Joan D. Beckman

     E-mail: beckm092@umn.edu

     Year Entered: 2004

     Degrees Received:
     North Dakota State University
     Zoology and Biotechnology majors
     B.S., 2004

     University of Minnesota
     Ph.D., 2010, Microbiology, Immunology, and Cancer Biology PhD Program
     M.D., 2012, Medical School

Honors and Awards:
-National Institute on Aging National Research Service Award for Individual Predoctoral MD/PhD Fellows, 2007-2011
-2008 Central Society for Clinical Research Trainee Travel Award
-2008 Midwestern Section American Federation for Medical Research Junior Scholar Award
-Best Poster Award, 2008 American Physician Scientists Association (APSA)/American Society for Clinical Investigation/Association of American Physicians (ASCI/AAP)
-2008 Science Award, National Institutes of Health Workshop on Vasculopathy in Sickle Cell Disease, Natcher Conference Center, Bethesda, MD
-Best Poster Award, 2008 Department of Medicine Robert P. Hebbel Research Day
-2008 ASH Travel Award

Thesis Advisor: Greg Vercellotti, M.D.

Thesis Research: 
Joan is currently working toward towards her Ph.D. in Microbiology, Immunology, and Cancer Biology.  Joan’s research interest is in vascular inflammation and blood vessel stasis that occurs in patients with sickle cell disease and transgenic sickle mice. The goals of her current research in the laboratory of Dr. Greg Vercellotti revolve around increasing our knowledge about the role of heme in the pathophysiology of SCD and other conditions using animal and cell culture models.

The major question in the Vercellotti lab is how do sickle patients defend or adapt to excessive oxidative stress and inflammation resulting from red blood cell hemolysis and the release of Hb, heme and iron into the vasculature.  Patients with sickle cell disease exhibit significantly elevated oxidative stress and inflammation and elevated cytoprotective genes, including heme oxygenase and ferritin. The Vercellotti group has demonstrated that heme-oxygenase -1 protein (HO-1) plays a critical role in metabolizing the excess heme generated during hemolysis and in modulating vaso-occlusion in murine models of sickle cell disease (SCD).  The products of HO-1 activity, carbon monoxide (CO), Fe2+ /ferritin, and biliverdin/bilirubin have demonstrable anti-oxidant and anti-inflammatory effects. Joan is currently investigating if the HO-1 product CO can work as a therapy for SCD.  Specifically, Joan is exploring the potential use of inhaled CO to modulate inflammatory cell differentiation in SCD models. 

In addition, Joan is exploring the new area of microRNA research.  Mature miRNAs are cleaved from ~70-nucleotide hairpin structures, called precursor miRNAs (pre-miRNAs), in the cytoplasm by the enzyme Dicer. Prior to this final step, pre-miRNAs are excised in the nucleus from a primary miRNA (pri-miRNA) transcript by the RNase III enzyme Drosha and its co-factor DiGeorge Critical Region 8 (DGCR8 also known as Pasha) which are necessary and sufficient for pri-mRNA processing.  Recent evidence has shown that DGCR8 relies on heme in order to function efficiently.  The ability of DGCR8 to function as a heme biosensor provides an elegant mechanism of linking heme levels to global protein synthesis and cellular differentiation.  This possibility has implications for sickle cells disease as well as in other heme-mediated disorders.  

Joan’s main residency interest is hematology/oncology.  Joan grew up and attended high school in Jamestown, North Dakota.  Joan is currently a member of the Health Sciences Orchestra. During her free time she enjoys reading, following baseball, watching movies, travel, and swimming.

Publications (pubmed):

Beckman JD, Chen C, Nguyen J, Thayanithy V, Subramanian S, Steer CJ, Vercellotti GM. Regulation of heme oxygenase-1 protein expression by miR-377 in combination with miR-217.  J Biol Chem. 2011 Feb 4;286(5):3194-202.

Belcher JD, Vineyard JV, Bruzzone CM, Chen C, Beckman JD, Nguyen J, Steer CJ, Vercellotti GM. Heme oxygenase-1 gene delivery by Sleeping Beauty inhibits vascular stasis in a murine model of sickle cell disease. J Mol Med. 2010 Jul;88(7):665-75.

Belcher JD, Beckman JD, Balla G, Balla J, Vercellotti G. Heme degradation and vascular injury. Antioxid Redox Signal. 2010;12:233-248.

Beckman JD, Belcher JD, Vineyard JV, Chen C, Nguyen J, Nwaneri MO, O'Sullivan MG, Gulbahce E, Hebbel RP, Vercellotti GM Md. Inhaled Carbon Monoxide Reduces Leukocytosis in a murine model of sickle cell disease. Am J Physiol Heart Circ Physiol. 2009;297:H1243-53.

Bruzzone CM, Belcher JD, Schuld NJ, Newman KA, Vineyard J, Nguyen J, Chen C, Beckman JD, Steer CJ, Vercellotti GM. Quantitative real-time polymerase chain reaction (qRT-PCR) restriction fragment length polymorphism (RFLP) method for monitoring highly conserved transgene expression during gene therapy. Transl Res. 2008 ;152:290-7.

Beckman JD, Grazul-Bilska AT, Johnson ML, Reynolds LP; Redmer DA. Effects of nitric oxide on expression of angiogenic factors by luteal pericytes. Endorine 2006;29:467-476.

Reynolds LP, Beckman JD, Kirsch JD, Kraft KC, Redmer, DA. Expression of Basic Fibroblast Growth Factor (bFGF) in ovine uterine and placental tissues of late pregnancy. Biology of Reproduction 1999, 60 (supp. 1).

Beckman JD,Reynolds LP, Redmer DA, Kirsch JD, Petry KD, Kraft KC, Redmer CB, Grazul-Bilska AT. Isolation and Characterization of Ovine Luteal Pericytes and endothelial cells and the study of vascular endothelial growth factor (VEGF) and nitric oxide (NO) interactions. In:Biology of Reproduction 2003, 68 (supp. 1): 137.

Beckman JD, Reynolds LP, Grazul-Bilska AT, Kirsch JD, Kraft KC, Johnson ML, Redmer DA.  2004.  Expression of angiogenic factors in ovine luteal pericytes exposed to nitric oxide.  Biol. Reprod. 70 (Suppl. 1).

Obrtlikova P, Ross JJ, Luttun A, Beckman JD, Keirstead SA, Kaufman DS. Transition of Human Embryonic Stem Cell-Derived Endothelial Cells to Smooth Muscle Cells in Culture as a Model for Vascular Development. Blood 2005;106 (11).