Hesham Tawfeek

Hesham Tawfeek

Title: Research Associate Professor

Department: Biological and Chemical Sciences

Campus: Long Island

Area(s) of Expertise: Cell Signaling, Molecular Biology, Bone Biology, and Osteoimmunology

Education Credentials: MBBCh (MD equivalent)

Joined New York Tech: 2024

Hesham Tawfeek graduated from El-Minia University Faculty of Medicine (El-Minia, Egypt) with an MBBCh Degree (Bachelor of Medicine, Bachelor of Surgery) and was trained in clinical medicine until 1997. From 1997 to 2011 he received training in basic science investigations through his roles as a research assistant, postdoctoral fellow, and instructor at the Endocrine Unit at Massachusetts General Hospital and Harvard Medical School (Boston, Mass.), and the Endocrine Division at Emory University School of Medicine (Atlanta, Ga.). Tawfeek established his independent research programs in 2011 when he joined the Department of Orthopaedics at Columbia University (New York, N.Y.) as a tenure-track assistant professor and then at the James J. Peters Veterans Affairs Medical Center (Bronx, N.Y.) and the Icahn School of Medicine at Mount Sinai (New York, N.Y.) under his federal appointment as a research health scientist.

Tawfeek was recruited to New York Tech's Department of Biological and Chemical Sciences in September 2024. As Research Associate Professor, Tawfeek leads a translational bone research program, employing innovative pharmacologic and genetic approaches and animal models to understand the mechanisms behind bone loss associated with aging, hormonal imbalances, and immobilization. His work focuses on uncovering the role of bone and immune cell interactions in bone health and disease. The objective of Tawfeek's research is to develop novel therapies for improving bone structure and reducing fractures in individuals with poor bone health. His scientific contributions to the fields of endocrinology, bone biology, and osteoimmunology have been well recognized. Recently, his laboratory has been employing preclinical models to understand and treat the challenging clinical problem of bone loss in immobilized individuals after spinal cord injury (SCI). In one project, his work led to the discovery of an unexpected role for T cells in SCI-induced bone loss. Briefly, the findings showed that T cell immuno-competence status appears to distinctly control the onset and magnitude of changes in bone structure after SCI. The results, thus far, provide important insight into the importance of promoting immune function as a new strategy to reduce bone loss in individuals with SCI. In another project, his investigations identified a novel role for excessive transforming growth factor-β (TGF-β) signaling in mediating bone loss after SCI. Importantly, treatment of SCI mice with TGF-β inhibitory antibody completely prevented trabecular bone loss and restored bone integrity both in acute and chronic SCI, respectively.

These findings have important and immediate translational implications for reducing the risk of fragility fractures in persons with motor paralysis after SCI. Tawfeek is a recipient of research awards and recognitions, and his research has been supported by grants from the National Institutes of Health, the Department of Veterans Affairs, the New York State Department of Health, and recently the Department of Defense. His work has been published in highly reputable journals such as Proceedings of the National Academy of Sciences, Cell Metabolism, Endocrinology, Molecular Endocrinology, American Journal of Physiology, PLoS One, Physiological Reports, and FASEB Journal. Tawfeek also serves on distinguished editorial and review boards such as Endocrinology, FASEB Journal, Bone, Frontiers in Endocrinology, the American Journal of Physiology, Journal of the Endocrine Society, and Journal of Spinal Cord Medicine.

