William Durante
University of Missouri-Columbia, MO·Physiology
When an artery is injured, for example by a procedure like angioplasty, or damaged by diabetes, the smooth muscle cells in its wall can multiply, move, and lay down excess collagen. Collagen is the stiff protein that gives tissue its strength.
- Fields
Physiology
Pharmacology
Medicine & Clinical Research
- Topics
glutaminase-1
glutamine metabolism
glutamate
- Grants
- 1 known grant, through May 2027
What they work on
- Determine how glutaminase-1 (GLS1), an enzyme that converts glutamine to glutamate and ammonia, controls the growth, migration, collagen production and survival of vascular smooth muscle cells, using GLS1 gene delivery and tests of each breakdown product.
- Test whether growth factors promote smooth muscle cell proliferation, migration and collagen synthesis by switching on GLS1 in cultured vascular cells.
- Establish whether blocking GLS1 with drugs, gene silencing, or deleting GLS1 specifically in smooth muscle cells reduces artery wall thickening after carotid artery injury in rodents.
- Investigate whether high glucose increases GLS1 and whether GLS1 drives artery remodeling, stiffening and hypertension in diabetic mice.
More about the research
This overgrowth thickens and stiffens the artery and can lead to re-narrowing of the vessel and to high blood pressure. Cardiovascular disease and stroke cost more lives than any other disease in the US. Understanding what fuels this abnormal artery remodeling could point to new treatments.
Why it matters
Abnormal thickening and stiffening of arteries after injury, and in diabetes, contributes to cardiovascular disease and hypertension. These conditions are leading causes of death in the US. If GLS1 proves to be a key driver of this remodeling, it could become a new drug target for preventing re-narrowing of injured arteries and for treating arterial stiffness and high blood pressure in people with diabetes.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Sadiya Parveen-Nesson
Louisiana State University, LA·Microbiology & Immunology
Test whether blocking glutaminase (GLS1), the enzyme that breaks down glutamine, restores the TB-killing ability of Mtb-infected macrophages, using siRNA knockdown, chemical inhibition and macrophages from macrophage-specific GLS1 knockout mice.
Santhi Ganesh
University of Michigan, MI·Genetics
Define the range of genetic variants underlying arterial fibrodysplasia using high-throughput targeted gene sequencing of patients with fibromuscular dysplasia (FMD) from clinical and biorepository collections.
Yuanjun Shen
Binghamton University, NY·Medicine & Clinical Research·Early-career
Examine how Vps34, an enzyme that drives smooth muscle overgrowth, is activated in PAH lung arteries through Akt-dependent loss of phosphorylation at Ser164, including candidate phosphatases identified by computer analysis.
The school
University of Missouri-Columbia: 21 labs on PI Pages, $509M a year on research, 260 research doctorates a year.
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