Mayank Verma , IT 2007
Improvement of muscular dystrophy phenotype by increased vasculature in mdx Mice
Major
Microbiology
Mentors
Atsushi Asakura : Neurology
Paul and Sheila : Wellstone Muscular Dystrophy Center
Brief Bio
I graduated from Hopkins High school in 2005 and entered the University of Minnesota right away. I like to read, watch T.V. and play smash bros.
Future Plans
After graduating in spring 2009, I would like to attend graduate school. My ultimate goal is to go into academia for teaching/research.
Why Research?
I like the freedom and independence. Not only do you get to learn about different topics, but you get to do it without the pressure of getting tested. Research also gives you more time to explorer tangents than any classroom activity.
What Did I Get from Research?
I expected to learn about muscular dystrophy and how research works.
How Did I Start?
I set up a meeting with my mentor to learn more about muscular dystrophy in high school and soon started volunteering in his lab. When I entered the University of Minnesota, he offered me a job.
My Advice for Another Student:
Do it. It is definitely a worthwhile experience in your undergraduate career.
Research Summary
Duchanne Muscular Dystrophy (DMD) is a genetic disorder in which the absence of the protein dystrophin causes a loss of the dystrophin associated protein complex (DAPC) linked to the extra-cellular complex in the muscle cells. This leads to the degradation of the muscle fiber the regeneration is not sufficient and several rounds of degeneration/regeneration results in a progressive deterioration of the muscles fiber.
It has been discovered that dystrophin is also present in the middle muscular/elastic tissue in the blood vessel. Blood vessels can be expected to have the same weaknesses as the muscles without dystrophin. Furthermore, the deterioration of the this elastic tissue can create a shortage of blood vessels and inadequate blood flow and as a result, the muscle fibers may become hypoxic, inducing further damage.
My project was to elucidate if the dystrophin deficient blood vessels have a significant effect on the pathology and physiology of the DMD model mice (mdx). For this study, mdx micewere bred with heterozygous Flt1+/- mice to yield double mutant mdx/Flt1+/- mice. Flt1 is an inhibitory receptor for Vascular Endothelial Growth Factor (VEGF) and the preliminary work conducted for this study showed that although homozygous Flt1 knockout mice die in the embryological stage, heterozygous Flt1 knockout mice are viable and display enhanced vascularization.