Recent Projects and Research

Selected Publications

  1. Tawfeek HA, Che J, Qian F, Abou-Samra AB. Parathyroid hormone receptor internalization is independent of protein kinase A and phospholipase C activation. Am J Physiol Endocrinol Metab. 2001;281(3)E545–57.
  2. Tawfeek HA, Qian F, Abou-Samra AB. Phosphorylation of the receptor for parathyroid hormone and parathyroid hormone-related peptide is required for internalization and regulates receptor signaling. Mol Endocrinol. 2002;16(1)1–13.
  3. Tawfeek HA, Abou-Samra AB. Important role for the V-type H(+)-ATPase and the Golgi apparatus in the recycling of PTH/PTHrP receptor. Am J Physiol Endocrinol Metab. 2004;286(5):E704–10.
  4. Bounoutas GS, Tawfeek HA, Frolich LF, Chung UI, Abou-Samra AB. Impact of impaired receptor internalization on calcium homeostasis in knock-in mice expressing a phosphorylation-deficient parathyroid hormone (pth) / pth-related peptide receptor. Endocrinology. 2006 ;147(10):4674–9.
  5. Tawfeek HA, Abou-Samra AB. Negative regulation of PTH-activated phospholipase C signaling by PTH/PTHrP receptor phosphorylation and Protein Kinase A. Endocrinology. 2008;149(8):4016–23.
  6. Aydin C, Aytan N, Mahon MJ, Tawfeek HA, Kowall NW, Dedeoglu A, Bastepe M. Extra-large XL{alpha}s (XXL{alpha}s), a variant of Gs{alpha}, is a distinct, membrane-anchored GNAS product that can mimic Gs{alpha}. Endocrinology. 2009; 150(8):3567–75.
  7. Terauchi M, Li J, Bedi B, Baek K, Tawfeek HA, Galley S, Gilbert L, Nanes M, Zayzafoon M, Guldberg R, Lamar D, Singer M, Lane T, Kronenberg HM, Weitzmann MN, Pacifici RT. T lymphocytes amplify the anabolic activity of parathyroid hormone through Wnt10b signaling. Cell Metab. 2009; 10(3):229–40.
  8. Bedi B, Li JY, Grassi F, Tawfeek H, Weitzmann MN, Pacifici R. Inhibition of antigen presentation and T cell costimulation blocks PTH-induced bone loss. Ann N Y Acad Sci. 2010;1192(1):215–21.
  9. Tawfeek HA, Bedi B, Li JY, Adams J, Kobayashi T, Weitzmann MN, Kronenberg HM, Pacifici R. Disruption of PTH receptor 1 in T cells protects against PTH-induced bone loss. PloS One. 2010; 20;5(8).
  10. Jau-Yi Li, Tawfeek H, Bedi B, Yang X, Adams J, Gao K, Zayzafoon M, Weitzmann MN, Pacifici R. Ovariectomy disregulates osteoblast and osteoclast formation through the T cell receptor CD40 ligand. Proc Natl Acad Sci USA. 2011; 108(2):768–73.
  11. Bedi B, Li JY, Tawfeek H, Baek KH, Adams J, Vangara SS, Chang MK, Kneissel M, Weitzmann MN, Pacifici R. Silencing of parathyroid hormone (PTH) receptor 1 in T cells blunts the bone anabolic activity of PTH. Proc Natl Acad Sci USA. 2012; 109(12):E725–33.
  12. Tawfeek HA, Abou-Samra AB. Disruption of Parathyroid Hormone and Parathyroid Hormone Related Peptide Receptor Phosphorylation Prolongs ERK1/2 MAPK Activation and Enhances c-fos Expression. Am J Physiol Endocrinol Metab. 2012; 302(11):E1363–72.
  13. Lee HG, Hsu A, Goto H, Nizami S, Lee JH, Cadet ER, Tang P, Shaji R, Chandhanayinyong C, Kweon SH, Oh DS, Tawfeek H, Lee FY. Aggravation of Inflammatory Response by Co-Stimulation with Titanium Particles and Mechanical Perturbations in Osteoblast- and Macrophage- like Cells. Am J Physiol Cell Biology. 2013 ; 304(5):C431–9
  14. Oh DS, Kim YH, Ganbat D, Han MH, Lim P, Back JH, Lee FY, Tawfeek H. Bone marrow absorption and retention properties of engineered scaffolds with micro-channels and nano-pores for tissue engineering: a proof of concept. Ceramics International. 2013; 39(7):8401–8410 15.
  15. Tascau L, Gardner T, Anan H, Yongpravat C, Cardozo CP, Bauman WA, Lee FY, Oh DS, Tawfeek HA. Activation of Protein Kinase A in Mature Osteoblasts Promotes a Major Bone Anabolic Response. Endocrinology. 2016 ;157(1):112–26.
  16. Harlow L, Sahbani K, Nyman JS, Cardozo CP, Bauman WA, Tawfeek HA. Daily Parathyroid Hormone Administration Enhances Bone Turnover and Preserves Bone Structure after Severe Immobilization-induced Bone Loss. Physiol Rep. 2017; 5(18), e13446.
  17. Graham Z, Siedlik JA, Harlow L, Sahbani K, Bauman WA, Tawfeek HA, Cardozo CP. Key glycolytic metabolites in paralyzed skeletal muscle are altered 7 days after spinal cord injury in mice. J Neurotrauma. 2019 Apr 10. doi: 10.1089/neu.2018.6144.
  18. Sahbani K, Cardozo CP, Bauman WA, Tawfeek HA. Abaloparatide exhibits greater osteoanabolic response and higher cAMP stimulation and β-arrestin recruitment than teriparatide. Physiol Rep. 2019 Oct;7(19):e14225. doi: 10.14814/phy2.14225.
  19. Graham ZA, Liu XH, Harlow L, Pan J, Azulai D, Tawfeek HA, Wnek RD, Mattingly AJ, Bauman WA, Yarrow JF, Cardozo CP. Effects of a High-Fat Diet on Tissue Mass, Bone, and Glucose Tolerance after Chronic Complete Spinal Cord Transection in Male Mice. Neurotrauma Rep. 2020;1(1):17-31. doi: 10.1089/neur.2020.0014.
  20. Sahbani K, Shultz LC, Cardozo CP, Bauman WA, Tawfeek HA. Absence of αβ T cells accelerates disuse bone loss in male mice after spinal cord injury. Ann N Y Acad Sci. 2021;1487(1):43–55.
  21. Sahbani K, Cardozo CP, Bauman WA, Tawfeek HA. Inhibition of TGF-β signaling attenuates disuse-induced trabecular bone loss after spinal cord injury in male mice. Endocrinology. 2022, 1;163(1) bqab230.
  22. Sahbani K, Pan J, Zaidi M, Cardozo CP, Bauman WA, Tawfeek HA. Abaloparatide Prevents Immobilization-induced Cortical but not Trabecular Bone Loss after Spinal Cord Injury. FASEB J. 2023; 37(6):e22984.

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Professional Honors and Awards

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