Harry C. Blair, MD

Professor of Pathology, Division of Clinical Chemistry

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.


American Board of Pathology (Anatomic Pathology and Clinical Pathology)


Metabolic Bone Disease

Education & Training
BA - Washington University, 1976
MD - Washington University, 1980
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.

NIH Research

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

Representative Publications

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

  • Tourkova IL, Liu L, Sutjarit N, Larrouture QC, Luo J, Robinson LJ, Blair HC.Adrenocorticotropic hormone and 1,25-dihydroxyvitamin D3 enhance humanosteogenesis in vitro by synergistically accelerating the expression of bone-specific genes. Lab Invest. 2017 97: 1072-1083. PMID: 28737765. PMCID: PMC5844701.
  • Blair HC, Larrouture QC, Li Y, Lin H, Beer-Stoltz D, Liu L, Tuan RS, Robinson LJ, Schlesinger PH, Nelson DJ. Osteoblast Differentiation and Bone Matrix Formation In Vivo and In Vitro. Tissue Eng Part B Rev. 2017 23: 268-280. PMID: 27846781. PMCID: PMC5467150.
  • Larrouture QC, Nelson DJ, Robinson LJ, Liu L, Tourkova I, Schlesinger PH, Blair HC. Chloride-hydrogen antiporters ClC-3 and ClC-5 drive osteoblast mineralization and regulate fine-structure bone patterning in vitro. Physiol Rep. 2015 Nov;3(11). pii: e12607. doi: 10.14814/phy2.12607. Epub 2015 Nov 24. PMID: 26603451. PMCID: PMC4673636.
  • Palagano E, Blair HC, Pangrazio A, Tourkova I, Strina D, Angius A, Cuccuru G, Oppo M, Uva P, Van Hul W, Boudin E, Superti-Furga A, Faletra F, Nocerino A, Ferrari MC, Grappiolo G, Monari M, Montanelli A, Vezzoni P, Villa A, Sobacchi C. Buried in the Middle but Guilty: Intronic Mutations in the TCIRG1 Gene Cause Human Autosomal Recessive Osteopetrosis. J Bone Miner Res. 2015 3010:1814-21. PMID: 25829125.
  • Elaidate, an 18-carbon trans-monoenoic fatty acid, inhibits β-oxidation in human peripheral blood macrophages. Zacherl JR, Mihalik SJ, Chace DH, Christensen TC, Robinson LJ, Blair HC. J Cell Biochem. 2014 115:62-70. PMID: 23904193.