Dandan Sun
University of Pittsburgh, PA·Neuroscience
After a stroke, the brain must clean up dead cells and debris, rebuild the insulation around nerve fibers, and reshape connections between neurons. Microglia, the brain's resident immune cells, do much of this work through phagocytosis, the process of engulfing and digesting material.
- Fields
Neuroscience
Pharmacology
Microbiology & Immunology
- Topics
microglia
Na+/H+ exchanger
intracellular pH
- Grants
- 1 known grant, through Jun 2027
What they work on
- Determine how deleting Nhe1, an acid-exporting membrane protein, only in microglia changes phagocytosis-related gene expression and debris clearance after ischemic stroke, using Cx3cr1-CreER;Nhe1 conditional knockout mice.
- Test how Nhe1-deficient microglia increase phagocytosis and cholesterol efflux through the LXR/RXR–APOE–TREM2 pathway, and how this supports remyelination after stroke.
- Examine how loss of microglial NHE1 boosts mitochondrial biogenesis and oxidative phosphorylation (OXPHOS), the cell's efficient energy production, to fuel microglial repair functions in post-stroke brains.
More about the research
How microglia adjust their energy metabolism to support this repair work is not well understood. Answering this could point to treatments for stroke, vascular dementia and Alzheimer's disease.
Why it matters
Microglia that fail to clear debris or that stay inflamed contribute to memory and thinking decline in vascular dementia and Alzheimer's disease. This work could establish NHE1 as a drug target for shifting microglia toward a repair-promoting state. Such a shift may improve brain repair and recovery of cognitive function in people after stroke and in related neurodegenerative diseases.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Dorothy Schafer
University of Massachusetts Chan Medical School, MA·Neuroscience
Determine whether microglia or other macrophages account for the reduced inflammation and improved remyelination seen in mice lacking UNC93B1, the chaperone eTLRs need, in acute and immune-mediated demyelination models.
Tae-Wan Kim
Columbia University, NY·Neuroscience
Determine how the neuronal signal SEMA3A promotes β-amyloid uptake and a disease-associated microglia gene profile in human iPSC-derived microglia (iMGLs), independently of the TREM2 receptor.
Kristian Doyle
University of Arizona, AZ·Neuroscience
Identify the pro-inflammatory lipid species released when myelin and cell membranes break down after stroke, and the inflammatory pathways they trigger in macrophages and microglia.
The school
University of Pittsburgh: 83 labs on PI Pages, $1.5B a year on research, 403 research doctorates a year.
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