Match tier
Listed
Presence
Current · Arkansas
Last published
2026
Sources
OpenAlex · ORCID
Refreshed
2026-10-03
Joseph J. Goellner
Research Instructor
Also affiliated: Monsanto (United States) (1994); Howard Hughes Medical Institute (1997); Pfizer (United States) (2003); Washington University in St. Louis (1982–1997); University of Arkansas Medical Center (2026); Central Arkansas Veterans Healthcare System (2008–2020); Washington University Medical Center (1985); Ehime University (1997)
Internal Med, College of Medicine
19 h-index
28 pubs
4,104 cited
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Joseph J. Goellner's research has explored fundamental biological processes, with a significant focus on immune system function and bone remodeling. His work has investigated the roles of specific molecular pathways, such as lymphotoxin signaling in the development of peripheral lymphoid organs and complement receptors in humoral immune responses. Goellner has also studied the mechanisms controlling bone mass, identifying osteocytes as a primary source of RANKL essential for osteoclast formation and examining the influence of PTH receptor signaling in osteocytes. His research extends to the role of FoxO-mediated defense against oxidative stress in osteoblasts and its impact on skeletal homeostasis. He has also contributed to studies on transgenic models, including those investigating aldosterone-driven cardiac hypertrophy and age-dependent cognitive deficits.
Metrics
- h-index: 19
- Publications: 28
- Citations: 4,104
Positions
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Research Instructor publications 2008–2026University of Arkansas for Medical Sciences Internal Med, College of Medicine Institutional directory
Selected Publications
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Wnt10b is required for the increase in cancellous bone caused by oxidized phospholipids blockade (2026)
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Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice (2025)
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Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation (2023)
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Osteoblasts Suppress Bone Resorption Via Production of Osteoprotegerin (2020)
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A Uromodulin Mutation Drives Autoimmunity and Kidney Mononuclear Phagocyte Endoplasmic Reticulum Stress (2020)
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Local Production of Osteoprotegerin by Osteoblasts Suppresses Bone Resorption (2020)
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Soluble RANKL contributes to osteoclast formation in adult mice but not ovariectomy-induced bone loss (2018)
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Mutant Profilin1 transgenic mice recapitulate cardinal features of motor neuron disease (2016)
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Osteocytes, not Osteoblasts or Lining Cells, are the Main Source of the RANKL Required for Osteoclast Formation in Remodeling Bone (2015)
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A DNA Segment Spanning the Mouse Tnfsf11 Transcription Unit and Its Upstream Regulatory Domain Rescues the Pleiotropic Biologic Phenotype of the RANKL Null Mouse (2014)
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Mouse and Human BAC Transgenes Recapitulate Tissue-Specific Expression of the Vitamin D Receptor in Mice and Rescue the VDR-Null Phenotype (2014)
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A Humanized Mouse Model of Hereditary 1,25-Dihydroxyvitamin D–Resistant Rickets Without Alopecia (2014)
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FoxO-Mediated Defense against Oxidative Stress in Osteoblasts Is Indispensable for Skeletal Homeostasis in Mice (2010)
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Control of Bone Mass and Remodeling by PTH Receptor Signaling in Osteocytes (2008)
Grants & Funding
As listed on this researcher's institutional profile.
- Center for Musculoskeletal Disease Research (CMDR) NIH/Nat. Inst. of General Medical Sciences Co-Investigator
Collaboration Network
Top Collaborators
Charles A. O’Brien
14 shared publications
In database
- Control of Bone Mass and Remodeling by PTH Receptor Signaling in Osteocytes
- Osteocytes, not Osteoblasts or Lining Cells, are the Main Source of the RANKL Required for Osteoclast Formation in Remodeling Bone
- FoxO-Mediated Defense against Oxidative Stress in Osteoblasts Is Indispensable for Skeletal Homeostasis in Mice
- Soluble RANKL contributes to osteoclast formation in adult mice but not ovariectomy-induced bone loss
- Local Production of Osteoprotegerin by Osteoblasts Suppresses Bone Resorption
Showing 5 of 14 shared publications
Jinhu Xiong
University of Arkansas for Medical Sciences
5 shared publications
In database
- Osteocytes, not Osteoblasts or Lining Cells, are the Main Source of the RANKL Required for Osteoclast Formation in Remodeling Bone
