Cardiac and ventilatory physiological data for mice exposed to acrolein. This dataset is associated with the following publication: Kurhanewicz, N., A. Ledbetter, A. Farraj, and M. Hazari. TRPA1 mediates the cardiac effects of acrolein through parasympathetic dominance but also sympathetic modulation in mice. TOXICOLOGY AND APPLIED PHARMACOLOGY. Academic Press Incorporated, Orlando, FL, USA, 347: 104-114, (2018).

This data shows the heart rate, heart rate variability and cardiac mechanical function of mice exposed to acrolein or ozone. This dataset is associated with the following publication: Kurhanewicz, N., R. McIntosh-Kastrinsky, H. Tong, A. Ledbetter, L. Walsh, A. Farraj, and M. Hazari. TRPA1 mediates changes in heart rate variability and cardiac mechanical function in mice exposed to acrolein. TOXICOLOGICAL AND APPLIED PHARMICOLOGY. Elsevier Science BV, Amsterdam, NETHERLANDS, 324: 51-60, (2017).

We have examined the potential for interactive cardiovascular effects of repeated, intermittent co-exposure to concentrated ambient particulate matter (CAPs) and acrolein, and the potential role of transient receptor potential cation channel A1 (TRPA1), which we previously linked to air pollution-induced cardiac arrhythmogenesis. Chemical and source characteristics of collected particles was evaluated, as well as wind and weather patterns during exposure. Female B6129 mice and Trpa1-/- mice (n=6) were exposed to filtered air (FA), CAPs (46 µg/m3 of PM2.5 approximately 160 nm diameter), Acrolein (0.42 ppm) or CAPs+Acrolein for 3hrs/day, 2days/week, for 4 weeks. Cardiac strain data, heart function and dimensions, and transmitral blood flow were investigated with echocardiography (40 MHz) before exposures, 1 day after the first exposure, and 1 day after the final exposure. Several other biological endpoints were evaluated but the key findings from ultrasound echocardiography assessments were: elapsed time between peak strain in adjacent wall segments (i.e. myocardial strain delay), a measure of myocardial dyssynchrony, increased by ~5-fold in B6129 mice after the final exposure to CAPs+Acrolein when compared to strain delay in B6129 mice exposed to FA, CAPs, or Acrolein alone, and when compared to strain delay in Trpa1-/- mice exposed to CAPs+Acrolein. There were no changes after the first exposure in any group. This dataset is associated with the following publication: Thompson, L., L. Walsh, B. Martin, J. Mcgee, C. Wood, K. Kovalcik, P. Pancras, N. Coates, A. Ledbetter, D. Davies, W. Cascio, M. Higuchi, M. Hazari, and A. Farraj. Ambient Particulate Matter and Acrolein Co-Exposure Increases Myocardial Dyssynchrony in Mice: Evidence for TRPA1 Involvement. TOXICOLOGICAL SCIENCES. Society of Toxicology, RESTON, VA, 167(2): 559-572, (2019).

Cardiovascular Physiologic and Systemic Responses to Sequential Exposure to Nitrogen Dioxide and Ozone in Rats. This dataset is associated with the following publication: Farraj , A., F. Malik, N. Coates , L. Walsh , D. Winsett , D. Terrell , L. Thompson, W. Cascio , and M. Hazari. Morning NO2 Exposure Sensitizes Hypertensive Rats to the Cardiovascular Effects of Same Day O3 Exposure in the Afternoon. INHALATION TOXICOLOGY. Informa Healthcare USA, New York, NY, USA, 28(4): 170-179, (2016).

Raw data for all figures and tables in manuscript for study analyzing the impact of living conditions on cardiovascular function in ApoE -/- mice. This dataset is associated with the following publication: Fiamingo, M., S. Toler, K. Lee, W. Oshiro, Q. Krantz, P. Evansky, D. Davies, M. Gilmour, A. Farraj, and M. Hazari. Depleted housing elicits cardiopulmonary dysfunction after a single flaming eucalyptus wildfire smoke exposure in a sex-specific manner in ApoE knockout mice.. Cardiovascular Toxicology. Humana Press Incorporated, Totowa, NJ, USA, 24: 852-869, (2024).

