Robert Campbell
Washington University in St Louis, MO·Medicine & Clinical Research
Ischemic stroke happens when a clot blocks blood flow to part of the brain, and roughly 700,000 people in the U.S. have one each year.
- Fields
Medicine & Clinical Research
Physiology
Microbiology & Immunology
- Topics
platelets
ischemic stroke
thrombosis
- Grants
- 3 known grants, through May 2030
What they work on
- Determine how the mitochondrial calcium uniporter (MCU), the channel bringing calcium into mitochondria, controls platelet activation, procoagulant platelet formation and platelet-neutrophil aggregates, including signaling through the enzyme Syk.
- Test whether deleting or blocking MCU in platelets improves cerebral blood flow and neurological outcomes in mouse models of ischemic stroke, using intravital microscopy to watch clots form in living vessels.
- Determine whether MCU and other regulators of procoagulant platelets are altered in platelets from human ischemic stroke patients and whether those changes, measured by sequencing, correlate with patient outcomes.
- Assess whether the prostacyclin receptor, a brake on platelet activation, cross-talks with the thrombin receptor PAR4, using genetically altered human megakaryocytes and platelets from humanized PAR4 mouse lines.
- Map how cathepsin G, a neutrophil enzyme, cleaves PAR4 and how the resulting tethered ligand activates integrin aIIbb3, granule release and aggregation, comparing the Ala120 and Thr120 PAR4 variants.
- Use humanized PAR4 mice to test how human PAR4 and its Ala120Thr variant shape platelet and neutrophil activity, infarct size and brain hemorrhage after experimental ischemia/reperfusion injury.
- Determine whether neutrophil extracellular traps (NETs), DNA-protein webs released by neutrophils, appear inside and outside brain vessels in stroke patients and mice, and whether patients' neutrophils are primed to release them.
- Test whether platelet-derived HMGB1, an alarm molecule released on platelet activation, drives NET formation during ischemic stroke injury.
- Test whether giving the endogenous neutrophil NET-inhibitory factor (nNIF) blocks NET release in experimental stroke and improves acute and long-term motor and neurological function.
More about the research
Today's main treatments either dissolve the clot or pull it out, and many patients are not eligible for either. New options depend on knowing which cells drive the damage. Platelets, the small blood cells that build clots, and neutrophils, inflammatory white blood cells, are the focus here. Across its grants the lab asks how platelets switch on, how they recruit and activate neutrophils, and whether blocking those steps protects the brain, combining patient blood samples, cell experiments, mouse stroke models and live imaging inside blood vessels.
Why it matters
Stroke and other clotting disorders are leading causes of death and long-term disability, and many patients cannot use existing clot-removing treatments. By pinpointing specific platelet pathways, mitochondrial calcium entry, the PAR4 receptor and platelet-triggered neutrophil traps, this work could identify drug targets that reduce brain injury without causing dangerous bleeding, and genetic markers such as PAR4 Thr120 that could help tailor anti-platelet therapy to an individual patient.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
The role of mitochondrial calcium uniporter in platelet function and thrombosis
NIH · Aug 2026 – May 2030
Platelet-Mediated Neutrophil Extracellular Traps Regulate Ischemic Stroke Injury
NIH · Aug 2024 – Mar 2027
HUMAN PLATELET PAR4: NOVEL ACTIVATION, INTERINDIVIDUAL VARIATION, AND NEUTROPHIL INTERACTIONS IN VIVO AND IN VITRO
NIH · Oct 2024 – Jan 2027
Closest labs
Rashmi Sood
Medical College of Wisconsin, WI·Physiology
Identify and phenotype the immune cell populations that change in the decidua, the uterine lining that meets the placenta, and track their trafficking into and out of the tissue as clots form and abruption develops in EPCR-deficient mice.
Jessica Brinkworth
University of Illinois Urbana-Champaign, IL·Microbiology & Immunology
Test whether neutrophils, front-line germ-killing white blood cells, from larger mammals kill Escherichia coli less effectively per cell, comparing direct killing and phagocytosis across 20 terrestrial species spanning 7 orders of magnitude in body mass.
Jocelyn Grunwell
Emory University, GA·Medicine & Clinical Research
Test whether markers of neutrophil cell death, including neutrophil extracellular traps (NETs), in blood and airway samples taken twice in the first week of intubation predict longer intubation or death in children with PARDS.
The school
Washington University in St Louis: 97 labs on PI Pages, $1.2B a year on research, 365 research doctorates a year.
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