Edward Sander
University of Iowa, IA·Biomedical Engineering
Scars form when a healing wound lays down too much stiff, disorganized tissue, and in the United States fibrosis and scarring cost about $20 billion a year to treat while still leaving many people with lasting problems. Surgeons have noticed that transplanting a patient's own fat into a wound site seems to reduce scarring, and fat cells in the skin have recently been recognized as players in normal early healing — but nobody knows what they are telling the cells that build scar tissue.
- Fields
Biomedical Engineering
Medicine & Clinical Research
Biology
- Topics
wound healing
fibrosis
scarring
- Grants
- 1 known grant, through Jul 2027
What they work on
- Determine whether secreted factors from human adipocyte-lineage cells inhibit, induce or reverse the conversion of fibroblasts into scar-forming myofibroblasts, using a myofibroblast conversion assay with fractionation, proteomics and inhibition/add-back experiments.
- Test whether myofibroblasts induced by adipokines, the signaling molecules released by fat cells, produce a different extracellular matrix than those induced by TGF-β1, the classic fibrosis signal, and whether that matrix is less scar-like.
- Measure how reciprocal communication between adipocyte-lineage cells and fibroblasts changes the composition and mechanics of the extracellular matrix, using 3D adipose spheroids and 3D in vitro wound models.
- Assess whether transplanting adipose stem cells, preadipocytes or mature adipocytes differentially alters fibroblast and myofibroblast behavior and matrix remodeling in a porcine wound model.
More about the research
This project aims to work out how human fat-lineage cells change the behavior of fibroblasts, the cells that produce and remodel the extracellular matrix (ECM), the protein scaffold that gives tissue its structure and mechanical properties.
Why it matters
Scarring and fibrosis after injury, surgery or disease are costly and often permanent, limiting movement, appearance and quality of life. Fat grafting already appears to reduce scarring in reconstructive surgery, but without knowing which fat cells or signals are responsible, treatments cannot be optimized. Determining how adipose-lineage cells control fibroblast conversion and matrix remodeling could guide better cell-based or drug therapies for wound healing and fibrosis.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Ryan Stowers
University of California-Santa Barbara, CA·Biomedical Engineering
Determine whether cardiomyopathy-driven remodeling of the extracellular matrix alters myocardial viscoelasticity, by mechanically testing human DCM and HCM heart tissue and pig disease-model tissue.
Sangkyun Cho
Johns Hopkins University, MD·Biomedical Engineering·Early-career
Test in real time whether releasing mechanical load drives cardiac myofibroblasts back toward a quiescent state, using iPSC-derived fibroblast reporter lines with fluorescently tagged marker genes such as CFP-TAGLN in a dynamically softening hydrogel.
Ryan Driskell
Washington State University, WA·Biology
Test whether Lef1, a Wnt-pathway transcription factor, is the master regulator of newborn papillary fibroblast function by switching it on in adult mouse skin fibroblasts and using wounding and chamber grafting assays to see if scarring gives way to regeneration.
The school
University of Iowa: 32 labs on PI Pages, $703M a year on research, 418 research doctorates a year.
Reach out
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