Zaynah Saraya
Pronouns: she/her
Research Mentor(s): Kurt Hankenson
Research Mentor School/College/Department: Orthopaedic Surgery / Medicine
Program:
Authors: Zaynah Saraya, Christina Capobianco , Kurt Hankenson
Session: Session 6: 3:40 pm – 4:30 pm
Poster: 14
Abstract
Approximately 15 million fractures occur yearly in the United States, however around 10% of these fractures will result in a nonunion or malunion, meaning that they will not heal without surgical intervention. Many factors can contribute to impaired fracture healing including age, ischemia, smoking, chronic inflammation, infection, and polytrauma. There is a pressing need to understand mechanisms that underlie impaired healing and understand the processes that facilitate fracture healing under healthy and impaired conditions. Our studies specifically focus on modulating gene expression and understanding how this impacts fracture callus formation and mineralization. Within the lab we have shown that global deletion of the gene thrombospondin 1 (TSP1) leads to impaired fracture callus formation and healing, however the exact mechanisms are not well defined. TSP1 has been shown to have roles in regulation of blood vessel growth, inflammation, and fibrosis. Our study seeks to assess how a deficiency in TSP1 impacts bone healing. Our lab has shown that TSP1 is highly expressed by the immune cells, specifically macrophages, during fracture callus formation. Thus, we hypothesize that inhibition of TSP1 in the immune population will have the same effect of impaired healing as a global deletion. We can assess this through analysis of cartilage and bone formation using Safranin-O/Fast green staining. Immunofluorescence can also be used to interrogate differences in blood vessel growth.
