Effects of exposure to fatty acids on the contraction and relaxation of aortic tissue (Figure 1 A-E) and the viability of the aortic tissue (Table 1). This dataset is associated with the following publication: Bass, V., S. Snow, J. Soukup, M. Schladweiler, A. Ghio, U. Kodavanti, and M. Madden. 12-Hydroxy Oleic Acid Impairs Endothelium Dependent Vasorelaxation. JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH - PART A: CURRENT ISSUES. Taylor & Francis, Inc., Philadelphia, PA, USA, 82(5): 383-386, (2020).

Figure 1. is Aortic Ring Responses Following 1hr Exposure with either 200µM OA, 12-OH-OA, or vehicle. Table 1. is Aortic Tissue Viability. This dataset is associated with the following publication: Bass, V., S. Snow, J. Soukup, M. Schladweiler, A. Ghio, U. Kodavanti, and M. Madden. 12-Hydroxy Oleic Acid Impairs Endothelium Dependent Vasorelaxation. JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH - PART A: CURRENT ISSUES. Taylor & Francis, Inc., Philadelphia, PA, USA, 82(5): 383-386, (2020).

Figure 1. is Aortic Ring Responses Following 1hr Exposure with either 200µM OA, 12-OH-OA, or vehicle. Table 1. is Aortic Tissue Viability. This dataset is associated with the following publication: Bass, V., S. Snow, J. Soukup, M. Schladweiler, A. Ghio, U. Kodavanti, and M. Madden. 12-Hydroxy Oleic Acid Impairs Endothelium Dependent Vasorelaxation. JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH - PART A: CURRENT ISSUES. Taylor & Francis, Inc., Philadelphia, PA, USA, 82(5): 383-386, (2020).

Aortic tissue cellular viability with different treatments. This dataset is associated with the following publication: Bass, V., S. Snow, J. Soukup, M. Schladweiler, A. Ghio, U. Kodavanti, and M. Madden. 12-Hydroxy Oleic Acid Impairs Endothelium Dependent Vasorelaxation. JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH - PART A: CURRENT ISSUES. Taylor & Francis, Inc., Philadelphia, PA, USA, 82(5): 383-386, (2020).

Studies have linked exposure to ultrafine particulate matter (PM) and adverse cardiovascular events. Particulate matter-induced oxidative stress is believed to be a key mechanism underlying observed adverse vascular effects. Advanced age is one factor known to decrease anti-oxidant defenses and confer susceptibility to the detrimental vascular effects seen following PM exposure. The present study was designed to investigate the vasomotor responses following ultrafine PM exposure in wild type (WT) and superoxide dismutase 2 deficient (SOD2+/-) mice which possess decreased anti-oxidant defense. Thoracic aortic rings isolated from young and aged WT and SOD2+/- mice were exposed to ultrafine PM in a tissue bath system. Aortic rings were then constricted with increasing concentrations of phenylephrine, followed by relaxation with rising amounts of nitroglycerin (NTG). Data demonstrated that ultrafine PM decreased the relaxation response in both young WT and young SOD2+/- mouse aortas, and relaxation was significantly reduced in young SOD2+/- compared to WT mice. Ultrafine PM significantly diminished the NTG-induced relaxation response in aged compared to young mouse aortas. After ultrafine PM exposure, the relaxation response did not differ markedly between aged WT and aged SOD2+/- mice. Data demonstrate that the greater vascular effect in aortic rings in aged mice ex vivo after ultrafine PM exposure may be attributed to ultrafine PM-induced oxidative stress and loss of anti-oxidant defenses in aged vascular tissue. Consistent with this conclusion is the attenuation of NTG-induced relaxation response in young SOD2+/- mice. This dataset is associated with the following publication: Carter, J., N. Madamanchi , G. Stouffer, M. Runge, W. Cascio, and H. Tong. Ultrafine Particulate Matter Exposure Impairs Vasorelaxant Response in Superoxide Dismutase 2 Deficient Murine Aortic Rings. JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH - PART A: CURRENT ISSUES. Taylor & Francis, Inc., Philadelphia, PA, USA, 81(5): 106-115, (2018).

Studies have linked exposure to ultrafine particulate matter (PM) and adverse cardiovascular events. Particulate matter-induced oxidative stress is believed to be a key mechanism underlying observed adverse vascular effects. Advanced age is one factor known to decrease anti-oxidant defenses and confer susceptibility to the detrimental vascular effects seen following PM exposure. The present study was designed to investigate the vasomotor responses following ultrafine PM exposure in wild type (WT) and superoxide dismutase 2 deficient (SOD2+/-) mice which possess decreased anti-oxidant defense. Thoracic aortic rings isolated from young and aged WT and SOD2+/- mice were exposed to ultrafine PM in a tissue bath system. Aortic rings were then constricted with increasing concentrations of phenylephrine, followed by relaxation with rising amounts of nitroglycerin (NTG). Data demonstrated that ultrafine PM decreased the relaxation response in both young WT and young SOD2+/- mouse aortas, and relaxation was significantly reduced in young SOD2+/- compared to WT mice. Ultrafine PM significantly diminished the NTG-induced relaxation response in aged compared to young mouse aortas. After ultrafine PM exposure, the relaxation response did not differ markedly between aged WT and aged SOD2+/- mice. Data demonstrate that the greater vascular effect in aortic rings in aged mice ex vivo after ultrafine PM exposure may be attributed to ultrafine PM-induced oxidative stress and loss of anti-oxidant defenses in aged vascular tissue. Consistent with this conclusion is the attenuation of NTG-induced relaxation response in young SOD2+/- mice. This dataset is associated with the following publication: Carter, J., N. Madamanchi , G. Stouffer, M. Runge, W. Cascio, and H. Tong. Ultrafine Particulate Matter Exposure Impairs Vasorelaxant Response in Superoxide Dismutase 2 Deficient Murine Aortic Rings. JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH - PART A: CURRENT ISSUES. Taylor & Francis, Inc., Philadelphia, PA, USA, 81(5): 106-115, (2018).

