Jackie A. Fretz, PhD

I obtained my BS in Biochemistry and Molecular Biology from the University of New Hampshire, and PhD in Biochemistry from the University of Wisconsin--Madison. My research career has focused on transcriptional regulation of cell fate. This has included NFATc1 in osteoclasts, the Vitamin D Receptor in osteoblasts, and EBF1 in mesenchymal progenitors.

Currently I am investigating the actions of EBF1 in mesenchymal progenitors and perivascular cells. In the bone this involves the actions of EBF1 in the vascular support cells (pericytes) to regulate bone vascularity, anabolism, and adipocyte differentiation. We have identified that the marrow adipocytes are a very different form of fat-storing cell than arises in other anatomical locations. This is primarily highlighted by the different way that these cells rely upon the presence of EBF1. Most interestingly Our investigations have revealed that EBF1 is essential to properly mobilize osteoblast progenitors into the bone lineage in the aging adult skeleton and following injury to mediate repair.

In the kidney EBF1 also participates in regulation of renal development and disease progression through it's ability of mesenchymal cells to modulate the vascularity of the glomerulus. Within the adult kidney podocytes use EBF1 to respond to glomerular injury and propagate sclerosis. Our work in kidney is also tied back to bone through the investigation of the pathology underlying chronic kidney disease-mineral bone disorders including regulation of FGF-23 in early chronic kidney disease.