- Soluble RANKL contributes to osteoclast formation in adult mice but not ovariectomy-induced bone loss
- Local Production of Osteoprotegerin by Osteoblasts Suppresses Bone Resorption
- A DNA Segment Spanning the Mouse Tnfsf11 Transcription Unit and Its Upstream Regulatory Domain Rescues the Pleiotropic Biologic Phenotype of the RANKL Null Mouse
- Osteoblasts Suppress Bone Resorption Via Production of Osteoprotegerin
Jeff D. Thostenson
MRC Biostatistics Unit
5 shared publications
In database
- Local Production of Osteoprotegerin by Osteoblasts Suppresses Bone Resorption
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice
- Osteoblasts Suppress Bone Resorption Via Production of Osteoprotegerin
- Wnt10b is required for the increase in cancellous bone caused by oxidized phospholipids blockade
J. Wesley Pike
University of Wisconsin–Madison (US)
3 shared publications
- Mouse and Human BAC Transgenes Recapitulate Tissue-Specific Expression of the Vitamin D Receptor in Mice and Rescue the VDR-Null Phenotype
- A Humanized Mouse Model of Hereditary 1,25-Dihydroxyvitamin D–Resistant Rickets Without Alopecia
- A DNA Segment Spanning the Mouse Tnfsf11 Transcription Unit and Its Upstream Regulatory Domain Rescues the Pleiotropic Biologic Phenotype of the RANKL Null Mouse
Elena Ambrogini
3 shared publications
In database
- FoxO-Mediated Defense against Oxidative Stress in Osteoblasts Is Indispensable for Skeletal Homeostasis in Mice
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Wnt10b is required for the increase in cancellous bone caused by oxidized phospholipids blockade
M. Piemontese
University of Arkansas for Medical Sciences (US)
3 shared publications
- Osteocytes, not Osteoblasts or Lining Cells, are the Main Source of the RANKL Required for Osteoclast Formation in Remodeling Bone
- Soluble RANKL contributes to osteoclast formation in adult mice but not ovariectomy-induced bone loss
- A DNA Segment Spanning the Mouse Tnfsf11 Transcription Unit and Its Upstream Regulatory Domain Rescues the Pleiotropic Biologic Phenotype of the RANKL Null Mouse
Keisha M. Cawley
University of Arkansas for Medical Sciences (US)
3 shared publications
- Soluble RANKL contributes to osteoclast formation in adult mice but not ovariectomy-induced bone loss
- Local Production of Osteoprotegerin by Osteoblasts Suppresses Bone Resorption
- Osteoblasts Suppress Bone Resorption Via Production of Osteoprotegerin
Nancy Cecile Bustamante-Gomez
University of Arkansas for Medical Sciences
3 shared publications
In database
- Local Production of Osteoprotegerin by Osteoblasts Suppresses Bone Resorption
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Osteoblasts Suppress Bone Resorption Via Production of Osteoprotegerin
Igor Gubrij
University of Arkansas for Medical Sciences (US)
3 shared publications
- Local Production of Osteoprotegerin by Osteoblasts Suppresses Bone Resorption
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Osteoblasts Suppress Bone Resorption Via Production of Osteoprotegerin
Michela Palmieri
University of Arkansas for Medical Sciences
3 shared publications
In database
- Local Production of Osteoprotegerin by Osteoblasts Suppresses Bone Resorption
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Osteoblasts Suppress Bone Resorption Via Production of Osteoprotegerin
Seong Min Lee
University of Wisconsin–Madison (US)
2 shared publications
- Mouse and Human BAC Transgenes Recapitulate Tissue-Specific Expression of the Vitamin D Receptor in Mice and Rescue the VDR-Null Phenotype
- A Humanized Mouse Model of Hereditary 1,25-Dihydroxyvitamin D–Resistant Rickets Without Alopecia
Maria Almeida
Orthopaedic Research
2 shared publications
In database
- FoxO-Mediated Defense against Oxidative Stress in Osteoblasts Is Indispensable for Skeletal Homeostasis in Mice
- Wnt10b is required for the increase in cancellous bone caused by oxidized phospholipids blockade
Robert S. Weinstein
Central Arkansas Veterans Healthcare System (US)
2 shared publications
- Control of Bone Mass and Remodeling by PTH Receptor Signaling in Osteocytes
- FoxO-Mediated Defense against Oxidative Stress in Osteoblasts Is Indispensable for Skeletal Homeostasis in Mice
Robert L. Jilka
Central Arkansas Veterans Healthcare System
2 shared publications
In database
- Control of Bone Mass and Remodeling by PTH Receptor Signaling in Osteocytes
- FoxO-Mediated Defense against Oxidative Stress in Osteoblasts Is Indispensable for Skeletal Homeostasis in Mice
Kathleen A. Bishop
University of Wisconsin–Madison (US)
2 shared publications
- Mouse and Human BAC Transgenes Recapitulate Tissue-Specific Expression of the Vitamin D Receptor in Mice and Rescue the VDR-Null Phenotype
- A DNA Segment Spanning the Mouse Tnfsf11 Transcription Unit and Its Upstream Regulatory Domain Rescues the Pleiotropic Biologic Phenotype of the RANKL Null Mouse
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