Studies have linked exposure to ultrafine particulate matter (PM) and adverse cardiovascular events. Particulate matter-induced oxidative stress is believed to be a key mechanism underlying observed adverse vascular effects. Advanced age is one factor known to decrease anti-oxidant defenses and confer susceptibility to the detrimental vascular effects seen following PM exposure. The present study was designed to investigate the vasomotor responses following ultrafine PM exposure in wild type (WT) and superoxide dismutase 2 deficient (SOD2+/-) mice which possess decreased anti-oxidant defense. Thoracic aortic rings isolated from young and aged WT and SOD2+/- mice were exposed to ultrafine PM in a tissue bath system. Aortic rings were then constricted with increasing concentrations of phenylephrine, followed by relaxation with rising amounts of nitroglycerin (NTG). Data demonstrated that ultrafine PM decreased the relaxation response in both young WT and young SOD2+/- mouse aortas, and relaxation was significantly reduced in young SOD2+/- compared to WT mice. Ultrafine PM significantly diminished the NTG-induced relaxation response in aged compared to young mouse aortas. After ultrafine PM exposure, the relaxation response did not differ markedly between aged WT and aged SOD2+/- mice. Data demonstrate that the greater vascular effect in aortic rings in aged mice ex vivo after ultrafine PM exposure may be attributed to ultrafine PM-induced oxidative stress and loss of anti-oxidant defenses in aged vascular tissue. Consistent with this conclusion is the attenuation of NTG-induced relaxation response in young SOD2+/- mice. This dataset is associated with the following publication: Carter, J., N. Madamanchi , G. Stouffer, M. Runge, W. Cascio, and H. Tong. Ultrafine Particulate Matter Exposure Impairs Vasorelaxant Response in Superoxide Dismutase 2 Deficient Murine Aortic Rings. JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH - PART A: CURRENT ISSUES. Taylor & Francis, Inc., Philadelphia, PA, USA, 81(5): 106-115, (2018).

Background Balloon injury (BI) of the rat carotid artery (CCA) is widely used to study intimal hyperplasia (IH) and decrease in lumen diameter (LD), but CCA's small diameter impedes the evaluation of endovascular therapies. Therefore, we validated BI in the aorta (AA) and iliac artery (CIA) to compare it with CCA. Methods Rats underwent BI or a sham procedure (control). Light microscopic evaluation was performed either directly or at 1, 2, 3, 4 and 16 weeks follow-up. The area of IH and the change in LD (LD at 16 weeks minus LD post BI) were compared. Results In the BI-groups the area of IH increased to 0.14 ± 0.08 mm2 (CCA), 0.14 ± 0.03 mm2 (CIA) and 0.12 ± 0.04 mm2 (AA) at 16 weeks (NS). The LD decreased with 0.49 ± 0.07 mm (CCA), compared to 0.22 ± 0.07 mm (CIA) and 0.07 ± 0.10 mm (AA) at 16 weeks (p < 0.05). The constrictive vascular remodelling (CVR = wall circumference loss combined with a decrease in LD) was -0.17 ± 0.05 mm in CIA but absent in CCA and AA. No IH, no decrease in LD and no CVR was seen in the control groups. Conclusions BI resulted in: (1.) a decrease in LD in CCA due to IH, (2.) a decrease in LD in CIA due to IH and CVR, (3.) no change in LD in AA, (4.) Comparable IH development in all arteries, (5.) CCA has no vasa vasorum compared to CIA and AA, (6.) The CIA model combines good access for 2 F endovascular catheters with a decrease in LD due to IH and CVR after BI.

Figure 1. Comparison of cell viability in response to exposure of cells to oleic acid (in ethanol), a hydroxy-metabolite, or methylated oleic acid as percent of the vehicle control response. Figure 2. Mitochondrial stress test extracellular flux using comparison of cellular oxygen consumption rate measures. Figure 3. Soluble mediator release comparison of cells exposed to oleic acid and its metabolites. Figure 4. Cellular iron-uptake following incubation with fatty acids. Supplement 2A. Lactate dehydrogenase activity release ( a measure of cell viability) is dose- and time-dependent. Supplement 2B. Oleic acid cellular association differs with vehicle utilized. This dataset is associated with the following publication: Bass, V., J. Soukup, A. Ghio, and M. Madden. Oleic Acid and Derivatives Affect Human Endothelial Mitochondrial Function Cell and Vasoactive Mediator Production. Lipids in Health and Disease. BioMed Central Ltd, London, UK, 19(1): 128, (2020).