Catherine Miney

Mentor: Dr. Jae-Sung Kim
College of Medicine
 
"I became involved with research because I grew up with a chronic autoinflammatory disease, and I have witnessed how developments in research have improved my treatment options over the years. I wanted to do research at the University of Florida in order to learn how to study medical literature, develop a project, and to work with a team in order to understand issues in medicine today and to progress towards developing new treatments and therapies for chronic illnesses."

Major

Biomedical Engineering

Minor

N/A

Research Interests

  • Autoimmune/Autoinflammatory Diseases
  • Mitochondrial Disorders
  • Molecular Biology

Academic Awards

  • UF Presidential Scholarship 2013
  • Anderson Scholar 2015
  • University Scholars Program 2016

Organizations

  • Phi Sigma Pi National Honor Fraternity
  • Tau Beta Pi Engineering Honor Society

Volunteer

  • Camp Counselor at Camp Korey
  • GatorTrax

Hobbies and Interests

  • Hiking
  • Rock climbing
  • Traveling
  • Running

Research Description

Mitochondrial Dysfunction after Hepatic Ischemia/Reperfusion
Reperfusion injury is the tissue damage caused after blood flow returns to a tissue after a period of ischemia. In our lab, we study the effect of ischemia reperfusion (IR) injury in various diseased liver models, including nonalcoholic fatty liver disease (NAFLD), aging, and colorectal liver metastases. In each of these models, we examine how IR injury affects mitochondria function and morphology. Mitochondria provide energy to hepatocytes by producing ATP through a proton motive force established across the membrane. The liver performs a huge number of functions including roles in digestion, storage and release of glucose, regulation of lipid storage, and the clearance of toxins. Hepatocytes contain hundreds of mitochondria in order to execute these metabolic functions. However, when mitochondria are exposed to oxidative stress such as IR, high conductance permeability transition pores open, leading to depolarization of mitochondria and uncoupling of oxidative phosphorylation in the electron transport chain. Subsequent removal of damaged mitochondria through mitophagy, a catabolic pathway responsible for removing dysfunctional mitochondria, is essential for cell survival. Mitophagy prevents the accumulation of dysfunctional mitochondria and their toxic byproducts. However, during reperfusion, calcium-dependent non-lysosomal proteases called calpains destroy proteins necessary for mitophagy to occur. Failure to dispose of dysfunctional mitochondria can lead to necrotic cell death. We are currently investigating how mitochondrial morphology and function are altered by IR-mediated defects in mitophagy, and how to prevent degradation of mitophagy proteins by calpains.