Neha Dole
University of Arkansas for Medical Sciences, AR·Physiology·Early-career
Bone is more than a frame for the body. It also takes part in controlling the body's energy use, and its cells wear down with age.
- Fields
Physiology
Biology
Medicine & Clinical Research
- Topics
bone biology
skeletal aging
osteoporosis
- Grants
- 2 known grants, through Jan 2028
What they work on
- Identify which bone cells produce Lipocalin-2 (LCN2), a secreted protein that rises with age, and define their contribution to skeletal aging in mice.
- Establish whether SLC22A17, an iron-importing receptor for LCN2, mediates LCN2's local effects on bone, including ferroptosis, an iron-dependent cell death program.
- Test whether the LCN2–SLC22A17 pathway is necessary and sufficient for bone decline in aging mice and whether targeting it reduces bone fragility.
- Determine whether obesity reprograms osteocyte energy metabolism through TGFβ signaling and whether removing osteocytic TGFβ rescues metabolic dysfunction in diet-induced obese mice.
- Identify TGFβ-responsive epigenetic factors that control osteocyte energy metabolism in obesity, using ChIP-Seq, ATAC-Seq and RNA-Seq to map gene regulation.
More about the research
Osteocytes, the cells buried in bone that make up about 95% of its cells, and osteoblasts, the bone-building cells, lie at the center of both stories. The lab studies how signals made inside bone drive two problems: bone loss with aging and the energy imbalance of obesity.
Why it matters
Older adults with fragile bones could benefit if the LCN2–SLC22A17 pathway proves to be a target for slowing skeletal aging, since current bone-building drugs work only short-term and bone loss returns after stopping. In obesity, understanding how bone cells shape energy balance could help therapies restore metabolism while protecting bone health.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Beata Lecka-Czernik
University of Toledo, OH·Physiology
Determine how fuel choice and aging change osteocyte function and whether these effects depend on PPARG, using aged C57BL/6 and osteocyte-specific PPARG knockout mice, bone organ cultures and MLO-Y4 osteocyte-like cells with PPARG knocked down, with transcriptomics and quantitative proteomics.
Erica Scheller
Washington University in St Louis, MO·Physiology
Define how fat breakdown in constitutive bone marrow adipocytes supports osteoblast bone formation during high sympathetic nerve activity, and test whether this protection persists in aged and post-menopausal states.
Weiming Mao
Indiana University-Purdue University-Indianapolis, IN·Pharmacology
Test whether activating canonical Wnt signaling prevents steroid-induced high eye pressure in mice, using Wnt reporter mice and conditional knockout mice that lack β-catenin, the pathway's key protein.
The school
University of Arkansas for Medical Sciences: 7 labs on PI Pages, $227M a year on research, 40 research doctorates a year.
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