Gordon Meares
Ohio State University, OH·Neuroscience
During an ischemic stroke, blood flow to part of the brain is blocked, cutting off oxygen and nutrients. Stroke is common and a leading cause of long-term disability, yet there are few treatments.
- Fields
Neuroscience
Pharmacology
Medicine & Clinical Research
- Topics
ischemic stroke
neuroinflammation
ER stress
- Grants
- 1 known grant, through May 2027
What they work on
- Test whether deleting PERK, an ER stress sensor, in astrocytes or microglia improves outcome after experimental stroke, using mice with cell-specific PERK loss and middle cerebral artery occlusion.
- Determine how PERK-driven slowdown of protein production and activation of JAK1, an enzyme that turns on inflammatory genes, contribute to brain inflammation and neuron death after stroke.
- Test whether ISRIB, a small molecule that restores protein production, improves functional outcome in mice after middle cerebral artery occlusion.
More about the research
Besides the rapid death of brain cells, a stroke triggers inflammation and endoplasmic reticulum (ER) stress in the cells that survive. ER stress is a cellular alarm that goes off when proteins fold badly. How ER stress affects astrocytes and microglia, the brain's support and immune cells, is unknown. This project studies one ER stress pathway as a possible driver of brain damage after stroke.
Why it matters
Stroke affects about 800,000 people in the United States each year and is the leading cause of long-term disability, with few treatments available. If removing PERK from glial cells or restoring protein production with a drug such as ISRIB improves recovery in mice, the PERK and JAK1 pathway could become a new target for reducing brain inflammation and neuron loss after stroke.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Jason D Huber
West Virginia University, WV·Pharmacology
Test whether NL-1, a compound that binds the mitochondrial protein mitoNEET, prevents ferroptosis (iron-dependent cell death) in a four-cell Transwell blood-brain barrier model after oxygen-glucose deprivation and reperfusion.
Risheng Xu
Johns Hopkins University, MD·Neuroscience·Early-career
Identify which mast-cell inflammatory signals, such as TNFα and CCL2, are controlled by the receptor Mrgprb2 after ischemic stroke induced by transient middle cerebral artery occlusion in mice.
Cameron Mccarthy
University of South Carolina-Columbia, SC·Physiology
Test whether loss of OGT, the enzyme that adds O-GlcNAc sugar tags to proteins, protects parenchymal arterioles from dysfunction before stroke in mice made diabetic with a high-fat diet and low-dose streptozotocin.
The school
Ohio State University: 71 labs on PI Pages, $1.6B a year on research, 882 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.