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 a VA Merit Investigator and Staff Pathologist. He is also on the faculty of the Department of Cell Biology and in the McGowan Institute for Regenerative Medicine.

Office Location:
University of Pittsburgh
705 Scaife Hall
DeSoto & Terrace Streets
Pittsburgh, PA 15261
Clinical Office:
Rm. 3013
Clinical Laboratory Building

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

Lab Admin. Office:
Fax: 412-647-5934
Telephone: 412-647-3762
Clinical Office: 412-647-6138
Email Address: hcblair@imap.pitt.edu


  • BA - Washington University, 1976
  • MD - Washington University, 1980


American Board of Pathology (Anatomic Pathology and Clinical Pathology)


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
Visiting Professor, Mahidol Medical School, Bankok, Thailand 2012.

Research Interests

Dr. Blair's current research activity includes:

R01 AR065407-01 (12/1/13-11/30/18)
Role PI (Multi PI award, Blair corresponding PI, 15% effort)
Regulation of Osteoclastogenesis by Calcium
This proposal characterizes the role of the Orai1 calcium channel in osteoclast formation, and in bone development, in human cells in vitro and in transgenic mouse models in vivo.

BX002490-01A1 10/1/2014-9/30/2018
Role PI (VA Merit award 27.5% effort)
Regulation of osteoblasts by ACTH and VEGF
We will study mechanisms by which hormones regulate the balance of bone formation and bone loss, studying human precursor cells differentiating in tissue cultures and using a mouse model. The growth and differentiation signals to be studied, tumor necrosis factor-alpha and vascular endothelial growth factor, are key regulators of bone health, and may also provide important insights regarding the mechanism of mineral deposition in other pathological processes. This is relevant to the risk for fractures and osteoporosis, major causes of disability Veterans. Osteoporosis is also of particular significance to female Veterans. The studies will include analysis of mechanisms that may allow undesirable side effects of therapy on bone, particularly effects of glucocorticoids, to be avoided.

Mechanisms of Bone Mineralization (Application for support pending)
Role PI (Multi PI award, Blair corresponding PI, 15% effort)
Novel Mechanisms Causing Delayed Mineralization Disorders
Delayed mineralization can cause weak bone or osteoporosis; some causes are well known, such as mineral transport defects, but the complete pathway of mineral transport during bone formation is not established. In the work proposed, we will study previously uncharacterized ion transporters that are highly active during bone formation, to determine how they support bone formation and the consequences when they are missing or dysfunctional.

Regulation of macrophage-family cells by fatty acids
Role PI (Application for support in preparation)
Membranes of somatic cells, such as red blood cells, incorporate fatty acids that reflect dietary intake. When excessive saturated and trans-unsaturated fats are incorporated, membrane fluidity is restored by fatty acid desaturases acting on the saturated fats. In health, when cells die macrophages recycle completely the cell components, including membranes. Cell membrane debris is exported, as cholesterol or cholesterol esters, for disposal by the liver or, as triglycerides or phospholipids, for lipid storage or re-use in membranes. When macrophages cannot fully recycle cell membranes, semi-liquid masses of partially oxidized fatty acids and cholesterol, foamy macrophages, and proliferating stromal cells accumulate in arterial walls, atherosclerosis. From ancient times, dietary excess has been known cause atherosclerosis. A dramatic increase of atherosclerotic disease in developed countries since ~ 1940 reflects in large part superabundant nutrition and altered dietary composition. Dietary changes include increased saturated and artificial trans-unsaturated fat intake. The biochemical basis of this epidemic of atherosclerosis reflects limited reverse transport capacity and a partial metabolic block in ?-oxidation caused by certain trans-fatty acid intermediates.

