Amiraj Banga
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Research Interest Structural and Functional Effects of Nanoparticle Toxicity on Barrier Epithelial Cell Function Carbon nanoparticles (CNP) are important components of the rapidly expanding nanotechnology field. Due to their size and unique electrical, mechanical and thermal properties, they have found widespread application in electronics, computers, aerospace, agriculture, pharmaceutical and other industries. The current and projected demand and production of these nanoscale materials will also lead to proportional opportunities for occupational and environmental exposures. The goal of this study is to elucidate the effect of carbon nanoparticle exposure on human health, be it injurious, benign or beneficial. The central hypothesis underlying the research is that manufactured, non functionalized CNPs, fullerenes (C60), single-walled nanotubes (SWCNT) and multi-walled nanotubes (MWCNT), when exposed to barrier epithelia (lung, intestine and kidney cells), exert a biological effect on the cell membrane and its associated cytoskeletal proteins that alters cell function by altering or dysregulating electrogenic transport mechanisms and barrier functions characteristic of these cell types. We are using established, well characterized, cell lines to study the epithelial cells lining each of the organs. The electrophysiological studies are being done to measure Trans Epithelial Electrical Resistance (TEER), that is a direct measure of cellular integrity and cellular viability, and Short Circuit Current (SCC), that is a measure of net ion movement across the cell and hence the hormonal responsiveness of the above mentioned types of cells. The effects of exposure are directly related to size, physico-chemical character, surface area and dose of CNP and are likely to alter cell function and injure the cells. The overall focus therefore, is to study carbon nanoparticle induced differential protein expression in barrier epithelia and its relationship to barrier cell functions. Most real world applications of CNTs involve some form of functionalization. Therefore, considering the exposure to derivatized form of CNT as a matter of great importance, effect of functionalized CNTs is also being evaluated. |
Stephanie Flaig
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Research Interest Polycystic kidney disease (PKD), is a genetic disorder that is characterized by the growth and accumulation of fluid-filled cysts in the kidney tubules and liver bile ducts. There are different forms of PKD, Autosomal Dominant Polycystic Kidney Disease (ADPKD), which is more common and Autosomal Recessive Polycystic Kidney Disease (ARPKD), is less common. The disease progresses and the fluid-filled cyst grow in size and eventually decrease renal function to the point of renal failure. Currently treatment is limited to cyst aspiration or organ transplantation, thus it is important to determine possible drug treatments. The cysts grow in size due to fluid and ion transport from the epithelial renal cells that line each cyst. Thus, it is important to identify the possible pathways and components of cyst fluid responsible for the fluid secretion and the cyst growth throughout the disease. Currently we are using mpkCCDcl4 (mouse principal cells of the kidney cortical collecting duct, clone 4) cell line, which are derived from the distal nephron and collecting duct of the kidneys. Through electrophysiological techniques we are investigating the secretory pathways of human PKD cyst fluid. We are also working on a study involving the drug treatment on a rat model using agonists of peroxisome proliferator activator receptor gamma (PPARγ), such as Pioglitazone and Rosiglitizone. PPARγ agonists are insulin-sensitizing agents that our laboratory has shown have a positive effect in reducing cyst growth in rodent models. We are determining if the cyst sizes decrease with treatment and without causing harmful sides effects, such as fluid retention. |
Shanta Lewis
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