 2011 July; 31(7): 1598–1606.
- O'Toole TE, Hellmann J, Wheat L, Haberzettl P, Lee J, Conklin DJ, Bhatnagar A, Pope CA 3rd. Episodic exposure to fine particulate air pollution decreases circulating levels of endothelial progenitor cells. Circ Res. 2010 Jul 23;107(2):200-3. Epub 2010 Jul 1.
- Keith RJ, Haberzettl P, Vladykovskaya E, Hill BG, Kaiserova K, Srivastava S, Barski O, Bhatnagar A. Aldose reductase decreases endoplasmic reticulum stress in ischemic hearts. Chem Biol Interact. 2009 Mar 16;178(1-3):242-9. Epub 2008 Nov 11.
- Haberzettl P, Vladykovskaya E, Srivastava S, Bhatnagar A. Role of endoplasmic reticulum stress in acrolein-induced endothelial activation. Toxicol Appl Pharmacol. 2009 Jan 1;234(1):14-24. Epub 2008 Oct 7.
- Haberzettl P, Schins RP, Höhr D, Wilhelmi V, Borm PJ, Albrecht C. Impact of the FcgammaII-receptor on quartz uptake and inflammatory response by alveolar macrophages. Am J Physiol Lung Cell Mol Physiol. 2008 Jun;294(6):L1137-48. Epub 2008 Apr 4.
- Haberzettl P, Duffin R, Krämer U, Höhr D, Schins RP, Borm PJ, Albrecht C. Actin plays a crucial role in the phagocytosis and biological response to respirable quartz particles in macrophages. Arch Toxicol. 2007 Jul;81(7):459-70. Epub 2007 Mar 21.
