John Belcher, PhD

Associate Professor of Medicine, Division of Hematology, Oncology and Transplantation

John Belcher

Contact Info

Mailing Address:
Division of Hematology, Oncology and Transplantation
420 Delaware Street SE, MMC 480
Minneapolis, MN 55455

Administrative Assistant Name
Barbara Porwit

Administrative Phone
612-624-5620

Administrative Email
porw0001@umn.edu

Administrative Fax Number
612-626-6919

PhD, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC

Cardiovascular Research Institute, University of California, San Francisco, CA

Summary

Dr. Belcher earned his PhD from Wake Forest University. He joined the Division of Hematology, Oncology and Transplantation (HOT) in 1996. In collaboration with other HOT investigators, Dr. Belcher’s research has been integral to a series of important discoveries demonstrating heme is central to the pathobiology of sickle cell anemia. Dr. Belcher’s laboratory work is committed to the successful translation of laboratory discoveries to clinical care.

Expertise

  • Sickle cell anemia
  • Heme metabolism
  • Gene therapy
  • Endothelial biology
  • Inflammation

Awards & Recognition

American Society of Hematology

Research

Research Summary/Interests

Dr. Belcher’s research is focused on hemoglobin, heme, and iron toxicity to the endothelium, as well as related cytoprotective responses. Currently, he is investigating heme-mediated inflammation and vaso-occlusion in sickle cell anemia through toll like receptor-4 signaling. His research is also exploring the cytoprotective effects of Nrf2, heme oxygenase-1, ferritin, haptoglobin, and hemopexin in the context of iron-mediated oxidative stress.

Cell and Molecular Biology; Sickle Cell Anemia; Endothelial Cells; Vascular Biology; Heme-mediated Inflammation; Gene Therapy

Publications

  • Belcher JD, Chen C, Nguyen J, Milbauer L, Abdulla F, Alayash AI, Smith A, Nath KA, Hebbel RP, and Vercellotti GM. Heme triggers TLR4 signaling leading to endothelial cell activation and vaso-occlusion in murine sickle cell disease. Blood 2014;123:377-390.
  • Belcher JD, Young M, Chen C, Nguyen J, Burhop K, Tran P, Vercellotti GM. MP4CO, a pegylated hemoglobin saturated with carbon monoxide is a modulator of HO-1, inflammation and vaso-occlusion in transgenic sickle mice. Blood. 2013;122(15):2757-2764.
  • Belcher JD, Nath KA, Vercellotti GM. Vasculotoxic and pro-inflammatory effects of plasma heme: Cell signaling and cytoprotective responses. Review. Oxidative Medicine. 2013;Article ID 831596.
  • Schaer DJ, Buehler PW, Alayash AI, Belcher JD, Vercellotti GM. Perspective Article. Hemolysis and free hemoglobin revisited: Exploring hemoglobin and hemin scavengers as a novel class of therapeutic proteins. Blood. 2013;121(8):1276-84.
  • 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;88(7):665-75.
  • Belcher JD, Beckman JD, Balla G, Balla J, Vercellotti G. Heme degradation and vascular injury. Antioxid Redox Signal. 2010;12(2):233-48. Review.a
  • Belcher JD, Chen C, Nguyen J, Milbauer L, Abdulla F, Alayash AI, Smith A, Nath KA, Hebbel RP, and Vercellotti GM. Heme triggers TLR4 signaling leading to endothelial cell activation and vaso-occlusion in murine sickle cell disease. Blood 2014;123:377-390.