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Basic Vision Research

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Across both the Evanston and Chicago campuses of Northwestern, physicians and scientists are actively pursuing new knowledge to improve the quality of life and options for adults and children with diseases and disorders of the eye. In addition to our faculty members with primary appointments in the Department of Ophthalmology, we collaborate in vision research with many faculty members outside our department, including Biomedical Engineering, Dermatology, Medicine, Neurobiology and Neuroscience.

RetinaCell Biology and Development
Carthew, Richard

Richard Carthew, PhD

Owen L. Coon Professor of Molecular Biosciences


The laboratory is interested in understanding how microRNAs specifically inhibit their target genes and the biological consequences of this regulation. The laboratory works on function of microRNAs to promote the differentiation of photoreceptor neurons in the fruit fly, Drosophila.

Johnson, Mark

Mark Johnson, PhD

Professor of Biomedical Engineering, Professor of Ophthalmology, Feinberg School of Medicine


Cellular mechanics and the hydrodynamics of glaucoma; the role of lipids in AMD; transport through connective tissues; esophageal transport; and chaos and diffusion.

RetinaDegenerations and Diabetic Retinopathy
Linsenmeier, Robert

Robert Linsenmeier, PhD

Professor of Biomedical Engineering, Professor of Neurobiology, Professor of Ophthalmology, Director of Northwestern Center for Engineering Education Research


The microenvironment of the mammalian retina, including oxygen and pH regulation in health and disease; engineering education research.

RetinaCircuitry and Function
Schmidt, Tiffany

Tiffany Schmidt, PhD

Assistant Professor of Neurobiology


The research is concerned with the role of retinal ganglion cell (RGC) subtypes in specific visual functions with emphasis on intrinsically photosensitive RGCs (ipRGCs).

Visual Processing
Segraves, Mark

Mark Segraves, PhD

Professor of Neurobiology


The laboratory uses the eye movement system as a model for how the brain of primates, including man, controls a variety of movements. Research work focuses upon areas of the rhesus monkey's prefrontal cortex and midbrain that help to control eye movements.

RetinaFunctional Imaging
Zhang, Hao

Hao Zhang, PhD

Professor of Biomedical Engineering, Professor of Ophthalmology, Feinberg School of Medicine


Novel optical imaging technologies for ophthalmic application.

Yongling Zhu Lab

Research Description

The laboratory develops genetic and viral technologies to delineate and target cell types in the retina, followed by combining electrophysiology, functional imaging and optogenetics to understand how specific subsets of neurons integrate into larger circuits that compute different neural representations of the visual world.

For more information, visit the faculty profile for Yongling Zhu, PhD.

Select Publications

  • Jo, A., Xu, J., Deniz, S., Cherian, S., DeVries, S.H., and Zhu, Y. (2018) Intersectional strategies for targeting amacrine and ganglion cell types in the mouse retina
  • Xu, J. and Zhu, Y. (2018) A rapid in vitro method to flip back the Double-fLoxed Inverted Open reading frame in a plasmid BMC Biotechnol. 18(1):52
  • Zhu, Y., Xu, J., Hauswirth, W.W., and DeVries, S.H.* (2014). Genetically targeted binary labeling of retinal neurons. J. Neuroscience. 34(23):7845–7861
  • Zhu, Y., Xu, J., and Heinemann, S. F. (2009). Two pathways of synaptic vesicle retrieval revealed by single vesicle imaging. Neuron, 61(3):397-411
  • Zhu, Y. and Stevens, C. F. (2008) Probing synaptic vesicle fusion by altering mechanical properties of the neuronal surface membrane Proc Natl Acad Sci U S A. 105(46):18018-18022


Lab Staff

  • Sercan Deniz: Postdoc fellow
  • Andrew Jo: Graduate student

Vijay P. Sarthy Lab

Research Description

The pattern of gene expression in eukaryotic cells is strongly influenced by interactions with neighboring cells. When cell-cell interactions are perturbed, changes in cellular gene activity are often observed. In the vertebrate retina, inherited or acquired rod and cone degeneration results in disruption of normal interactions between photoreceptors and their support cells, the Müller cells. Under these conditions many genes such as the glial intermediate filament protein (GFAP) gene, ciliary neurotrophic factor (CNTF) gene and basic fibroblast growth factor (bFGF) gene are upregulated in neighboring Müller cells.

We use techniques such as single cell RT-PCR and differential display to study changes in gene expression patterns in Müller cells. Major goals of our current research are to elucidate the molecular mechanisms responsible for transcriptional activation and to determine the extracellular inductive signal and the signal transduction pathways involved. Our recent cell transfection studies and experiments with GFAP-lacZ transgenic mice suggest that GFAP gene activation in Müller cells is regulated by a cell type-specific, inducible enhancer and that GFAP gene is activated through the JAK-STAT pathway. The work on gene regulation is crucial for development of strategies for using Müller cell-specific promoters to test the biological effects of growth factors and cytokines in animals models of retinal degeneration and more importantly for designing cell type-specific vectors for targeted delivery in gene therapy.

