Impact of Stress Hormones and IUGR Fetal Conditions on Myoblast Function

Authors

Hannah E. Riley, University of Nebraska LincolnFollow
Kristin A. Beede, University of Nebraska LincolnFollow
Dustin T. Yates, University of Nebraska LincolnFollow

Date of this Version

Spring 2016

Document Type

Poster

Citation

UCARE Poster session, University of Nebraska-Lincoln Research Fair, April 2016, Lincoln, NE.

Comments

Copyright © 2016 Hannah Riley, Kristin Beede, and Dustin Yates

Abstract

Chronic fetal stress causes adaptive responses that result in intrauterine growth restriction (IUGR). Maternal stressors including heat stress, illness, and obesity cause placental dysfunction that harshens the intrauterine environment by inducing hypoxia and nutrient restriction. IUGR fetuses have restricted growth through the last trimester and after birth. The objective of this study was to test the effects of stress hormones on myoblast proliferation rates. L6 cells and primary myoblasts that were isolated from IUGR fetal sheep in a previous study were used to study the effects of stress hormones on myoblast proliferation and myoblast gene expression. Incubation in epinephrine-spiked media initially reduced L6 cell proliferation at 4 hours but then increased proliferation at 48 and 96 hours. TNFa, IL-6 and TWEAK all increased proliferation rates, but the quickest and most profound increase was with IL-6. Although IUGR fetal myoblasts showed greater proliferation rates than controls, proliferation rates didn’t change with increasing amounts of norepinephrine or insulin in controls or IUGR myoblasts. Together our findings show that increased exposure to stress hormones have a positive effect on myoblast proliferation, especially in relatively short durations (48-96 hours).