Archana Sanjay
University of Connecticut, CT·Biology
Broken bones that heal slowly or not at all are a serious public health problem, and there are few drugs that boost bone repair. Healing begins when progenitor cells in the periosteum, the thin layer covering bone, multiply right after an injury.
- Fields
Biology
Physiology
Medicine & Clinical Research
- Topics
bone regeneration
fracture healing
nonunion
- Grants
- 1 known grant, last ended Aug 2026
What they work on
- Test whether Rspo2 and Rspo3 are needed in mesenchymal progenitors for fracture healing, by deleting these genes at the time of fracture in mice and assessing repair with microCT, histology and mechanical testing.
- Determine whether the R-spondin receptor Lgr6 is required for bone healing by examining fracture repair and Wnt signaling in Lgr6 knockout mice.
- Deliver Rspo2 protein to bone injury sites and measure its effects on BMP and Wnt signaling, activation and differentiation of progenitor cells, and overall bone healing.
More about the research
These cells then turn into osteoblasts, which build bone, and chondrocytes, which build cartilage. It is still poorly understood how these stem-like cells are switched on after injury. This project studies a signaling pair that may control them: R-spondin (Rspo) proteins and their Lgr receptors.
Why it matters
Delayed and non-healing fractures of long bones and the skull and face are a significant clinical problem. Showing that R-spondin–Lgr signaling controls the cells that repair bone could reveal new drug targets. Delivering Rspo2 to injuries may offer a new way to speed fracture healing and reduce nonunion.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Alexander Knights
Washington University in St Louis, MO·Medicine & Clinical Research·Early-career
Determine how Rspo2-driven Wnt/β-catenin signaling controls the appearance and behavior of scar-promoting synovial cells in PTOA, using transgenic reporter mice, multi-omic analyses and in vitro differentiation assays.
Deneen M Wellik
University of Wisconsin-Madison, WI·Biology
Trace what Hoxa11-expressing muscle interstitial cells become in living mice, using Hoxa11-CreERT2 lineage labeling (a genetic switch that permanently marks these cells) after muscle injury and during induced muscle hypertrophy (growth).
Fernando Fierro
University of California-Davis, CA·Physiology
Uncover how spermine synthase (SMS) deficiency impairs bone mineralization, testing whether excess spermidine blocks hypusination, the chemical activation of the protein eIF5A, and disrupts mitochondrial release of calcium phosphate.
The school
University of Connecticut: 31 labs on PI Pages, $434M a year on research, 360 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.