Research Interests

• Endocrine hormonal controls in skeletal stem cells and osteoprogenitors for bone homeostasis and regeneration
• Microenvironment within the stem cell niche of bone
• Alternative in vitro models for bone research

The bone, functioning as an endocrine organ, intricately interacts with various hormonal signals. Bone regeneration is a complex and highly orchestrated process that involves the coordinated actions of numerous cell types over time. Despite the complex nature of this process, approximately 5% of fractures result in non-union, causing prolonged pain, immobility, and necessitating subsequent surgeries. The stress-associated hormone, glucocorticoids, plays an important role in regulating bone mass as well as the process of fracture healing.

My research group is dedicated to unraveling the cellular and molecular mechanisms of glucocorticoid receptor signaling in skeletal stem/progenitor cells both during both bone regeneration and homeostasis. Additionally, we aim to gain insights into the microenvironment within the stem cell niche of the bone. Moreover, we explore alternative in vitro models designed for bone research, with a specific focus on bone regeneration.

Our comprehensive approach broadens our perspectives, providing a foundation for identifying novel targets that can contribute to progress in the field of bone health.

1. Mechanisms of glucocorticoid action in skeletal stem/progenitor cells during bone regeneration (in collaboration with Prof. Dr. Tuckermann and Prof. Dr. Ignatius) - DFG funded project within the CRC 1149 (danger response, disturbance factors and regenerative potential after acute trauma)
2. Glucocorticoid and Notch signaling crosstalk in bone
3. Molecular mechanism of rare jaw tumors – ossifying fibroma (in collaboration with Prof. Dr. Tuckermann)
4. Callus organoids

Remark, L.H., Leclerc, K., Ramsukh, M., Lin, Z., Lee, S., Dharmalingam, B., Gillinov, L., Nayak, V. V., El Parente, P., Sambon, M., et al. (2023). Loss of Notch signaling in skeletal stem cells enhances bone formation with aging. Bone Res. 11:50. doi.org/10.1038/s41413-023-00283-8

Lee, S., Krüger, B.T., Ignatius, A., and Tuckermann, J. (2022). Distinct Glucocorticoid Receptor Actions in Bone Homeostasis and Bone Diseases. Front. Endocrinol. (Lausanne). 12, 1–8. doi: 10.3389/fendo.2021.815386

Ahmad, M., Kroll, T., Vettorazzi, S., Dorn, K., Mengele, F., Lee, S., Nandi, S., Yilmaz, D., Tangudu, N.K., Pachmayr, J., et al. (2022). Inhibition of Cdk5 increases osteoblast differentiation , bone mass and improves fracture healing. Bone Res. 10:33. doi.org/10.1038/s41413-022-00195-z

Hachemi, Y., Rapp, A.E., Lee, S., Dorn, A., Krüger, B.T., Kaiser, K., Ignatius, A., and Tuckermann, J. (2021). Intact Glucocorticoid Receptor Dimerization Is Deleterious in Trauma-Induced Impaired Fracture Healing. Front. Immunol. 11, 1–12. doi: 10.3389/fimmu.2020.628287

Lee, S., Remark, L.H., Josephson, A.M., Leclerc, K., Lopez, E.M., Kirby, D.J., Mehta, D., Litwa, H.P., Wong, M.Z., Shin, S.Y., et al. (2021). Notch-Wnt signal crosstalk regulates proliferation and differentiation of osteoprogenitor cells during intramembranous bone healing. Npj Regen. Med. 6, 29. doi.org/10.1038/s41536-021-00139-x

Lee, S., Liu, P., Ahmad, M., and Tuckermann, J.P. (2021). Leukemia inhibitory factor treatment attenuates the detrimental effects of glucocorticoids on bone in mice. Bone 145, 115843. doi.org/10.1016/j.bone.2021.115843

Lee, S., Remark, L.H., Buchalter, D.B., Josephson, A.M., Wong, M.Z., Litwa, H.P., Ihejirika, R., Leclerc, K., Markus, D., Yim, N.L., et al. (2020). Propranolol Reverses Impaired Fracture Healing Response Observed With Selective Serotonin Reuptake Inhibitor Treatment. J. Bone Miner. Res. 35, 932–941. DOI: 10.1002/jbmr.3950

Josephson, A.M., Bradaschia-Correa, V., Lee, S., Leclerc, K., Patel, K.S., Lopez, E.M., Litwa, H.P., Neibart, S.S., Kadiyala, M., Wong, M.Z., et al. (2019). Age-related inflammation triggers skeletal stem/ progenitor cell dysfunction. Proc. Natl. Acad. Sci. U. S. A. 116, 6995–7004. doi.org/10.1073/pnas.1810692116

Lee, S., Liu, P., Teinturier, R., Jakob, J., Tschaffon, M., Tasdogan, A., Wittig, R., Hoeller, S., Baumhoer, D., Frappart, L., et al. (2017). Deletion of Menin in craniofacial osteogenic cells in mice elicits development of mandibular ossifying fibroma. Oncogene 37, 616–626. doi:10.1038/onc.2017.364

Further publications by Dr. Sooyeon Lee can be found in our publications directory.