Neha S. Dole
Assistant Professor
Also affiliated: University of California, San Francisco (2017–2024); Endocrine Society (2020); UConn Health (2012–2016); University of San Francisco (2021)
Faculty Researcher
Physiology and Cell Biology, College of Medicine
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Neha S. Dole's research focuses on the role of osteocytes in bone health and disease, particularly in the context of aging and metabolic dysfunction. Her work investigates how these bone cells regulate bone quality and integrity, examining the molecular signaling pathways involved, including transforming growth factor beta (TGFβ) and microRNAs (miRs).
Dole is the Principal Investigator on an NIH/National Institute of Diabetes and Digestive and Kidney Diseases grant totaling $140,899, which aims to unravel the role of osteocytes in metabolic dysfunction associated with obesity. Her recent publications explore how aging impairs osteocytic regulation of collagen and bone quality, how high-fat and high-carbohydrate diets affect bone fragility through TGFβ-dependent control of osteocyte function, and how fluid shear stress impacts osteocyte signaling. She also studies the effects of specific microRNAs, such as miR-100 and miR181a/b-1, on osteocyte function and bone properties, and investigates the role of lipocalin-2 in osteocyte ferroptosis and osteoblast crosstalk via Wnt signaling.
Her collaborative network includes several researchers from the University of Arkansas for Medical Sciences, with whom she has co-authored multiple publications. These collaborators include Vivek Khanal (4 shared publications), Madeline Carroll (3 shared publications), Amy Y. Sato (2 shared publications), and Ryan M. Allen (2 shared publications). Dole maintains an active lab website to disseminate her research.
Metrics
- h-index: 14
- Publications: 26
- Citations: 617
Selected Publications
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Osteocytic Lipocalin-2 regulates bone formation locally through iron-dependent ferroptosis and Wnt suppression (2026)
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Global Transcriptional Profiling of Adipose Tissue Uncovers Unique Sex-Dependent Mechanisms in Acute Obesity: Implications for Adipose-Heart Interorgan Crosstalk (2025)
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Lipocalin-2 Regulates Osteocyte Ferroptosis and Osteocyte-Osteoblast Crosstalk via Wnt Signaling to Control Bone Formation (2025)
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High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function (2024)
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miR181a/b-1 controls osteocyte metabolism and mechanical properties independently of bone morphology (2023)
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The Multifaceted Effects of Osteocytic TGFβ Signaling on the Skeletal and Extraskeletal Functions of Bone (2023)
Federal Grants 1 $140,899 total
Unraveling the role of osteocytes in metabolic dysfunction associated with obesity
Grants & Funding
As listed on this researcher's institutional profile. Federal awards with verified records are shown above.
- Role of subchondral bone osteocytes in post-traumatic osteoarthritis US Department of Defense Principal Investigator
- Vivek Khanal ASBMR 2025 President's Award American Society for Bone and Mineral Research Principal Investigator
- ABI P. Prather NIH T32 FY26 Y3 State of Arkansas Principal Investigator
Collaboration Network
Top Collaborators
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
- Lipocalin-2 Regulates Osteocyte Ferroptosis and Osteocyte-Osteoblast Crosstalk via Wnt Signaling to Control Bone Formation
- Global Transcriptional Profiling of Adipose Tissue Uncovers Unique Sex-Dependent Mechanisms in Acute Obesity: Implications for Adipose-Heart Interorgan Crosstalk
- Osteocytic Lipocalin-2 regulates bone formation locally through iron-dependent ferroptosis and Wnt suppression
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
- The Multifaceted Effects of Osteocytic TGFβ Signaling on the Skeletal and Extraskeletal Functions of Bone
- miR181a/b-1 controls osteocyte metabolism and mechanical properties independently of bone morphology
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
- Lipocalin-2 Regulates Osteocyte Ferroptosis and Osteocyte-Osteoblast Crosstalk via Wnt Signaling to Control Bone Formation
- Osteocytic Lipocalin-2 regulates bone formation locally through iron-dependent ferroptosis and Wnt suppression
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
- miR181a/b-1 controls osteocyte metabolism and mechanical properties independently of bone morphology
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
- miR181a/b-1 controls osteocyte metabolism and mechanical properties independently of bone morphology
- Lipocalin-2 Regulates Osteocyte Ferroptosis and Osteocyte-Osteoblast Crosstalk via Wnt Signaling to Control Bone Formation
- Osteocytic Lipocalin-2 regulates bone formation locally through iron-dependent ferroptosis and Wnt suppression
- Lipocalin-2 Regulates Osteocyte Ferroptosis and Osteocyte-Osteoblast Crosstalk via Wnt Signaling to Control Bone Formation
- Osteocytic Lipocalin-2 regulates bone formation locally through iron-dependent ferroptosis and Wnt suppression
- Lipocalin-2 Regulates Osteocyte Ferroptosis and Osteocyte-Osteoblast Crosstalk via Wnt Signaling to Control Bone Formation
- Osteocytic Lipocalin-2 regulates bone formation locally through iron-dependent ferroptosis and Wnt suppression
- The Multifaceted Effects of Osteocytic TGFβ Signaling on the Skeletal and Extraskeletal Functions of Bone
- miR181a/b-1 controls osteocyte metabolism and mechanical properties independently of bone morphology
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
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