Title

The Effect Of In Vitro Silica Treatment On Lung Fibroblasts

Author(s)

Nicole Wyman

School Name

Governor's School for Science and Math

Grade Level

12th Grade

Presentation Topic

Cell and Molecular Biology

Presentation Type

Mentored

Mentor

Mentor: Dr. LaRue; Department of Pathology and Laboratory Medicine, Medical University of South Carolina

Written Paper Award

1st Place

Abstract

Pulmonary fibrosis is a debilitating lung disease that is caused by an over proliferation of fibroblasts, which scars the lung tissue. Currently, the disease is regularly modeled by an in vivo approach, which does not allow for the molecular level examination that an in vitro model would. Silica is often used as a stimulus for pulmonary fibrosis, with in vivo experiments, so it was used in this in vitro experiment. To test the impact of silica on lung fibroblasts, lung samples were extracted from an Ly5.1 mouse, the type of mouse for basic research, and plated to allow for fibroblast proliferation. The fibroblasts were treated with varying doses of silica and then tested for alpha-smooth muscle actin (-SMA) and collagen I (Col I) protein levels. TGF-beta (TGF-ß) treatment was used as a positive control as it has been shown in previous to induce activation in NIH3T3 fibroblast cells. The TGF-ß treatment resulted in an increase of both alpha-smooth muscle actin and collagen I levels, demonstrating the activation of fibroblasts. The silica treatment resulted in an increase of collagen I levels in the lower dose, but a decrease in the higher doses. Fibroblast death may have caused this decrease in collagen I levels. Silica treatment did not affect the alpha-smooth muscle actin levels. The constant alpha-smooth muscle actin levels and decrease in collagen I levels suggests that the untreated fibroblasts were activated, creating a successful in vitro model of pulmonary fibrosis.

Location

Owens 202

Start Date

4-16-2016 9:45 AM

COinS
 
Apr 16th, 9:45 AM

The Effect Of In Vitro Silica Treatment On Lung Fibroblasts

Owens 202

Pulmonary fibrosis is a debilitating lung disease that is caused by an over proliferation of fibroblasts, which scars the lung tissue. Currently, the disease is regularly modeled by an in vivo approach, which does not allow for the molecular level examination that an in vitro model would. Silica is often used as a stimulus for pulmonary fibrosis, with in vivo experiments, so it was used in this in vitro experiment. To test the impact of silica on lung fibroblasts, lung samples were extracted from an Ly5.1 mouse, the type of mouse for basic research, and plated to allow for fibroblast proliferation. The fibroblasts were treated with varying doses of silica and then tested for alpha-smooth muscle actin (-SMA) and collagen I (Col I) protein levels. TGF-beta (TGF-ß) treatment was used as a positive control as it has been shown in previous to induce activation in NIH3T3 fibroblast cells. The TGF-ß treatment resulted in an increase of both alpha-smooth muscle actin and collagen I levels, demonstrating the activation of fibroblasts. The silica treatment resulted in an increase of collagen I levels in the lower dose, but a decrease in the higher doses. Fibroblast death may have caused this decrease in collagen I levels. Silica treatment did not affect the alpha-smooth muscle actin levels. The constant alpha-smooth muscle actin levels and decrease in collagen I levels suggests that the untreated fibroblasts were activated, creating a successful in vitro model of pulmonary fibrosis.