Patrick Belvitch
University of Illinois Chicago, IL·Medicine & Clinical Research
In acute respiratory distress syndrome (ARDS), leaky blood vessels in the lungs let protein-rich fluid flood the tiny air sacs. This starves the body of oxygen and often causes respiratory failure and death in critically ill patients.
- Fields
Medicine & Clinical Research
Physiology
Biology
- Topics
acute respiratory distress syndrome
acute lung injury
pulmonary vascular leak
- Grants
- 1 known grant, through May 2029
What they work on
- Determine how CARMIL1, a regulator of actin filament growth, shapes edge actin structures in lung endothelial cells, using biochemistry and advanced imaging after silencing CARMIL1 or overexpressing normal or variant forms.
- Test whether changing CARMIL1 levels alters endothelial barrier integrity, using multiple assays of local and overall permeability in cultured lung endothelial cells.
- Characterize endothelial CARMIL1 in mouse lung injury by delivering endothelial-targeted siRNA or lentiviral constructs and measuring vascular leak after inflammatory or infectious insults.
- Link human LRRC16A gene variants associated with better ARDS outcomes to cellular mechanisms by comparing variant and normal CARMIL1 constructs in endothelial cells.
More about the research
Normally, the endothelial cells that line these vessels form a tight barrier. During severe infection or inflammation, gaps open between them. People carrying certain variants of the gene LRRC16A appear to have better ARDS outcomes, but nobody knows why. Explaining that link could reveal how lung vessels stay sealed and suggest new ways to treat the disease.
Why it matters
Patients with ARDS, a frequently fatal lung failure triggered by severe infection or inflammation, currently lack treatments that stop fluid leaking from lung blood vessels. Explaining how CARMIL1 and its human variants affect the endothelial barrier could point to new therapeutic targets that strengthen lung vessels. It could also help explain why some critically ill patients fare better than others.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Jamie Meegan
University of South Alabama, AL·Physiology·Early-career
Test whether cell-free hemoglobin released from fragile red blood cells during sepsis disrupts the lung microvascular endothelial cell barrier by oxidizing low-density lipoprotein to oxidized LDL.
Barry M. Gumbiner
University of Virginia, VA·Biology
Determine whether surface regulation of VE-cadherin, the adhesion protein linking endothelial cells, is a shared mechanism for responses to histamine, angiopoietins, Tie2 and S1P, using endothelial cells from different microvascular beds.
Yutong Zhao
Ohio State University, OH·Medicine & Clinical Research
Test whether blocking the mitochondrial deubiquitinase USP30 in endothelial cells reduces white blood cell adhesion and migration and preserves the vessel barrier, and whether deleting it lessens Pseudomonas- or sepsis-induced lung injury in mice.
The school
University of Illinois Chicago: 42 labs on PI Pages, $532M a year on research, 359 research doctorates a year.
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