Event Title

Effect of Genetic Variants in the Connective Tissue Growth Factor Gene on Scarring-Related Phenotypes

Faculty Sponsor(s)

Heather Doherty

Location

Hartman Union Building Courtroom

Presentation Type

Event

Start Date

4-28-2017 4:00 PM

End Date

4-28-2017 5:00 PM

Abstract

Connective tissue growth factor (CTGF) is a primary protein involved in wound healing. After tissue damage occurs, expression of CTGF signals specialized cells called myofibroblasts to break down and repair damaged extracellular matrix (ECM) and deposit structural proteins like collagen and fibronectin. Overexpression of CTGF can result in excess ECM deposition leading to formation of a scar, known as fibrosis. Fibrosis is an important clinical complication following heart attack, chronic lung disorders, and liver disease. Studies show that genetic variants in CTGF affect fibrosis risk. Using mouse fibroblasts in cell culture, we examined differences in two CTGF variants (C213R, C228F) versus the wild-type CTGF protein. We hypothesize that there will be differences between wild-type CTGF and variants in collagen and fibronectin expression as well as cell migration in a scratch test assay used to mimic wound healing. Currently, we have observed that compared to wild-type CTGF the C228F variant has reduced cell migration and has potential to influence wound healing. Determining the impacts of these variants on CTGF may lead to anti-fibrotic therapies to reduce or prevent tissue damage caused by fibrosis.

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Apr 28th, 4:00 PM Apr 28th, 5:00 PM

Effect of Genetic Variants in the Connective Tissue Growth Factor Gene on Scarring-Related Phenotypes

Hartman Union Building Courtroom

Connective tissue growth factor (CTGF) is a primary protein involved in wound healing. After tissue damage occurs, expression of CTGF signals specialized cells called myofibroblasts to break down and repair damaged extracellular matrix (ECM) and deposit structural proteins like collagen and fibronectin. Overexpression of CTGF can result in excess ECM deposition leading to formation of a scar, known as fibrosis. Fibrosis is an important clinical complication following heart attack, chronic lung disorders, and liver disease. Studies show that genetic variants in CTGF affect fibrosis risk. Using mouse fibroblasts in cell culture, we examined differences in two CTGF variants (C213R, C228F) versus the wild-type CTGF protein. We hypothesize that there will be differences between wild-type CTGF and variants in collagen and fibronectin expression as well as cell migration in a scratch test assay used to mimic wound healing. Currently, we have observed that compared to wild-type CTGF the C228F variant has reduced cell migration and has potential to influence wound healing. Determining the impacts of these variants on CTGF may lead to anti-fibrotic therapies to reduce or prevent tissue damage caused by fibrosis.