Harry C. Blair, MD
Professor of Pathology

Dr. Blair

Dr. Blair is the Director of the Division of Clinical Chemistry in the Section of Laboratory Medicine and is also in the faculty of the Department of Cell Biology and Physiology.

Office Location:
University of Pittsburgh
705 Scaife Hall
DeSoto & Terrace Streets
Pittsburgh, PA 15261

Clinical Office:
Rm. 5514
Magee-Womens-Hospital

Contact Information:
Office Telephone: 412-383-9616
Lab Telephone: 412-624-2471

Lab Admin. Ofc.: (Secretary)
Fax: 412-647-8567
Telephone: 412-647-8409

Clinical Office: 412-641-5391
Email Address: hcblair@imap.pitt.edu

Education

  • BA - Washington University, 1972
  • MD - Washington University, 1980

Certifications

American Board of Pathology (Anatomic Pathology and Clinical Pathology)

Specialties

Metabolic Bone Disease

Awards and Honors (since 2000)

Visiting Scholar, Wolfson College, and Member, Senior Common Room, Wadham College, Oxford University, 2002-03.
Visiting Professor, Consiglio Nazionale delle Ricerche (CNR), Milano, Italy, Spring 2010

Research Interests

Dr. Blair's current research activity is centered on:
  • The role of calmodulin and cGMP in osteoclast control. This work considers how Ca+2 interacts with cGMP, itself modified by NO. Goals: 1) Determine the physiological role of intracellular calcium puffs at the acid secretion site. 2) Modify production of cGMP-dependent protein kinase or calmodulin-dependent phosphatase and study the effects on osteoclastic activity. 3) Characterize the interaction of cGMP and Ca+2 signals in osteoclasts. NIH 1RO1 AG12951-05; 99-00 direct $161,935.

  • Phytoestrogen regulation of bone turnover. We are studying which cells in bone turnover respond to estrogens, and the receptor(s) that mediate this response. Goals: 1) Determine the response of osteoclast regulatory proteins to isoflavone SERMs. 2) Assess the activity of isoflavones when ERs are eliminated. 3) Characterize ER-independent actions of isoflavones in osteoclast membranes. AR 46587-01 2000-01 direct $142,553.

  • Regulation of osteoclasts in hyperparathyroid bone. This work is considering how cytokines expressed in response to PTH, notably a membrane form of the kit ligand, m-SCF, interact with basal signals for osteoclast formation. Its goals are to: 1) Characterize the interactions of m-SCF, CSF-1, and RANK-ligand in osteoclast formation. 2) Determine how m-SCF functions in ectopic mast cell and alternative osteoclast development. Department of Veterans Affair's Merit Award; current year $110,000 direct costs.

  • Downregulation of osteoclastic activity. This project is in development, and includes studies considering key mechanisms affecting human bone turnover related to major disease states. It will determine the relative roles of apoptotic and reversible mechanisms in regulation of bone degradation by 1) glucocorticoids, via receptors in (pre) osteoclastic and osteoblastic cells; and 2) bone-associated pH eluted antimetabolites, via interference with osteoclastic secretory mechanisms or osteoblastic differentiation/activation signals.

Selected Publications

View Dr. Blair's publications on PubMed

Liu L, Schlesinger PH, Slack NM, Friedman PA, Blair HC, High capacity Na+/H+ exchange activity in mineralizing osteoblasts. J Cell Physiol. 2011 Jun;226(6):1702-12. doi: 10.1002/jcp.22501.

Yaroslavskiy BB, Turkova I, Wang Y, Robinson LJ, Blair HC, Functional osteoclast attachment requires inositol-1,4,5-trisphosphate receptor-associated cGMP-dependent kinase substrate. Lab Invest. 2010 Oct;90(10):1533-42. Epub 2010 Jun 21.

Zaidi M, Sun L, Robinson LJ, Tourkova IL, Liu L, Wang Y, Zhu LL, Liu X, Li J, Peng Y, Yang G, Shi X, Levine A, Iqbal J, Yaroslavskiy BB, Isales C, Blair HC, ACTH protects against glucocorticoid-induced osteonecrosis of bone. Proc Natl Acad Sci U S A. 2010 May 11;107(19):8782-7. Epub 2010 Apr 26.

Frattini A, Blair HC, Sacco MG, Cerisoli F, Faggioli F, Cato EM, Pangrazio A, Musio A, Rucci F, Sobacchi C, Sharrow AC, Kalla SE, Bruzzone MG, Colombo R, Magli MC, Vezzoni P, Villa A. Rescue of ATPa3-deficient murine malignant osteopetrosis by hematopoietic stem cell transplantation in utero. Proc Natl Acad Sci USA 102: 14629-14634, 2005.

Sun L. Sharrow AC, Zhang Z, Iqbal J, Papachristou DJ, Zaidi S, Peng Y, Zhu L-L, Yaroslavskiy BB, Zhou H, Zallone A, Sairam MR, Kumar TR, Bo W, Braun J, Cardoso-Landa L, Schaffler MB, Moonga BS, Blair HC*, Zaidi M* (*Joint senior authors) FSH Directly Regulates Bone Mass: Implications for Understanding the Pathogenesis of Osteoporosis Due to Hypogonadism. Cell 2006 125: 247-60.

Borysenko CW, Garcia Palacios V, Griswold, RD, Li Y, Iyer A, Yaroslavskiy BB, Sharrow AC, Blair HC. DR3 mediates apoptosis in human osteoblasts under narrowly regulated conditions. J Cell Physiol 2006 209: 1021-8.

Iqbal, J, Sun L, Blair HC, Zaidi, M. FSH Stimulates TNF Production From Immune Cells. A Novel Mechanism for Hypogonadal Bone Loss. Proc Natl Acad Sci U S A. 2006 103: 14925-30.

Blair HC, Wells A, Isales CM. Pituitary Glycoprotein Hormone Receptors in Non-endocrine Organs. Trends Endocrinol Metab. 2007 18: 227-33.

Yaroslavskiy BB, Sharrow AC, Wells A, Robinson LJ, Blair HC. Necessity of Inositol-1,4,5-trisphosphate Receptor-1 and ?-Calpain in Nitric Oxide Induced Osteoclast Motility. J Cell Science. 2007 120: 2884-94.

Sharrow AC, Li Y, Micsenyi A, Griswold RD, Wells A, Monga SP, Blair HC. Modulation of Osteoblast Gap-junction Connectivity by Serum, TNFalpha, and TRAIL. Experimental Cell Res 2007 (In press).