North Texas Eye Research Institute Faculty and Staff

NTERI Faculty

Faculty

 

Suchismita Acharya PhD
Research Assistant Professor
Published work

Our current research is focused on expanding the chemical toolbox for neural signaling and anti-inflammation/anti-oxidant pathways to understand the mechanism of action of the disease pathology associated with glaucomatous optic neuropathy, Alzheimer Diseases, Ischemic stroke as well as angiogenesis. Our lab integrates medicinal chemistry, chemical biology, bio-engineering, and drug delivery via nanotechnology. We employ synthetic organic and organometallic chemistry to generate small molecule library for low throughput as well as high throughput screening (target based as well as phenotypic).

Sai Chavala MD
Professor and Director of Translational Research
Published work
Our laboratory focuses understanding the molecular underpinnings of acquired and inherited retinal degenerations. Our goal is to develop novel therapies and restore vision for patients suffering from vision impairment secondary to retinal disease.  Currently, our lab focuses on stem cell-like regenerative approaches to replace damaged or lost retinal cells.

Abbot Clark, PhD, FARVO
Professor and Executive Director
Published work
Abe Clark’s laboratory studies the cell and molecular mechanisms responsible for a variety of eye diseases, especially glaucoma. Glaucoma is a leading cause of irreversible vision loss and blindness in the world. Dr. Clark’s lab has discovered a number of new disease pathways involved in glaucomatous elevation of intraocular pressure. His lab also has identified novel neuroprotective therapies to protect specific retinal neurons, retinal ganglion cells, that are damaged in glaucoma, and also protect the optic nerve and visual centers in the brain. Abe currently mentors 9 graduate students and serves on the editorial board of 4 scientific journals. He has published over 190 peer-reviewed manuscripts and has been invited to present his scientific work at over 110 national and international scientific meetings.

Adnan Dibas PhD
Research Assistant Professor
Very little is known about how and why the optic nerve is progressively damaged in glaucoma, a leading disease for blindness worldwide. Currently glaucoma medication involves only pressure lowering medication, however vision loss continues.  Conditions known to cause glaucoma such as hypoxia, and ischemia were found to be associated with increased in the expression of ASIC channels and blockers of such proteins increased survival of neurons in animals. Currently, our lab is involved in testing such blockers in different models of retinal injuries. Also, our lab is interested in steroid-induced trafficking in ocular tissues which in known to cause glaucoma in ~ 30% of human.

Dorette Ellis PhD
Associate Professor
Glaucoma is a disease of the eye that results in blindness. There are two prominent problems in glaucoma. One is high pressure caused by fluid build-up in the front of the eye and the other is loss of structures called retinal ganglion cells in the back of the eye. I am interested in understanding how retinal ganglion cells function and how to help the cells survive in glaucoma. I am also interested in understanding how the fluid in the front of the eye is able to build-up and how to decrease the fluid in glaucoma. Understanding how fluid builds-up and how cells die will allow us to develop therapeutic strategies for the treatment of glaucoma.

Shaoqing He PhD
Research Assistant Professor
Published work
My research interest focuses on the pathological mechanisms of glaucoma. The characteristic events occurring during progression of glaucoma are the death of nerve cells in the eye (retinal ganglion cells) and damage to the optic nerve. We are testing the hypothesis that transcription factors, the proteins controlling gene expression, and astrocytes, one type of supporting cells in the nervous system, play a crucial role in both events.  Therefore, my efforts are dedicated to understand the interaction of nerve cells and astrocytes, and to reveal the roles of transcription factors in neuronal cell death, particularly through the activation of astrocytes.

Raghu Krishnamoorthy PhD
Assistant Professor
My laboratory is involved in projects aimed at understanding the role of the endothelin family of vasoactive peptides in glaucomatous neurodegeneration. The goal is to develop endothelin receptor antagonists as neuroprotective agents for the treatment of glaucoma. Another project focusses on the POU domain transcription factor POU4F2 (Brn3b) and study its role in neuroprotection in a rodent model of glaucoma.

Yang Liu MD PhD
Research Assistant Professor
Published work
Dr. Liu’s research interests focus on understanding the mechanisms related to glaucoma neurodegeneration and developing effective neuroprotective strategies. Current studies include phosphoproteomics changes in the retina following optic nerve injury, establishing conditionally immortalized retinal cell lines.

Weiming Mao PhD
Assistant Professor and Associate Director of Research
Visual Science Graduate Program Advisor
Published work
Glaucoma is a leading cause of blindness. My research team uses various models including cultured cells, perfusion cultured eyes, and mice to study the disease mechanism. We are currently focusing on three projects: 1) determine how two glaucoma-associated cell signaling pathways, the TGFβ and Wnt pathways, interact with each other in the eye; 2) determine the genes that cause glucocorticoid-induced glaucoma; and 3) determine the proteins that change the “scaffold” inside ocular cells.

Colleen McDowell PhD
Assistant Professor
Published work
One of the major risk factors for the development of glaucoma is an increased pressure inside the eye. An increase of pressure occurs in the eye when fluid is not drained properly through the drainage structures in the front of the eye. Research in my laboratory aims to understand what regulates the arrangement and construction of the drainage structures and how changes in this makeup prevent proper drainage in the eye. In addition, the buildup of pressure in the eye can damage the visual sensing structures in the back of the eye, leading to blindness. My laboratory also studies specific subtypes of cells in the visual sensing structures of the eye that are more or less susceptible to glaucoma damage. These experiments will help identify pathways of destruction that will serve as new targets for the development of effective glaucoma treatments, and may also lead to the discovery of more sensitive ways to diagnose glaucoma and follow glaucoma progression.

