Harry C. Blair, MD
Professor of Pathology

Dr. Blair

Dr. Blair is a member 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

I investigate the regulation of bone turnover and the mechanisms by which bone is deposited and resorbed. I use human models including human mesenchymal stem cells, which differentiate into bone-forming osteoblasts, and human monocytes, which differentiate into macrophages and osteoclasts. I also study selected related topics in clinical chemistry; currently these include the mechanisms by which trans-fatty acids cause pathology by interfering with fatty acid catabolism in macrophages. Major current projects include regulation of osteoclast formation by calcium; the role of glycoprotein hormones, traditionally thought of as pituitary-endocrine regulators, in direct action on bone turnover. New projects in development include regulation by PTH of osteoblast transport, and osteoblast acid transport and matrix vesicle activity. Research support added over the past year includes an RO1 (multi PI, I am the submitting PI), and my VA Merit was recently scored in the funding range. Two additional RO1 applications are pending review.

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 β-oxidation caused by certain trans-fatty acid intermediates.

NIH Research

View Dr. Blair's NIH RePORT on nih.gov

Selected Publications

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

  • Follicle Stimulating Hormone Receptor in Mesenchymal Stem Cells Integrates Effects of Glycoprotein Reproductive Hormones. Tourkova IR, Witt MR, Li L, Larrouture Q, Liu L, Luo Jianhua, Robinson LJ, Blair HC. Marrow (NYAS) in press.
  • Follistatin-like protein 1 regulates chondrocyte proliferation and chondrogenic differentiation of mesenchymal stem cells.Chaly Y, Blair HC, Smith SM, Bushnell DS, Marinov AD, Campfield BT, Hirsch R.Ann Rheum Dis. 2014 Mar 21. doi: 10.1136/annrheumdis-2013-204822. [Epub ahead of print] PMID: 24641944 [PubMed - as supplied by publisher]
  • Thyroid and bone: macrophage-derived TSH- splice variant increases murine osteoblastogenesis. Baliram R, Chow A, Huber AK, Collier L, Ali MR, Morshed SA, Latif R, Teixeira A, Merad M, Liu L, Sun L, Blair HC, Zaidi M, Davies TF. Endocrinology. 2013 Dec;154(12):4919-26. doi: 10.1210/en.2012-2234. Epub 2013 Oct 18. PMID: 24140716 [PubMed - indexed for MEDLINE]
  • Elaidate, an 18-carbon trans-monoenoic fatty acid, inhibits -oxidation in human peripheral blood macrophages. Zacherl JR, Mihalik SJ, Chace DH, Christensen TC, Robinson LJ, Blair HC. J Cell Biochem. 2014 Jan;115(1):62-70. doi: 10.1002/jcb.24633. PMID: 23904193 [PubMed - in process]
  • RANKL cytokine: from pioneer of the osteoimmunology era to cure for a rare disease. Lo Iacono N, Pangrazio A, Abinun M, Bredius R, Zecca M, Blair HC, Vezzoni P, Villa A, Sobacchi C. Clin Dev Immunol. 2013;2013:412768. doi: 10.1155/2013/412768. PMID: 23762088 [PubMed - indexed for MEDLINE]. PMCID: PMC3671266.