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Faculty Information

Despina Sitara, Ph.D. M.Sc. B.Sc.
Assistant Professor
Basic Science and Craniofacial Biology
Room 902S Dental Center, 421 First Avenue
Fax: 212-995-4553



2010, Post-doctoral training, Harvard School of Public Health, Boston, US

2008, Post-doctoral training, Harvard School of Dental Medicine, Boston, US

2004, Ph.D., Queen Mary University of London, London, UK

2000, M.Sc., University of Bristol, Bristol, UK

1998, B.Sc. (Hons), University of the West of England, Bristol, UK


Research Interests / Professional Overview:

The focus of our research is to understand the mechanisms by which bone interacts with the bone marrow environment and how the mineral content of bone influences the fate of hematopoietic stem cells. In addition, we are investigating the role of phosphate-regulating molecules in skeletal mineralization and renal function. For our studies we are using genetically altered mouse models and employing a variety of approaches including generation of bone marrow chimeras, molecular biology, biochemistry, histology, immunohistochemistry, and cell culture.


Project I:

Hematopoietic disorders such as bone marrow failure and immune dysfunction (e.g. aplastic anemia, lymphopenia, rheumatoid arthritis), as well as certain cancers (e.g. leukemia, lymphoma, myeloma), involve a link between skeletal formation and establishment of the marrow. It is well known that endochondral ossification, the process of cartilage replacement by bone, is an essential prerequisite for the development of normal hematopoiesis in the bone marrow. Bone components such as cells, extracellular matrix and minerals, are involved in the regulation of hematopoietic stem cell (HSC) function in the adult mammal. In addition, vitamin D, a well known modulator of calcium homeostasis and bone mineralization, also plays a role in hematopoietic differentiation. In our studies we are investigating the interplay of bone with the hematopoietic environment and how bone–derived factors regulate their crosstalk. The goal of our studies is to determine the mechanistic basis for this skeleto-hematopoietic link by addressing how a genetic defect in bone development influences the marrow environment that is needed for blood cell differentiation and normal hematopoiesis. For our studies we are using a genetically altered mouse model with impaired bone mineralization and we are currently characterizing the hematopoietic phenotype of this model. In this project we are employing a variety of histological, immunological and, cell culture approaches, as well as, in vivo bone marrow transplantation experiments to test whether hematopoietic defects result directly from alterations in the chondro-osseous microenvironment, or stem from abnormalities in the hematopoietic stem cells. Our studies will establish whether bone-produced molecules could be used as potential therapeutic targets in developing strategies for treatment of hematological disorders associated with bone changes.


Project II:

Phosphate is an essential ion for many biological processes including bone growth and development. Phosphate balance is primarily determined by processes that regulate the efficiency of intestinal phosphate absorption and renal phosphate excretion. In recent years it has become evident that the bone and kidneys are closely linked and influence each other’s functions. Our lab is interested in understanding how phosphate homeostasis is regulated in vivo. The goal of our studies is to identify and characterize molecules that affect mineral metabolism and determine possible inter-dependencies/-relationships among hormones known to regulate phosphate, including parathyroid hormone (PTH) and vitamin D. For our studies we are using knock-out and transgenic mouse models with altered phosphate metabolism to investigate the effects of these genetic manipulations on mineral homeostasis and skeletogenesis. The bone phenotype of these mice is carefully and extensively analyzed by molecular biology and biochemical approaches, as well as, mCT, histomorphometry, histology and, in situ hybridization. Our findings will contribute to a better understanding of phosphate disturbances as well as treatment of skeletal disorders caused by altered phosphate metabolism and associated with renal disease.


Project III:

Our lab is interested in determining the role of phosphate in tooth development. Previous studies have showed that disruption in serum phosphate levels leads to bone and tooth abnormalities. We have showed that ablation of FGF-23 in mice, a hormone that regulates circulating phosphate levels, results in disrupted morphology, mineralization, and protein expression within the dentoalveolar complex. Our research focuses on investigating the mechanisms by which systemic phosphate impacts mineralization. For our studies we are using mouse models to determine how phosphate homeostasis is regulated in vivo and we use histology, immunohistochemistry, and electron microscopy analyses. Our studies will identify molecules that have significant impact on development and maintenance of healthy teeth and supporting structures, and our findings will lead to new approaches for developing more effective treatments for tooth disorders associated with impaired phosphate metabolism.