The dataset is an excel spreadsheet containing the raw data used to generate the tables and figures in the manuscript. This dataset is associated with the following publication: Thompson, L., J. Shanahan, C. Perez, N. Coates, C. King, M. Hazari, J. Brown, and A. Farraj. Early Proteome Shift and Serum Bioactivity Precede Diesel Exhaust-induced Impairment of Cardiovascular Recovery in Spontaneously Hypertensive Rats. Scientific Reports. Nature Publishing Group, London, UK, 9(1): 6885, (2019).

This dataset includes QTc and RR values related to the electrocardiogram of rats exposed to either air or diesel exhaust. This dataset is associated with the following publication: Hazari , M., J. Lancaster, J. Starobin, A. Farraj , and W. Cascio. Diesel exhaust worsens cardiac conduction instability in dobutamine-challenged Wistar-Kyoto and spontaneously hypertensive rats. Cardiovascular Toxicology. Humana Press Incorporated, Totowa, NJ, USA, 17(2): 120-129, (2017).

Background Monolysocardiolipin acyltransferase (MLCL AT) catalyzes the acylation of monolysocardiolipin to cardiolipin in mammalian tissues. We previously reported that cardiac cardiolipin levels, MLCL AT and cardiolipin synthase activities were all elevated in rats made hyperthyroid by thyroxine treatment. In this study, we examined if cardiac mitochondrial MLCL AT activity was dependent upon the biosynthesis and level of cardiolipin in the heart. Rat heart mitochondrial MLCL AT activity was determined under conditions in which the levels of cardiac cardiolipin and cardiolipin synthase activity were either reduced or unaltered using four different disease models in the rat. In addition, these parameters were examined in a murine model of cardiac cell differentiation. Results In rats made hypothyroid by treatment with 6-n-propyl-2-thiouracil in the drinking water for 34 days, cardiac cardiolipin content was decreased 29% (p < 0.025) and this was associated with a 32% decrease (p < 0.025) in cardiolipin synthase and a 35% reduction (p < 0.025) in MLCL AT activities. Streptozotocin-induced diabetes or hyperinsulinemia in rats did not affect cardiac cardiolipin content nor MLCL AT and cardiolipin synthase activities. Finally, cardiolipin content, MLCL AT and cardiolipin synthase activities were unaltered during murine P19 teratocarcinoma cell differentiation into cardiac myocytes. In all models, phospholipase A2 activities were unaltered compared with controls. Conclusion We propose a general model in which the expression of MLCL AT activity is regulated in concert with the biosynthesis and level of cardiolipin in the heart.

This dataset includes raw data used to generate figures for the manuscript describing the effects of noise and ozone on cardiovascular function in rats. This dataset is associated with the following publication: Hazari, M., K. Phillips, K. Stratford, A.M. Khan, L. Thompson, W. Oshiro, G. Hudson, D. Herr, and A. Farraj. Exposure to intermittent noise exacerbates the cardiovascular response of Wistar-Kyoto Rats to Ozone Inhalation and Arrhythmogenic Challenge. Cardiovascular Toxicology. Humana Press Incorporated, Totowa, NJ, USA, 21(4): 336-348, (2021).

This dataset contains data of blood miRNA, cardiovascular biomarkers (i.e. inflammation, coagulation, and blood lipids), omega-3 index levels, as well as ambient PM2.5, O3 and NO2 concentrations from the panel study "PISCES". This dataset is associated with the following publication: Chen, H., S. Zhang, B. Yu, Y. Xu, A. Rappold, D. Diaz-Sanchez, J. Samet, and H. Tong. Circulating microRNAs as putative mediators in the association between short-term exposure to ambient air pollution and cardiovascular biomarkers. ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY. Elsevier Science Ltd, New York, NY, USA, 239(113604): 1, (2022).