Date of Award

Spring 4-30-2025

Document Type

Honors Project

Degree Name

Bachelor of Science

Department

Biological Sciences

Department Chair or Program Director

Baker, Dianne

First Advisor

Morriss, Ginny

Second Advisor

Baker, Dianne

Third Advisor

Sipe, Laura

Major or Concentration

Biology

Abstract

Myotonic dystrophy type 1 (DM1) is a genetic disease that causes muscle wasting and affects multiple organ systems. DM1 is caused by expanded CTG repeats in the 3’ untranslated region of the dystrophia myotonica protein kinase (DMPK) gene (Harper, 2001). Skeletal muscle relies on capillaries for nutrient delivery and waste clearance (Olfert, 2016). Skeletal muscle and capillaries communicate via a variety of chemicals, including PDGF-BB which both skeletal muscle and endothelial cells secrete and have receptors for (Hamaguchi, 2023). Platelet derived growth factor receptor β (PDGFRβ), when bound to platelet derived growth factor BB (PDGF-BB), induces angiogenesis (Wang, 2012). In a mouse model of DM1, PDGFRβ signaling was found to be deregulated (Morriss, 2018). Previously unpublished data from our lab revealed human umbilical vein endothelial cells (HUVECs) transfected with expanded CTG repeats displayed severe endothelial tube degradation over a 24-hour period based on length and width measurements. At hours 15, 18, 21, and 24, significant degradation of length (µm) was observed in DM1 compared to control transfection conditions and at hour 18, significant width (µm) degradation was also observed. Future work is needed to determine whether deregulated PDGFRβ signaling is a cause of endothelial tube degradation observed in DM1.

Download

Share

COinS