Natalie Rovaldi
Pronouns: she/her/hers
Research Mentor(s): Yadav Wagley
Research Mentor School/College/Department: Orthopaedic Surgery / Medicine
Program:
Authors: Natalie Rovaldi
Session: Session 6: 3:40 pm – 4:30 pm
Poster: 88
Abstract
EPDR1 was recently identified as a novel human osteoblast effector gene using functional genomics approach1,2. Further works have shown that knock-down of EPDR1 in human mesenchymal stem/progenitor cells (hMSC) biases the cells towards adipocytic lineage and enhances expression of inflammatory marker genes during osteoblastogenic differentiation. Although the loss of Epdr1 is associated with decreased osteoblastic gene markers in murine bone marrow stromal cells (BMSC), it is currently unknown how Epdr1 gene expression is regulated during BMSC differentiation into osteoblasts and adipocytes. A series of experiments have been conducted to explore the expression pattern of Epdr1 gene in BMSC during differentiation into osteoblasts and adipocytes. Mouse bone marrow stromal cells (BMSC) were harvested from the long bones (tibia and femur) and were induced to differentiate into osteoblastic and adipogenic cells over the span of eight to ten days. RNA from these cells were isolated at various lengths of time and reverse-transcribed into DNA, and marker genes for osteoblast and adipocytes were amplified using PCR. Our preliminary data suggests a modest increase of Epdr1 during the osteoblastic differentiation of murine BMSC whereas the expression of Epdr1 decreased as the cells differentiated into adipocytes. Since Epdr1 is a secreted protein, we additionally aim to evaluate osteoblast and adipocyte differentiation of BMSC in the presence of recombinant EPDR1. In next steps of these experiments, mouse preosteoblast and preadipocyte cell lines will be cultured and differentiated into osteoblast and adipocytes, and genetic manipulation techniques utilizing small interfering RNA (siRNA) will be utilized to understand the molecular implications of loss of Epdr1 function into cell differentiation models. Completion of these experiments would allow us to therapeutically intervene Epdr1 for maintenance of bone mineral density in pathological conditions and osteoporotic conditions in vivo using genetic mouse models.
