Joseph Miano
Augusta University, GA·Physiology
Coronary artery disease (CAD), the narrowing of the arteries that feed the heart, is driven partly by the smooth muscle cells in the artery wall. When these cells lose their normal identity, they can help build disease.
- Fields
Physiology
Genetics
Medicine & Clinical Research
- Topics
coronary artery disease
atherosclerosis
vascular smooth muscle cells
- Grants
- 1 known grant, through Nov 2028
What they work on
- Define the coronary artery disease that develops in mice lacking Lmod1 only in vascular smooth muscle cells, using mouse genetics, spatial gene-activity profiling and immuno-electron microscopy of artery tissue.
- Determine how nuclear LMOD1 works with MYBBP1A, a protein that supports ribosomal RNA production, using structure–function studies and click chemistry to track newly made RNA in smooth muscle cells.
- Test whether MYBBP1A itself is needed for RNA production in vascular smooth muscle cells and for protection from coronary disease, using a new mouse in which Mybbp1a can be deleted.
- Map how the Lmod1 gene is switched on in living mice, using chromosome conformation capture and prime editing of an SRF-binding CArG box and a nearby FOXO3 site that carries a CAD-linked human variant.
More about the research
Large human genetic studies (genome-wide association studies, or GWAS) have linked a gene called Leiomodin1 (LMOD1) to CAD risk. LMOD1 helps build the cell's internal scaffold (cytoskeleton) and marks vascular smooth muscle cells (VSMCs), but its job in living animals and how it is switched on were unknown. The lab previously showed that Lmod1 is directly controlled by SRF and Myocardin, two proteins that act as a master switch for smooth muscle genes. It also found that losing the gene causes a fatal muscle disorder of the internal organs in newborn humans and mice.
Why it matters
Coronary artery disease remains a major cause of heart attacks. LMOD1 carries a genetic variant linked to CAD in humans, but its role in the artery wall has been unclear. By showing how LMOD1 keeps coronary smooth muscle cells healthy and how its levels are controlled, this work could lay groundwork for treatments that preserve LMOD1 levels or its partnership with MYBBP1A, which may lower CAD risk.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Daniel Li
Stanford University, CA·Genetics·Early-career
Determine how losing ZEB1, a transcription factor linked to coronary artery disease risk, changes gene activity, epigenetic state and plaque features in smooth muscle–derived cells, using a Zeb1 knockout mouse model of atherosclerosis.
Guizhen Zhao
University of Houston, TX·Physiology
Define whether the BAF60c–PPARγ axis protects against atherosclerosis, using male and female mice with smooth-muscle-specific knockout or transgenic overexpression of BAF60c, a chromatin-remodeling subunit.
Robert Wirka
University of North Carolina at Chapel Hill, NC·Genetics
Track individual smooth muscle cells as they multiply and choose fates during atherosclerosis, using a barcoding mouse model compatible with single-cell RNA sequencing, with and without Twist1 knockout.
The school
Augusta University: 11 labs on PI Pages, $166M a year on research, 37 research doctorates a year.
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