Intracellular Localization of M10, a Caspase Cleavage Product of The Hepatoctye Growth Factor Receptor, in Primary Skin Fibroblasts

School Name

Governor's School for Science & Mathematics

Grade Level

12th Grade

Presentation Topic

Physiology and Health

Presentation Type

Mentored

Mentor

Mentor: Galina Bogatkevich, Medical University of South Carolina

Abstract

Scleroderma, or systemic sclerosis, causes fibrosis of the skin and organs due to an overproduction of collagen. Furthermore, scleroderma has a very poor prognosis, and currently there are no effective treatments available. But recent research has shown that there may be a possible form of therapy through the use of a specific peptide from the MET (Mesenchymal-Epithelial Transition factor) Tyrosine Kinase receptor, called M10. In scleroderma patients, the interaction between MET and HGF (Hepatocyte Growth Factor), the ligand which protects against fibrosis, is impaired. Previous research on the peptide M10, also known as TRPASFWETS, indicated that it can be used as a potential form of therapy for scleroderma patients due to its anti-fibrotic properties. Therefore, the aim of this research is to determine the location of M10 within primary skin fibroblasts from a patient at the Medical University of South Carolina. It was hypothesized that, in order to achieve anti-fibrotic effect, M10 would have to be transported into the nucleus. The goals were achieved by culturing the primary skin fibroblasts in the presence of M10, incubating for 48 hours, and followed by performing immunofluorescence microscopy. The results indicate that M10 was present in the cytoplasm and co-localized with the protein beta-actin. Therefore, M10, after 48 hours, was located in the cytoplasm and not in the nucleus as hypothesized. Future work will include treating these cells with M10 for a shorter period of time followed by immunofluorescence microscopy to see whether M10 is ever localized in the nucleus.

Start Date

3-25-2017 11:59 PM

Presentation Format

Written Only

Group Project

No

COinS
 
Mar 25th, 11:59 PM

Intracellular Localization of M10, a Caspase Cleavage Product of The Hepatoctye Growth Factor Receptor, in Primary Skin Fibroblasts

Scleroderma, or systemic sclerosis, causes fibrosis of the skin and organs due to an overproduction of collagen. Furthermore, scleroderma has a very poor prognosis, and currently there are no effective treatments available. But recent research has shown that there may be a possible form of therapy through the use of a specific peptide from the MET (Mesenchymal-Epithelial Transition factor) Tyrosine Kinase receptor, called M10. In scleroderma patients, the interaction between MET and HGF (Hepatocyte Growth Factor), the ligand which protects against fibrosis, is impaired. Previous research on the peptide M10, also known as TRPASFWETS, indicated that it can be used as a potential form of therapy for scleroderma patients due to its anti-fibrotic properties. Therefore, the aim of this research is to determine the location of M10 within primary skin fibroblasts from a patient at the Medical University of South Carolina. It was hypothesized that, in order to achieve anti-fibrotic effect, M10 would have to be transported into the nucleus. The goals were achieved by culturing the primary skin fibroblasts in the presence of M10, incubating for 48 hours, and followed by performing immunofluorescence microscopy. The results indicate that M10 was present in the cytoplasm and co-localized with the protein beta-actin. Therefore, M10, after 48 hours, was located in the cytoplasm and not in the nucleus as hypothesized. Future work will include treating these cells with M10 for a shorter period of time followed by immunofluorescence microscopy to see whether M10 is ever localized in the nucleus.