Thiagarajan Ganesh
University of Missouri-Kansas City, MO·Biomedical Engineering
Bone is not a static material: it adds and removes tissue in response to how it is loaded, which is why exercise strengthens it. The cells thought to sense that loading are osteocytes, which sit inside tiny cavities in the bone and reach out to each other through long, thin extensions in a connected network.
- Fields
Biomedical Engineering
Physiology
Engineering
- Topics
osteocytes
bone mechanobiology
mechanotransduction
- Grants
- 1 known grant, through May 2027
What they work on
- Develop multiplexed confocal imaging models of osteocytes and their dendritic networks in loaded and unloaded mouse bone to predict how these cells respond to altered mechanical loads with aging.
- Build macro- and micro-scale three-dimensional finite element and fluid-structure interaction models of osteocyte lacunae to compute strains and shear stresses on cells and dendrites at three load levels and two ages.
- Correlate computed mechanical strain with Wnt/beta-catenin signaling activity, measured as beta-galactosidase reporter activity in TOPGAL mice, to define a strain threshold for activation of bone-forming pathways.
- Compare male and female TOPGAL mice at 6 and 18 months after loading of the ulna, testing how sex and aging change the mechanical stimulus needed to activate osteocyte signaling.
- Use 3D printed physical models of the lacunar-canalicular system, the network of cavities and channels housing osteocytes, to study how fluid flows through the network as a whole.
More about the research
With age, the shapes of those cavities and channels change, and bone responds less well to loading. This project asks how mechanical loading is converted into a biological signal inside osteocytes, and how aging alters that conversion, in both male and female mice.
Why it matters
Osteoporosis is an age-related loss of bone mass that leaves people vulnerable to fractures, and exercise-based loading is known to build bone but works less well with age. Identifying the strain and fluid shear levels needed to switch on bone-forming signaling in osteocytes, and how those thresholds shift with age and differ between males and females, could help tailor exercise interventions or drug targets to older patients at fracture risk.
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.
Sarah Dallas
University of Missouri-Kansas City, MO·Physiology
Determine how osteoblast movement, differentiation and fate are tied to collagen assembly and mineralization, using live-cell and intravital imaging of mice with GFP-tagged type I collagen and bone-lineage fluorescent reporters.
Neha Dole
University of Arkansas for Medical Sciences, AR·Physiology·Early-career
Identify which bone cells produce Lipocalin-2 (LCN2), a secreted protein that rises with age, and define their contribution to skeletal aging in mice.
The school
University of Missouri-Kansas City: 7 labs on PI Pages, $57M a year on research, 94 research doctorates a year.
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