Jackie Fretz, PhD

Assistant Professor of Orthopaedics and Rehabilitation; Assistant Professor of Pathology

Departments & Organizations

Orthopaedics & Rehabilitation



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 always 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 researching the actions of EBF1 in mesenchymal development. 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 cell than arises in other locations and this is primarily highlighted by the different way that these cells rely upon the presence of EBF1. 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.  Our work in kidney is also tied back to bone through the investigation of the pathology underlying chronic kidney disease-mineral bone disorders.

Education & Training

PhD University of Wisconsin-Madison, Biochemistry (2007)
BS University of New Hampshire, Biochemistry and Molecular Biology (2002)
Research Scientist Yale School of Medicine
Postdoctoral Fellowship Yale School of Medicine

Honors & Recognition

  • John Haddad Young Investigator AwardAmerican Society for Bone and Mineral Research (2010)

  • Young Investigator AwardAmerican Society for Bone and Mineral Research (2009)

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Contact Info

Jackie Fretz, PhD
Lab Location
Tompkins Memorial Pavilion
789 Howard Avenue, Ste 522/515

New Haven, CT 06519
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Office Location
Tompkins Memorial Pavilion
789 Howard Avenue, Ste 522A

New Haven, CT 06519
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Mailing Address
Orthopaedics & RehabilitationPO Pox 708071

New Haven, Connecticut 06520-8071

Curriculum Vitae

EBF1 regulates bone vasculature

Deletion of EBF1 from the mesenchymal lineage results in expanded marrow sinusoids, an increase in marrow adipogenesis, and increased numbers of vessels traversing the mineralized portion of cortical bone. This is due to the actions of EBF1 in the pericyte cells lining the vessels of bone. Regulation of bone vasculature is essential to fracture repair, oncogenic engraftment, maintenance of the hematopoeitic niche, and mineral homeostasis.

Bone anabolism decreases when EBF1 is deleted

Mobilization of pericytes to replace and continue anabolic bone growth in the adult skeleton is an essential function of mineral homeostasis. In the absence of EBF1 fewer osteoblasts are recruited to bone surfaces in middle aged mice and as demonstrated by calcein and alizarin red labeling, bone anabolism slows.

Trichrome staining of 3 month old Ebf1-/- mouse kidney

Ebf1 deletion results in hypoplastic kidneys with a thinned cortex and immature peripheral glomeruli. By 3 months surviving mice exhibit interstitial fibrosis, glomerulosclerosis, tubular dilation, and hematuria.