Nanoparticle-induced Stress Leads to Elevated Reactive Oxygen Species, Punctate Mitochondria, and Apoptosis in Human Lung Cells
Presentation Type
Poster
Keywords
Nanoparticles, carbon black, reactive oxygen species, apoptosis, mitochondria, lung cells
Department
Biology
Major
Biology
Abstract
As a major component of air pollution, carbon black (CB) is a nanoparticle that poses a threat to many urban communities. A nanoparticle is any particle that is between 20 and 100 nm in diameter. CB is created from car emissions, combustion, and industry. It is known to worsen asthma and bronchitis when inhaled. CB is also linked to cardiovascular diseases and lung cancer. While it has been elucidated that CB kills cells through apoptosis, the specific pathway by which this occurs is currently unknown. The purpose of this project was to shed more light onto this process. For our model system, human bronchial epithelial cells (16HBE14o-) cells were used. Between concentrations of 40 and 100 µg/mL, CB caused a significant decrease in cell density. Evidence for apoptosis was given by counting apoptotic nuclei. There was a significant increase in percent apoptotic nuclei per field of view in cells exposed to CB 50 and 100 µg/mL for 24 and 48 hours compared to mock-treated cells. To observe whether CB induced morphological changes in the mitochondria, cells were transfected with fluorescent protein and imaged using an ultraviolet microscope. Cells exposed to CB 50 µg/mL and 100 µg/mL had higher levels of punctacte mitochondria than cells treated with mock. Finally, the concentrations of proteins known to be involved in apoptosis were surveyed using an antibody array, though, due to minimal detection of protein induction, the results were inconclusive. Further studies will pursue CB's effect on proteins involved in the mitochondrial apoptotic pathway.
Faculty Mentor
Dr. Jay Brewster
Funding Source or Research Program
Academic Year Undergraduate Research Initiative, Summer Undergraduate Research in Biology
Location
Waves Cafeteria
Start Date
1-4-2016 2:00 PM
End Date
1-4-2016 3:00 PM
Nanoparticle-induced Stress Leads to Elevated Reactive Oxygen Species, Punctate Mitochondria, and Apoptosis in Human Lung Cells
Waves Cafeteria
As a major component of air pollution, carbon black (CB) is a nanoparticle that poses a threat to many urban communities. A nanoparticle is any particle that is between 20 and 100 nm in diameter. CB is created from car emissions, combustion, and industry. It is known to worsen asthma and bronchitis when inhaled. CB is also linked to cardiovascular diseases and lung cancer. While it has been elucidated that CB kills cells through apoptosis, the specific pathway by which this occurs is currently unknown. The purpose of this project was to shed more light onto this process. For our model system, human bronchial epithelial cells (16HBE14o-) cells were used. Between concentrations of 40 and 100 µg/mL, CB caused a significant decrease in cell density. Evidence for apoptosis was given by counting apoptotic nuclei. There was a significant increase in percent apoptotic nuclei per field of view in cells exposed to CB 50 and 100 µg/mL for 24 and 48 hours compared to mock-treated cells. To observe whether CB induced morphological changes in the mitochondria, cells were transfected with fluorescent protein and imaged using an ultraviolet microscope. Cells exposed to CB 50 µg/mL and 100 µg/mL had higher levels of punctacte mitochondria than cells treated with mock. Finally, the concentrations of proteins known to be involved in apoptosis were surveyed using an antibody array, though, due to minimal detection of protein induction, the results were inconclusive. Further studies will pursue CB's effect on proteins involved in the mitochondrial apoptotic pathway.