The Role of uPARAP, a Cell Surface Collagen Receptor, In Mouse Model of Emphysema

School Name

Governor's School for Science & Mathematics

Grade Level

12th Grade

Presentation Topic

Cell and Molecular Biology

Presentation Type

Mentored

Mentor

Mentor: Lynn Schnapp, Medical University of South Carolina

Abstract

The purpose of this research was to determine whether or not the collagen uptake receptor, uPARAP, plays a role in the matrix remodeling of the lungs during the development of emphysema. This research was completed using knock out (KO) uPARAP mice that had been smoked with tobacco or not smoked, and smoking and non-smoking wild type (WT) mice. Many methods were used during this research to draw conclusions, including genotyping, protein assays, white blood cell differential, and quantitative real-time polymerase chain reaction. From genotyping, it was confirmed that all of the study mice involved in the experiment were organized correctly. The protein assays showed that there appears to be no significant difference between the protein concentrations of the non-smoking and smoking WT and KO uPARAP mice. The white blood cell differential showed that there appears to be a greater amount of neutrophils in the lung tissue of the KO uPARAP mice than the WT mice, both before and after smoking. The results of quantitative real-time polymerase chain reaction seemed to confirm that pattern by displaying that there may be greater expression of a neutrophil chemoattractant in the mice that had the largest number of neutrophils. Quantitative real-time polymerase chain reaction also showed that uPARAP does not appear to be regulated by smoke, and collagen expression in the lungs may decrease with smoking.

Start Date

3-25-2017 11:59 PM

Presentation Format

Written Only

Group Project

No

COinS
 
Mar 25th, 11:59 PM

The Role of uPARAP, a Cell Surface Collagen Receptor, In Mouse Model of Emphysema

The purpose of this research was to determine whether or not the collagen uptake receptor, uPARAP, plays a role in the matrix remodeling of the lungs during the development of emphysema. This research was completed using knock out (KO) uPARAP mice that had been smoked with tobacco or not smoked, and smoking and non-smoking wild type (WT) mice. Many methods were used during this research to draw conclusions, including genotyping, protein assays, white blood cell differential, and quantitative real-time polymerase chain reaction. From genotyping, it was confirmed that all of the study mice involved in the experiment were organized correctly. The protein assays showed that there appears to be no significant difference between the protein concentrations of the non-smoking and smoking WT and KO uPARAP mice. The white blood cell differential showed that there appears to be a greater amount of neutrophils in the lung tissue of the KO uPARAP mice than the WT mice, both before and after smoking. The results of quantitative real-time polymerase chain reaction seemed to confirm that pattern by displaying that there may be greater expression of a neutrophil chemoattractant in the mice that had the largest number of neutrophils. Quantitative real-time polymerase chain reaction also showed that uPARAP does not appear to be regulated by smoke, and collagen expression in the lungs may decrease with smoking.