Baerbel Rohrer
Medical University of South Carolina, SC·Medicine & Clinical Research
Age-related macular degeneration (AMD) is a leading cause of blindness in older adults. It damages the macula, the central part of the retina.
- Fields
Medicine & Clinical Research
Microbiology & Immunology
Biomedical Engineering
- Topics
age-related macular degeneration
retinal pigment epithelium
Bruch's membrane
- Grants
- 2 known grants, through Apr 2028
What they work on
- Characterize a perfused 3D RPE/choroid tissue chip built from stem cells, measuring gene expression by single-cell RNA sequencing, complement activation, Bruch's membrane formation and extracellular vesicles.
- Determine how the AMD risk genes CFH and ARMS2/HTRA1 alter complement activity, by building chips that pair risk-genotype RPE with non-risk choroid cells or vice versa.
- Test how the RPE/choroid chip responds to AMD-related stressors (cigarette smoke, fatty acid exposure and altered flow rate) under different genetic risk backgrounds.
- Determine whether antibodies against elastin damage Bruch's membrane through immune-cell killing and complement attack, using a smoke-induced eye disease mouse model and elastin-immunized mice.
- Test whether alpha-1 antitrypsin, a natural elastase inhibitor, preserves Bruch's membrane in mouse models, and analyze the MarketScan database for links between its use and AMD onset.
More about the research
Its early triggers are still unknown. Treating late-stage disease may also be less effective, because by then many inflammatory factors are at work. Early AMD centers on a few tissues. The retinal pigment epithelium (RPE) is a cell layer that supports the light-sensing cells. Bruch's membrane (BrM) is a thin layered sheet beneath the RPE. The choroid is the blood-vessel bed that feeds the retina. A common early sign is activation of complement, a part of the immune system that tags and attacks targets. Both projects study how damage and complement activity in this RPE–BrM–choroid region start AMD. One uses an engineered human tissue chip, and the other uses mouse models and patient data.
Why it matters
This work could identify early-stage treatment targets for age-related macular degeneration, which steals central vision from many older adults. Possible targets include complement activity in the RPE and elastin breakdown in Bruch's membrane. Alpha-1 antitrypsin is an existing elastase inhibitor, so it could be a candidate for slowing the disease before damage becomes widespread.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Dwight Stambolian
University of Pennsylvania, PA·Genetics
Differentiate eight patient-derived iPSC lines into retinal pigment epithelium, four with CFH risk alleles and four gene-corrected isogenic controls, and quantify mRNA, protein and function of complement components, regulators and receptors.
Jianhai Du
West Virginia University, WV·Biochemistry
Trace how retinal pigment epithelium cells use the amino acid proline as fuel alongside glucose, using tracer methods and mass spectrometry.
Jason Miller
University of Michigan, MI·Medicine & Clinical Research·Early-career
Determine the composition of lipid droplets, small fat-storage compartments, in human retinal pigment epithelium (RPE) cultures fed different lipid loads, using mass spectrometry.
The school
Medical University of South Carolina: 19 labs on PI Pages, $321M a year on research, 271 research doctorates a year.
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