Anne Delany
University of Connecticut, CT·Physiology
Glucocorticoids are stress hormones that the body needs for healthy bone, yet too much of them weakens the skeleton. Excess can come from steroid medications taken throughout the body or from conditions such as Cushing's disease.
- Fields
Physiology
Genetics
Medicine & Clinical Research
- Topics
microRNA
miR-433
glucocorticoids
- Grants
- 1 known grant, last ended Oct 2026
What they work on
- Characterize the bone structure and bone formation of male and female mice whose osteoblasts express a miR-433 'tough decoy' inhibitor, comparing mature and aging animals.
- Identify the genes and pathways that miR-433 directly targets in osteoblast-lineage cells, using an unbiased screening approach, to explain how this small RNA restrains bone-forming cell development.
- Determine at the molecular level how miR-433 limits glucocorticoid responsiveness, including its effects on glucocorticoid receptor residence in the nucleus of mesenchymal cells.
- Test how blocking miR-433 changes the skeletal response of decoy mice to excess glucocorticoids given from outside the body.
More about the research
It is the most common secondary cause of osteopenia, or low bone mass. Cells normally keep tight control over how strongly they respond to these hormones, and this project studies one small RNA that helps set that response in bone-forming cells.
Why it matters
Glucocorticoid excess, from steroid drugs or Cushing's disease, is the most common secondary cause of bone loss. Learning how miR-433 links bone formation to glucocorticoid sensitivity could guide new strategies to protect the skeletons of patients who need long-term steroid treatment.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Amjad Javed
University of Alabama at Birmingham, AL·Biology
Measure natural Runx2 protein levels and stability in skeletal tissues of mice lacking Sp7, a bone-specific transcription factor, to test whether Sp7 is needed to keep Runx2 protein stable.
John Fowlkes
University of Kentucky, KY·Physiology
Determine how deficiencies of insulin and insulin-like growth factor 1 (IGF-1) each contribute to diabetic bone disease at the tissue, cellular and molecular levels in models of type 1 diabetes.
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.
The school
University of Connecticut: 31 labs on PI Pages, $434M a year on research, 360 research doctorates a year.
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