Selected Publications

View Dr. Blair's publications on Google Scholar or PubMed

  1. Frattini A, Blair HC, Sacco MG, Cerisoli F, Faggioli F, Catò 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 U S A. 2005 102: 14629-34. PMID: 16195375; PMC1253616.
  2. Sun L, Blair HC, Peng Y, Zaidi N, Adebanjo OA, Wu XB, Wu XY, Iqbal J, Epstein S, Abe E, Moonga BS, Zaidi M. Calcineurin regulates bone formation by the osteoblast. Proc Natl Acad Sci U S A. 2005 102: 17130-5. PMID: 16286645; PMC1288002.
  3. Yaroslavskiy BB, Zhang Y, Kalla SE, García Palacios V, Sharrow AC, Li Y, Zaidi M, Wu C, Blair HC. NO-dependent osteoclast motility: reliance on cGMP-dependent protein kinase I and VASP. J Cell Sci. 2005 118: 5479-87. PubMed PMID: 16291726; PMC in process.
  4. Yaroslavskiy BB, Sharrow AC, Wells A, Robinson LJ, Blair HC. Necessity of inositol (1,4,5)-trisphosphate receptor 1 and mu-calpain in NO-induced osteoclast motility. J Cell Sci. 2007 120: 2884-94. PMID: 17690304; PMC2976040.
  5. Tondelli B, Blair HC, Guerrini M, Patrene KD, Cassani B, Vezzoni P, Lucchini F. Fetal liver cells transplanted in utero rescue the osteopetrotic phenotype in the oc/oc mouse. Am J Pathol. 2009 174: 727-35. PMID: 19218349; PMC2665735.
  6. Blair HC, Yaroslavskiy BB, Robinson LJ, Mapara MY, Pangrazio A, Guo L, Chen K, Vezzoni P, Tolar J, Orchard PJ. Osteopetrosis with micro-lacunar resorption because of defective integrin organization. Lab Invest. 2009 89: 1007-17. PMID: 19546854; PMC2856930.
  7. Robinson LJ, Blair HC, Barnett JB, Zaidi M, Huang CL. Regulation of bone turnover by calcium-regulated calcium channels. Ann N Y Acad Sci. 2010 1192: 351-7. PMID: 20392259 PMC in process.
  8. Wilson DC, Marinov AD, Blair HC, Bushnell DS, Thompson SD, Chaly Y, Hirsch R. Follistatin-like protein 1 is a mesenchyme-derived inflammatory protein and may represent a biomarker for systemic-onset juvenile rheumatoid arthritis. Arthritis Rheum. 2010 62: 2510-6. PMID: 20506332; PMC2921021.
  9. 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 90: 1533-42. PMID: 20567233; PMC3114438.
  10. Zhou Y, Lewis TL, Robinson LJ, Brundage KM, Schafer R, Martin KH, Blair HC, Soboloff J, Barnett JB. The role of calcium release activated calcium channels in osteoclast differentiation. J Cell Physiol. 2011 226: 1082-9. PMID: 20839232; PMC4020518.
  11. Blair HC, Robinson LJ, Huang CL, Sun L, Friedman PA, Schlesinger PH, Zaidi M. Calcium and bone disease. Biofactors. 2011 37: 159-67. PMID: 21674636; PMC3608212.
  12. Liu L, Alonso V, Guo L, Tourkova I, Henderson SE, Almarza AJ, Friedman PA, Blair HC. Na+/H+ exchanger regulatory factor 1 (NHERF1) directly regulates osteogenesis. J Biol Chem. 2012 287: 43312-21. PMID: 23109343; PMC3527918.
  13. Robinson LJ, Mancarella S, Songsawad D, Tourkova IL, Barnett JB, Gill DL, Soboloff J, Blair HC. Gene disruption of the calcium channel Orai1 results in inhibition of osteoclast and osteoblast differentiation and impairs skeletal development. Lab Invest. 2012 92: 1071-83. PMID: 22546867; PMC3387291.
  14. Wang B, Yang Y, Liu L, Blair HC, Friedman PA. NHERF1 regulation of PTH-dependent bimodal Pi transport in osteoblasts. Bone. 2013 52: 268-77. PMID: 23046970; PMC3513631.
  15. Zacherl JR, Mihalik SJ, Chace DH, Christensen TC, Robinson LJ, Blair HC. Elaidate, an 18-carbon trans-monoenoic fatty acid, inhibits ?-oxidation in human peripheral blood macrophages. J Cell Biochem. 2014 115:62-70. PubMed PMID: 23904193. PMC in process.
  16. Chaly Y, Blair HC, Smith SM, Bushnell DS, Marinov AD, Campfield BT, Hirsch R. Follistatin-like protein 1 regulates chondrocyte proliferation and chondrogenic differentiation of mesenchymal stem cells. Ann Rheum Dis. 2014 Mar 21. doi: 10.1136/annrheumdis-2013-204822. [Epub ahead of print] PMID: 24641944; PMC: in process.