Current Funding:

Whitehead Fellowship for Junior Faculty in Biomedical & Biological Sciences

American Heart Association (AHA) Scientist Development Grant

American Society for Bone and Mineral Research (ASBMR) Career Enhancement Award


Current Lab Members:

Lindsay Coe, Ph.D.: Assistant Research Scientist, e-mail:

Miranda Foster: NYUCD student, e-mail:

Jessica Li: NYUCD student, e-mail:

Khushali Shah: NYUCD student, e-mail:




Pub Med Articles:

Sitara D


Representative Publications:

1. Coe LM, Vadakke Madathil S, Casu C, Lanske B, Rivella S, Sitara D. (2014). FGF-23 is a negative regulator of prenatal and postnatal erythropoiesis. J Biol Chem, 2014 Feb 7. [Epub ahead of print]

2. Vadakke Madathil S, Coe LM, Casu C, Sitara D. (2014). Klotho deficiency disrupts hematopoietic stem cell development and erythropoiesis. Am J Pathol, 184(3):827-41.

3. Yuan Q, Sitara D, Sato T, Densmore M, Saito H, Schüler C, Erben RG, Lanske B. (2011). PTH ablation ameliorates the anomalies of Fgf23-deficient mice by suppressing the elevated vitamin D and calcium levels. Endocrinology, 152(11) (p.4053-61).

4. Correa D, Hesse E, Seriwatanachai D, Kiviranta R, Saito H, Yamana K, Neff L, Atfi A, Coillard L, Sitara D, Maeda Y, Warming S, Jenkins NA, Copeland NG, Horne WC, Lanske B, Baron R. (2010). Zfp521 is a target gene and key effector of parathyroid hormone-related peptide signalling in growth plate chondrocytes. Developmental Cell, 19(4) (p. 533-46).

5. Chu EY, Fong H, Blethen FA, Tompkins KA, Foster BL, Yeh KD, Nagatomo KJ, Matsa-Dunn D, Sitara D, Lanske B, Rutherford RB, and Somerman MJ. (2010). Ablation of systemic phosphate-regulating gene fibroblast growth factor 23 (Fgf23) compromises the dento-alveolar complex. Anatomical Record, 293(7) (p. 1214-1226).

6. Greenblatt MB, Shim JH, H, Zou W, Sitara D, Schweitzer M, Hu D, Lotinum S, Sano Y, Baron R, Park JM, Arthur S, Xie M, Schneider MD, Zhai B, Gygi S, Davis R, and Glimcher LH. (2010). A MAPK pathway essential for bone homeostasis. Journal of Clinical Investigation, 120(7) (p. 2457-2473).

7. Fong H, Chu EY, Tompkins KA, Foster BL, Sitara D, Lanske B, Somerman MJ. (2009). Aberrant cementum phenotype associated with the hypophosphatemic hyp mouse. Journal of Periodontology, 80(8) (p.1348-1354).

8. DeLuca S, Sitara D, Kang K, Marsell R, Jonsson K, Taguchi T, Erben RG, Razzaque MS, Lanske B. (2008). Amelioration of the premature aging-like features of Fgf-23 knockout mice by genetically restoring the systemic actions of FGF-23. Journal of Pathology, 216(3) (p.345-355).

9. Sitara D, Kim S, Razzaque MS, Bergwitz C, Taguchi T, Schüler C, Erben RG, Lanske B. (2008). Genetic evidence of serum phosphate-independent functions of Fgf-23 on bone. PLoS Genetics, 4(8):e1000154.

10. Sitara D, Razzaque MS, St-Arnaud R, Taguchi T, Erben RG, Lanske B. (2006). Genetic ablation of vitamin D activation pathway reverses biochemical and skeletal anomalies in Fgf-23 null animals. American Journal of Pathology, 169(6) (p.2161-2170).

11. Razzaque MS, Sitara D, Taguchi T, St-Arnaud R, Lanske B. (2006). Premature aging-like phenotype in fibroblast growth factor 23 is a vitamin D-mediated process. The FASEB Journal, 20(6) (p.720-722).

12. Sitara D, Razzaque MS, Hesse M, Yoganathan S, Taguchi T, Erben RG, Jüppner H, Lanske B. (2004). Homozygous ablation of fibroblast growth factor-23 results in hyperphosphatemia and impaired skeletogenesis, and reverses hypophosphatemia in Phex-deficient mice. Matrix Biology, 23 (p.421-432).