Karsten Gronert
University of California-Berkeley, CA·Neuroscience
Glaucoma and other optic nerve diseases blind people by killing retinal ganglion cells (RGCs), the neurons that carry visual signals from the eye to the brain. Prostaglandins, fat-derived signaling molecules, are already major drug targets in the eye: anti-inflammatory NSAIDs block their production, and prostaglandin-boosting drugs lower eye pressure.
- Fields
Neuroscience
Pharmacology
Medicine & Clinical Research
- Topics
prostaglandin D2
lipid mediators
retina
- Grants
- 1 known grant, through Apr 2030
What they work on
- Define which retinal cells make and respond to prostaglandin D2 (PGD2), a fat-derived signaling molecule, in healthy retina and how raised eye pressure (ocular hypertension) shuts this pathway down.
- Determine how the PGD2 receptors DP1 and DP2 maintain healthy retinal ganglion cells and macroglia, the retina's support cells, and keep inflammation in astrocytes and microglia in check.
- Test whether drugs that activate DP1 and/or DP2 protect retinal ganglion cells and optic nerve axons from degeneration caused by ocular hypertension in rodent models.
More about the research
Yet little is known about what prostaglandins do inside the retina itself, or whether they help protect its neurons.
Why it matters
People with glaucoma and other diseases that kill retinal ganglion cells could eventually benefit from new neuroprotective eye treatments. Because prostaglandin drugs are already used in the eye, showing that amplifying PGD2 receptor signaling protects these neurons could point to a new therapeutic strategy, and may also inform how routine ocular NSAID use affects the retina.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Shahid Husain
Medical University of South Carolina, SC·Pharmacology
Determine how class I and IIb histone deacetylases (HDACs), enzymes that tighten DNA packaging, contribute to retinal ganglion cell death in rats with ocular hypertension (high eye pressure).
Raghu Krishnamoorthy
University of North Texas Health Science Center, TX·Pharmacology
Determine whether endothelin-1 (ET-1), a blood-vessel-tightening protein, acts through its ETA and ETB receptors to reduce mitophagy, the removal of damaged mitochondria, in retinal ganglion cells.
Matthew Veldman
Medical College of Wisconsin, WI·Neuroscience
Determine when srebf2, a master regulator of cholesterol production, is needed in zebrafish retinal ganglion cells for optic nerve regeneration, using srebf2 activity reporter lines.
The school
University of California-Berkeley: 46 labs on PI Pages, $1.1B a year on research, 825 research doctorates a year.
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