Samuel A Herberg, PhD
- Assistant Professor of Ophthalmology
- Assistant Professor of Biochemistry and Molecular Biology
- Assistant Professor of Cell and Developmental Biology
Education & Fellowships
- Postdoctoral Fellow: Wake Forest University Baptist Medical Center, 2018, Regenerative Medicine
- Postdoctoral Fellow: Case Western Reserve University, 2017, Biomedical Engineering
- Postdoctoral Fellow: Augusta University in Augusta Georgia, 2014, Tissue Engineering
- PhD: Augusta University in Augusta Georgia, 2013, Cellular Biology
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My scientific training spans the fields of cellular biology, tissue engineering, and regenerative medicine. I now aim to train these skills on important problems in ocular biology.
The trabecular meshwork (TM) modulates homeostatic aqueous humor outflow resistance. Multifactorial dysregulation of the TM is the principal cause of elevated intraocular pressure (IOP) that is associated with irreversible vision loss in primary open-angle glaucoma (POAG). The lack of adequate animal and in vitro model systems for detailed mechanistic investigation of TM biology and outflow physiology has hampered the development of new POAG treatment modalities. We're developing a novel bioengineered 3D in vitro TM construct, integrated on a custom microfluidics chip, that recapitulates the complex TM tissue composition, architecture, and functions. This TM-on-a-chip model has the potential to significantly advance our mechanistic insight of how outflow resistance is modulated on the cellular and tissue level under homeostatic and glaucomatous conditions.
The site of retinal ganglion cell (RGC) injury in glaucoma occurs at the lamina cribrosa (LC), a porous collagenous network that provides structural support to RGC axons as they exit the globe. Biomechanical strain on the LC induced by IOP elevation is thought to cause direct mechanical failure of the collagen matrix. In collaboration with Dr. Preethi Ganapathy, we are investigating cellular mechanisms that alter LC biomechanics in response to dynamic IOP fluctuation, and how this affects RGC axon function.
In addition to my primary research projects in ocular biology, I am interested in SLC13A5 - a transporter that mediates Na+-coupled entry of citrate into cells. Loss-of-function mutations in SLC13A5 in humans cause severe neonatal epilepsy and defective skeletal and tooth development. Citrate is critical for multiple metabolic pathways. As ~70% of citrate in the body is in bone and teeth, it is likely that the Ca2+-chelating property of citrate is obligatory for its role in these tissues. However, the source of citrate in mineralized tissues and the precise role of SLC13A5 in tooth/bone physiology are not well understood. Our primary goal is to determine what SLC13A5 does in teeth/bone and why loss of function in SLC13A5 impacts dental/skeletal development in humans. Surprisingly, Slc13a5-/- mice do not have epilepsy, but they do show enamel hypoplasia in both incisors and molars, and decreased bone mineral density that gets corrected with age. The relatively mild skeletal phenotype in Slc13a5-/- mice raises an important question: Is mouse an appropriate model to delineate the mechanisms underlying the brain or dental/skeletal pathology arising from loss of function in SLC13A5 in humans? Major functional differences exist between mouse Slc13a5 and human SLC13A5. To that end, we have generated a humanized mouse that expresses human SLC13A5 in place of mouse Slc13a5. This unique mouse model allows us to investigate the biological role of the citrate transporter SLC13A5 in teeth/bone in a manner that is relevant to humans.
SUNY Distinguished Professor Emeritus
- Richard Cross, PhD
- David Turner, PhD