Cameron Millar PhD
Research Assistant Professor
Experienced eye researcher and educator, with both academic and industrial experience, committed to the investigation of ocular anterior segment physiology, aqueous humor dynamics, pharmacology, and glaucoma.  Experienced with in vivo (live animal) and organ perfusion paradigms, as well as small animal research surgical techniques, in the following species: mouse, rat, rabbit, monkey, and bovine.

Aiguo Ni PhD
Research Assistant Professor
Published work
Retinal stem cells are the primitive cells that can develop into different specific cell types in the eye. My research interests lie in ocular regenerative medicine. More specifically, one of my interests is to isolate or generate retinal stem cells and/or mature ocular cells such as retinal pigmented epithelial cells to replace cells and tissues lost during disease progression. The other is to use generated stem cells or mature cells as tools for disease modeling and drug screening to help developing new therapeutic strategies to treat degenerative eye diseases.

Iok-Hou Pang PhD
Professor and Chair of Department of Pharmaceutical Sciences
Published work
Dr. Pang’s research interests mainly focus on the understanding of glaucoma etiology, pathology, and pharmacology, especially on glaucoma neuroprotection.  His is working to delineate essential molecular and cellular mechanisms, as well as characterize receptors and signal transduction pathways related to the abnormal changes in glaucoma.  His laboratory is using rodents and primary cultures of retinal and optic nerve cells as study models to clarify biological events leading to the disease and its prevention and protection.

Dorota Stankowska PhD
Research Assistant Professor
Published work
My research focusses on mechanisms underlying the neuroprotective effects of transcription factor Brn3b in a rat model of ocular hypertension. Our studies have shown that following elevated intraocular pressure (IOP) mediated axonal injury in rats, administration of rAAV-Brn3b, promotes neuroprotection of retinal ganglion cells and optic nerve axons. Additionally, intravitreal rAAV-Brn3b administration significantly restored the visual acuity in IOP-elevated rat eyes. The long term goals are to uncover novel molecular targets of Brn3b and explore their potential to be developed as neuroprotective agents for the treatment of glaucoma.

Tara Tovar-Vidales PhD
Research Assistant Professor
Published work
Dr. Tovar-Vidales research goal is to understand the pathology of the trabecular meshwork (TM) and the optic nerve head (ONH) in glaucoma. The TM is the main dynamic resistor that regulates the aqueous humor outflow and causes elevated intraocular pressure in the anterior chamber of the eye. This elevated pressure is transduced towards the back of the eye and results in a remodeling of the ONH. The ONH is the resident of two types of cells, ONH astrocytes  and lamina cribrosa cells (LC). ONA and LC cells have been implicated in the pathophysiology of glaucoma. I focus primarily on growth factors and their signaling pathways to determine if they alter mRNA and protein expression of the TM and the ONH cells. I wish to understand the roles of these growth factors in normal tissue and in the glaucoma pathophysiology.

Hongli Wu PhD
Assistant Professor
Published work
The central theme of my research is to understand the function of thiol-regulating enzymes and evaluate their therapeutic potential in eye diseases. Of primary interest is the age-related macular degeneration (AMD), the most common retinal disorder that affects 25 million people worldwide, yet its pathogenesis remains poorly understood. The following are our major projects:

  • Examine how retinal thiol redox dysregulation leads to AMD pathogenesis.
  • Characterize glutaredoxin 2 (Grx2), a thiol redox-regulating enzyme, knockout mice as a new animal model for AMD.
  • Identify/screening Grx2 inducers from natural products for AMD treatment.

Thomas Yorio PhD
Professor
Dr. Yorio’s laboratory focuses on glaucoma.  Areas of interest include aqueous humor dynamics, endothelin pharmacology in glaucoma, identifying potential targets for neuroprotection and in the area of glucocorticoid pharmacology and ocular hypertension, specifically on understanding the role of glucocorticoid receptor (GR) beta in dampening the ocular hypertensive response of glucocorticoids.

Gulab Zode PhD
Assistant Professor
My research focus is to understand how cellular processes including unfolded protein response pathway and autophagy regulate protein misfolding and to develop targeted treatments for glaucoma based on the understanding of these pathways. We have developed two novel glaucoma mouse models as well as established various genetic tools to study protein misfolding and biological functions of unfolded protein response pathway and autophagy in glaucoma pathogenesis. We recently discovered that endoplasmic reticulum stress is associated with trabecular meshwork damage and elevation of intraocular pressure, leading to blindness. We are currently targeting these pathways using genetic and pharmacological manipulations for the treatment of glaucoma.

Staff

Marcy Butler

Mahshid Carter

Patricia Foster

Sherri Harris

Ramesh Kasetti

Linya Li

Xiaobin Liu

Hai-Ying Chen Ma

Biraj Mahato

Sandra Neubauer

Tien Phan

Anirudh Sethi

Wei Zhang

 

This page was last modified on October 24, 2016