Photo of Donald Bloch

Donald Bloch, MD

The Bloch Laboratory at Massachusetts General Hospital investigates the role of the bone morphogenetic protein signal transduction pathway in a broad spectrum of human diseases

Overview

Principal Investigator, Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital

Associate Physician, Rheumatology Unit, Department of Medicine, Massachusetts General Hospital

Associate Professor of Medicine, Harvard Medical School

 

The Bloch Laboratory investigates the role of the bone morphogenetic protein signal transduction pathway in a broad spectrum of human diseases, including iron overload syndromes, anemia, inflammation, Sjogren’s syndrome, non-alcohol related fatty liver disease, calciphylaxis and atherosclerosis. In addition, members of the laboratory investigate the structure and function of human autoantigens, with the intention of determining the role of these antigens in the pathogenesis of autoimmune diseases. The laboratory also studies the functional significance of genetic polymorphisms associated with hypertension.

 

The current research program focuses on three areas:

The role of the bone morphogenetic protein signaling pathway on the pathogenesis of human diseases, including inflammation, anemia, vascular calcification and atherosclerosis.

Ongoing studies use mice lacking components of the BMP signaling pathway to investigate the role of the BMP signaling in iron homeostasis and the innate immune system. In addition, we are examining the effects of blocking BMP receptors, using small molecule inhibitors, on the anemia of inflammation and the development of atherosclerosis.

Identification and characterization of novel, primary biliary cirrhosis-related, human autoantigens.

We have used the antibodies in the serum from more than 700 patients with this organ specific autoimmune disease to study the structure and function of two novel cellular structures: the PML-Sp100 nuclear body and the cytoplasmic mRNA processing body. Mutations in the gene encoding one autoantigen within the PML-Sp100 nuclear body, designated Sp110, were found to cause an immunodeficiency disorder known as “VODI” (veno-occlusive disease with immunodeficiency). Ongoing studies are examining the role of Sp110 in the maturation of cells involved in host defense, including B and T lymphocytes and monocytes.

The functional analysis of genetic polymorphisms associated with hypertension.

In collaboration with Dr. Newton-Cheh in the Division of Cardiology and Emmanuel Buys in the Anesthesia Center for Critical Care Research , we are characterizing the functional significance of genetic polymorphisms associated with increased blood pressure. A rare polymorphism in the gene encoding atrial natriuretic peptide (ANP) was found to be associated with decreased blood pressure. We showed that the polymorphism was within the seed sequence of microRNA 425, making the mRNA encoding ANP relatively resistant to degradation and increasing the level of circulating ANP. Ongoing studies are examining the functional significance of polymorphisms within other component of the ANP signaling pathway.

 

 

 

 

Group Members

Principal Investigator:

  • Donald Bloch, MD

Faculty Members:

  • Aranya Bagchi, MD
  • Rajeev Malhotra, MD
  • David Rhee, MD, PhD

Research Fellows:

  • Sara Vandenwijngaert, PhD
  • Florian Wunderer, MD

Research Projects

  • The role of the BMP signal transduction pathway in the pathogenesis of human diseases, including iron overload syndromes, anemia, inflammation, Sjogren’s syndrome, non-alcohol related fatty liver disease, calciphylaxis and atherosclerosis.
  • The structure and function of primary biliary cirrhosis autoantigens in the PML-nuclear body and the mammalian, cytoplasmic mRNA processing body.
  • The function of Sp110 and its role in the pathogenesis of VODI.
  • The functional significance of polymorphisms associated with hypertension.

Publications

Contact

Contact Us

Bloch Laboratory

Thier 5

55 Fruit Street Boston, MA 02114
  • Near Public Transit
  • Accessible
  • Phone: 617-726-3780
  • Fax: 617-726-2872
  • Email Us

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