Bellido Laboratory

Under the leadership of Teresita Bellido, PhD, the Bellido Laboratory investigates the mechanisms of signal transduction among and within bone cells, with particular emphasis on the biology of osteocytes. The laboratory employs in vitro, ex vivo and in vivo models to study how hormones and mechanical force act on bone cells and affect their function and life span.

Active Research

Current projects investigate the regulation of the osteocyte-derived genes by PTH; the mechanisms by which PTH, mechanical stimulation, and canonical Wnt signaling regulate bone homeostasis through actions on osteocytes; interventions that counteract the deleterious effects of glucocorticoid excess on bone and muscle; and the role of osteocytes in multiple myeloma musculoskeletal disease.

Collaborative projects investigate the role of the transcription factor Nrf2 in the protection of the skeleton induced by berry diets; the function of connexin43 in bone; the role of estrogen receptor beta in osteocytes for mechanobiology; and the regulation of cartilage function by PTH receptor signaling. The laboratory receives funding from the NIH, VA and the biopharma industry.

As Principal Investigator (PI) or Project Leader

10/1/2016-9/31/2018, PharmaMar S.A. Characterization of Aplidin® (plitidepsin) effects on multiple myeloma (MM)-induced bone disease. Role: PI

9/30/2014-8/31/2019, NIH-NCCAM R01-AT008754 and O2S1-AT008754. Berries and bone. Role: PI of subcontract IU-Purdue University; PI C Weaver

10/1/2013-9/30/2017, VA I01 BX002104 Merit Award. Osteocyte control of bone remodeling through the PTH receptor. Role: PI

09/2011-08/2017, NIH R01 AR059357. FAK/Pyk2 signaling pathway and bone formation. Role: PI

04/2017-03/2022, NIH R01 CA209882. Contribution of Osteocytes to the Musculoskeletal Effects of Multiple Myeloma. Role MPI with GD Roodman

06/2017, NSF Support for Junior Investigators at the ORS Musculoskeletal Biology Workshop at Sun Valley, Idaho. Role: PI

As co-Investigator, Mentor or Collaborator

12/1/15-11/30/2020, NIH R01 AR068332. CaMKK2 Inhibition as a Dual-Action Bone Anabolic and Anti-Catabolic Therapy in Osteoporosis. Role: Co-Investigator. PI: U Sankar.

4/1/2015-3/31/2020, NIH R01AR067210. Osteocyte apoptosis and regulation of bone resorption with aging. Role: Co-Investigator. PI: LI Plotkin

4/1/2013-3/31/2018, NIH R01. Control of FGF23 bioactivity via circulating alphaKlotho. Role: Co-Investigator. PI.: KE White

7/1/2016-6/30/2017, AAOF – American Association of Orthodontics Foundation. The effect of intermittent PTH on mandibular condylar cartilage. Role: co-Investigator. PI: A Utreja

12/1/2011-11/31/2020, VA I01 BX001478 Merit Award. Harnessing the anabolic potential of Wnt signaling to improve bone health. Role Co-I; PI: AR Robling

Sato AY, Tu X, McAndrews KA, Plotkin LI, Bellido T. Prevention of Glucocorticoid Induced-Apoptosis of Osteoblasts and Osteocytes by Protecting against Endoplasmic Reticulum (ER) Stress in vitro and in vivo in Female Mice.  Bone, 73: 60-68, 2015

Tu X,* Delgado-Calle J,* Condon K, Maycas M, Zhang H, Carlesso N, Taketo MM, Burr D, Plotkin LI, Bellido T. Osteocytes mediate the anabolic actions of canonical Wnt/βcatenin signaling in bone. Proceedings of National Academy of Sciences, 112 (5) E478-E486, 2015. [Epub ahead of print] (Highlighted in Nature Reviews Endocrinology; and in Nature Reviews Rheumatology) *Both first authors

Delgado-Calle J, Anderson J, Cregor MD, Hiasa M, Chirgwin JM, Carlesso N, Yoneda T, Mohammad KS, Plotkin LI, Roodman GD, Bellido T. Bidirectional Notch signaling and osteocyte-derived factors drive tumor cell proliferation and bone destruction in multiple myeloma. Cancer Research, 2016, DOI: 10.1158/0008-5472.CAN-15-1703.

Sato AY, Cregor M, Delgado-Calle J, Condon KW, Allen MR, Peacock M, Plotkin LI, Bellido T. Protection from Glucocorticoid-Induced Osteoporosis by Anti-Catabolic Signaling in the Absence of Sost/Sclerostin. Journal of Bone and Mineral Research, 31(10): 1791-1802, 2016

Pellegrini GG, Morales CC, Wallace TC, Plotkin LI, Bellido T. Avenanthramides prevent osteoblast and osteocyte apoptosis and induce osteoclast apoptosis in an Nrf2-independent manner. Nutrients, 2016 8, 423-427; doi:10.3390/nu8070423

Maycas M, McAndrews KA, Sato AY, Pellegrini GG, Brown DM, Allen MR, Plotkin LI, Gortazar AR, Esbrit P, Bellido T. PTHrP-Derived Peptides Restore Bone Mass and Strength in Diabetic Mice: Additive Effect of Mechanical Loading. Journal of Bone and Mineral Research doi 0.1002/jbmr.3007, 2016.

Delgado-Calle J, Tu X, Pacheco-Costa R, McAndrews K, Edwards R, Pellegrini G, Kuhlenschmidt K, Olivos N, Robling A, Peacock M, Plotkin LI, Bellido T. Control of Bone Anabolism in Response to Mechanical Loading and PTH by Distinct Mechanisms Downstream of the PTH Receptor. Journal of Bone and Mineral Research doi: 10.1002/jbmr.3011, 2016.

Sato AY, Richardson D, Cregor M, Davis HM, Au ED, McAndrews K, Zimmers TA, Organ JM,  Peacock M, Plotkin LI, Bellido T. Glucocorticois induce bone and muscle atrophy by tissue-specific mechanisms upstream of E3 ubiquitin ligases. Endocrinology (in press)

Pellegrini GG, Cregor M, McAndrews K, Morales CC, Doyle McCabe L, McCabe GP, Peacock M, Burr D, Weaver C, Bellido T. Nrf2 regulates mass accrual and the antioxidant endogenous response in bone differently depending on the sex and age. PLoS ONE (in press)

Delgado-Calle J, Anderson J, Cregor M, Condon K, Kuhstoss S, Plotkin LI, Bellido T,* and Roodman GD*. Genetic Deletion of Sost or Pharmacological Inhibition of Sclerostin Prevent Multiple Myeloma-induced Bone Disease without Affecting Tumor Growth. Leukemia (in press) * Corresponding authors

Research Team

Teresita M. Bellido, PhD

Teresita M. Bellido, PhD

Professor of Anatomy & Cell Biology
Jesus Delgado-Calle, PhD

Jesus Delgado-Calle, PhD

Assistant Research Professor of Anatomy & Cell Biology

Additional Research Team Members

Other research team members include Amy Y. Sato, PhD (Postdoctoral fellow), Emily Atkinson (Graduate student), Kevin McAndrews, MS (Research Technician), Melony Cregor (Research Technician), and Jessica H. Nelson (Research Technician)