Javier Sotelo, Jr.

Major and Classification

Health Promotion and Disease Prevention and Masters in Global Medicine

Faculty Mentor

Robert Maxson, Ph.D.


Keck School of Medicine, Dornsife College of Letters, Arts and Sciences

McNair Project

“Effects of Defective STAT3/Wnt pathways on Cardiac Neural Crest Cell Migration and Heart Development”

Project Abstract

Approximately one out of every one hundred live births is affected by a congenital heart disease that results in high embryo and infant mortality. Previous research has aimed to uncover the underlying genetic and microbiological causes of these heart disorders. One proposed mechanism is the failure of neural crest cells to migrate during early stages of embryonic development due to malfunctioning or missing protein pathways. The STAT3/Wnt protein pathway is believed to affect neural crest cell migration. It is thought that malfunctioning or missing STAT3/ Wnt proteins results in congenital heart disease. Preliminary studies have revealed that some mice with defective or missing STAT3/Wnt proteins displayed heart diseases. The purpose of this study was to further investigate how defective STAT3/Wnt protein pathways affect neural crest cell migration during the neonatal stages of cardiogenesis. Our aim was to uncover the causes, at a genetic and microbiological level, of embryonic heart diseases. By examining 5 STAT3/Wnt mutated mice, we were able to preliminarily determine that there was no correlation between defective STAT3/Wnt protein pathways and cardiac neural crest cell migration. Additionally, there was no correlation between the defective STAT3/Wnt protein pathways and deformities in the heart during cardiogenesis. However, due to our limited sample size, further research is needed to definitively rule out a correlation between STAT3/Wnt proteins and cardiac neural crest cell migration. Unexpected results from this study have indicated that there might be some correlation between defective STAT3/ Wnt protein pathways and development of the thymus.