Don M. Wojchowski, Ph.D.
Maine Medical Center Research Institute
81 Research Dr
Scarborough ME, 04074
Phone: (207) 396-8258
Fax: (207) 396-8179
Don Wojchowski is a native of Maine (and greater Portland) who graduated from Colby College; acquired biomedical research training at Boston's Children's Hospital; completed doctoral studies within a cell biology training program at the University of Massachusetts, Amherst; and then pursued postdoctoral studies at Harvard Medical School. Subsequently (from 1987-2003) Dr. Wojchowski served as assistant, associate and full Professor at The Pennsylvania State University (and as Immunobiology Program Director) with a research focus on hematopoiesis. He has served on several NIH study sections and national review committees, and is the recipient of several NIH career development awards. In October 2003, Dr. Wojchowski returned to Maine to join MMCRI. In 2005, Dr. Wojchowski was appointed Director of MMCRI's NIH sponsored COBRE Center of Excellence in Stem Cell Biology and Regenerative Medicine.
One focus of our laboratory's investigations is on key regulators of erythropoiesis, especially within clinically relevant anemia contexts. EPO/EPOR effects, and molecular action mechanisms are one prime example. Using combined approaches of knocked-in EPOR alleles, primary progenitor cell systems, transcriptome and phosphoproteomic analyses, we've discovered that the EPOR regulates much more than BCL-XL and survival [J Clin Invest 116:683-94]. Intriguing new major EPOR targets include cyclin G2 (a cell cycle brake) [BLOOD 110:2361-70]; Podocalyxin (a cell surface adhesion/migration factor) [BLOOD 110:509-18]; Spi2A (an atypical intracellular serpin) [under revision for Journal of Experimental Medicine]; TRIB3 (an E3 ubiquitin ligase adaptor) [BLOOD 111:5390-9]; and DAPK2 (an autophagy-linked S/T kinase) [BLOOD 112:886-90]. For each, we've now developed novel knockout mouse models with exciting initial phenotypes. Recent phosphoproteomic analyses, in addition, are revealing new connections between EPO/EPOR and cell migration events.
The importance of such work is underlined by EPO's ability to cytoprotect ischemically injured cardiac, neural and renal tissues; and to modulate tumorigenesis. In addition, novel EPO mimetics are emerging with distinct EPOR activation properties that merit mechanistic attention as they enter the clinic - and we are actively investigating such important new agents [BLOOD 113:4955-62].
Our global interrogations of erythropoietic regulators have further uncovered a handful of regulators that are proving to play important emerging roles in the development of renal, vascular, bone and hematopoietic stem cells. Exciting new collaborative investigations are being forged to gain insight into these factors, and their roles during injury and regenerative responses in these frequently clinically compromised tissues.
[note: For a further listing of publications please click here]
Sathyanarayana P, Dev A, Pradeep A, Ufkin M, Licht JD, Wojchowski DM. Spry1 as a novel regulator of erythropoiesis, EPO/EPOR target, and suppressor of JAK2. Blood. 2012;119:5522-31. PMCID: PMC3369686.
Singh S, Dev A, Verma R, Pradeep A, Sathyanarayana P, Green JM, Narayanan A, Wojchowski DM. Defining an EPOR- regulated transcriptome for primary progenitors, including Tnfr-sf13c as a novel mediator of EPO- dependent erythroblast formation. PLoS One. 2012;7:e38530. PMCID: PMC3396641.
Singh S, Verma R, Pradeep A, Leu K, Mortensen RB, Young PR, Oyasu M, Schatz PJ, Green JM, Wojchowski DM. Dynamic ligand modulation of EPO receptor pools, and dysregulation by polycythemia-associated EPOR alleles. PLoS One. 2012;7:e29064. PMCID: PMC3257245.
Wojchowski D. Eugene Goldwasser (1922-2010). Nature. 2011;470:40 (invited overview).
Dev A, Fang J, Sathyanarayana P, Pradeep A, Emerson C, Wojchowski DM. During EPO or anemia challenge, erythroid progenitor cells transit through a selectively expandable proerythroblast pool. Blood. 2010;116:5334-46. PMCID: PMC3012546.
Wojchowski DM, Sathyanarayana P, Dev A. Erythropoietin receptor response circuits. Curr Opin Hematol. 2010;17:169-76. PMCID: PMC2855390.
Sathyanarayana P, Houde E, Marshall D, Volk A, Makropoulos D, Emerson C, Pradeep A, Bugelski PJ, Wojchowski DM. CNTO 530 functions as a potent EPO mimetic via unique sustained effects on bone marrow proerythroblast pools. Blood. 2009;113:4955-62. PMCID: PMC2686145.
Sathyanarayana P, Dev A, Fang J, Houde E, Bogacheva O, Bogachev O, Menon M, Browne S, Pradeep A, Emerson C, Wojchowski DM. EPO receptor circuits for primary erythroblast survival. Blood. 2008;111:5390-9. PMCID: PMC2396729.
Fang J, Menon M, Zhang D, Torbett B, Oxburgh L, Tschan M, Houde E, Wojchowski DM. Attenuation of EPO-dependent erythroblast formation by death-associated protein kinase-2. Blood. 2008;112:886-90. PMCID: PMC2481541.
Sathyanarayana P, Menon M, Bogacheva O, Bogachev O, Niss K, Kapelle W, Houde E, Fang J, Wojchowski DM. Erythropoietin modulation of podocalyxin and a proposed erythroblast niche. Blood. 2007;110:509-18. PMCID: PMC1924484.
Fang J, Menon M, Kapelle W, Bogacheva O, Bogachev O, Houde E, Browne S, Sathyanarayana P, Wojchowski DM. EPO modulation of cell-cycle regulatory genes, and cell division, in primary bone marrow erythroblasts. Blood. 2007;110:2361-70. PMCID: PMC1988929.
Menon M, Karur V, Bogacheva O, Bogachev O, Cuetara B, Wojchowski DM. Signals for stress erythropoiesis are integrated via an erythropoietin receptor phosphotyrosine-343-Stat5 axis J Clin Invest. 2006;116:683-94. PMCID: PMC1386105.