Amy C. Engevik, PhD

portrait of a scientist
Assistant Professor
Department: Regenerative Medicine & Cell Biology
Programs: Cell Injury, Inflammation



Research Interests:

Dr. Engevik received her PhD from the University of Cincinnati and joined the MUSC faculty in 2021 following postdoctoral work studying gut epithelial biology and the basic mechanisms underlying enteric disease in the Department of Surgery at the Vanderbilt University Medical Center.

Dr. Engevik’s graduate work centered around wound healing from gastric ulcers. This work identified a role for the developmental morphogen, Sonic hedgehog, secreted into the circulation from gastric parietal cells, in the promotion of gastric wound repair. Other work similarly correlated the appearance of Spasmolytic Polypeptide/TFF2-expressing Metaplastic (SPEM) cell lineages with re-epithelialization and effective healing of ulcer wounds in young, but not aged mice. Extensions of this latter work demonstrated the ability of gastric organoids transplanted from young mice and containing SPEM lineages to promote normal ulcer repair in older mice.

Dr. Engevik’s postdoctoral work also focused on basic gut epithelial function, in the context of the cellular mechanisms leading to the life-threatening chronic secretory diarrhea observed in Microvillus Inclusion Disease (MVID). MVID is a rare congenital disorder in humans associated with inactivating mutations of the myosin Vb (MYO5B) gene. Dr. Engevik’s MVID studies focused on the functional characterization of a genetic loss-of function mouse model of MYO5B. Detailed examination of the cellular localization of apical membrane ion transporters in this model supported the overarching hypothesis that loss of hydration promoting apical transporters, coupled with the maintenance of chloride secretion via the cystic fibrosis transmembrane conductance regulator (CFTR), promoted water loss from the intestinal epithelium to cause MVID-associated diarrhea. Work using a genetically engineered swine model of MVID also suggested that defects in sodium absorption coupled to maintenance of CFTR mediated chloride secretion in the intestine was responsible for the pathogenesis of MVID associated diarrhea.

Dr. Engevik’s current research continues to focus on the function of MYO5B in apical cellular transport, but on a different facet of human disease pathology associated with this gene. Cholestasis or reduction of bile secretion from the liver in MVID patients was initially thought to be a byproduct of the nutritional interventions necessitated by diarrheal malabsportion. However, incidences of isolated cholestasis have recently been associated with a specific subset of MYO5B mutations. Dr. Engevik’s ongoing work will explore the hypothesis that aberrant bile salt transporter regulation or localization in liver and/or bile duct cells but not intestinal cells is the underlying cause of isolated liver pathology and cholestasis in this setting.


PubMed Collection