A second project is concerned with molecular cloning, regulation and function of neurotransmitter transporters—a family of membrane proteins that are involved in the uptake of neurotransmitters. We are particularly interested in the role of taurine and glutamate transporters in retinal ischemia and glutamate neurotoxicity. We have already cloned and characterized GABA, taurine and glutamate transporters from retina. We have also localized the transporters to specific retinal cell types and shown that phosphorylation may play a key role in regulating transporter function.

For more information visit Dr. Sarthy's faculty profile page.


View Dr. Sarthy's publications at PubMed


Email Dr. Sarthy

Phone 312- 503-3031

Tsutomu Kume Lab

Susan Quaggin Lab

Our lab focuses on the basic biology of vascular tyrosine kinase signaling in development and diseases of the blood and lymphatic vasculature.  Our projects include uncovering the molecular mechanisms of diabetic vascular complications, thrombotic microangiopathy, glomerular diseases and glaucoma.  Utilizing a combination of mouse genetic, cell biologic and proteomic approaches, we have identified key roles for Angiopoietin-Tie2 and VEGF signaling in these diseases.  Members of the lab are developing novel therapeutic agents that target these pathways.  

For more information, please see the faculty profile of Susan Quaggin, MD


See Dr. Quaggin's publication in PubMed


Email Dr. Quaggin

Robert Lavker/Han Peng Lab

Research Description

The Lavker/Peng laboratory focuses on the biology of epithelial stem cells and the roles of microRNAs (miRNAs) in regulating epithelial homeostasis. Initial investigations on microRNAs (miRNAs) focused on corneal epithelial-preferred miRNAs. Specifically, miR-205 undergoes a unique form of regulation through an interaction with the corneal-preferred miR-184 to maintain SHIP2 levels. SHIP2, a lipid phosphatase, is a target of miR-205, which enhances keratinocyte survival through PI3K-Akt signaling. This miRNA also positively regulates keratinocyte migration by altering F-actin organization and decreasing cell-substrate adhesion. The lab has also focused on miR-31, which targets factor inhibiting hypoxia-inducible factor-1 (FIH-1). FIH-1 impairs epithelial differentiation via attenuation of Notch signaling. Our results define a previously unknown mechanism for keratinocyte fate decisions where Notch signaling potential is, in part, controlled through a miR-31/FIH-1 nexus. This provides a rationale for development of treatment regimens in patients with diseases affecting abnormal epithelial differentiation (e.g., psoriasis) using inhibitors of FIH-1.

The laboratory has also been interested in the roles of autophagy in stratified epithelia. We were the first to use single cell RNA sequencing assay and established a comprehensive atlas of genes of the anterior segmental epithelia from wild-type and autophagy-deficient mice. In addition, we showed how ciliogenesis and autophagy are coordinately regulated in the corneal epithelium. Furthermore, we have demonstrated that depletion of miRs-103/107 in vitro and in vivo resulted in an inhibition of autophagy at the end stage and that PLD1/PKC/dynamin1 pathway plays a critical role in regulation of end-stage autophagy. This was the first demonstration of how end-stage autophagy is regulated in stratified epithelia. We have also reported that autophagy has a positive role in proliferative capacity of the limbal epithelium. Our laboratory has demonstrated that autophagy plays protective roles against a variety of stress (e.g., nitrogen mustard-induced corneal injury) in the cornea.

Our group is actively engaged in conducting research in skin and corneal inflammation. We demonstrated that enhancement of autophagy activates myeloid anti-inflammatory M2 macrophages in mouse skin. We also demonstrated that ACE2 deficiency resulted in a cytokine storm-driven corneal inflammation. We examined the efficacy of a novel synthetic high-density lipoprotein nanoparticle (HDL NPs)-based eye drop in alleviating corneal inflammation. HDL NP can also delivery functional microRNAs (e.g., miR-205) into corneal epithelial cells.


For publication information and more, see the Lab faculty’s profiles:

Robert Lavker, PhD, Han Peng, PhD

Contact Lavker/Peng Lab

Contact the Lavker/Peng Lab at 312-503-2043 or visit us on campus in the Montgomery Ward Building, 303 E. Chicago Avenue, Ward 9-120, Chicago, Illinois, 60611.


Robert M. Lavker, PhD, Han Peng, PhD

Postdoctoral Fellows

Elwin Dean Clutter II, Ph.D.

Elif Kayaalp Nalbant, Ph.D.

Seyedeh Parisa Foroozandehasl, Ph.D.


Wending Yang, PhD

Richard Longnecker Lab

Nikia Laurie Lab

Research Description

Retinoblastoma, the most common pediatric cancer of the eye, is a devastating and sometimes fatal pediatric cancer. Within the United States, the majority of retinoblastoma patients are diagnosed before their second birthday and many lose their sight due to this disease. Outside of the United States, advanced retinoblastoma is an even greater clinical challenge in developing countries, where the mortality rate among children diagnosed with advanced metastatic retinoblastoma is as high as 80%.

Our laboratory mission is to understand the molecular mechanisms associated with retinoblastoma progression in order to facilitate the identification of novel therapeutic targets. We are accomplishing our mission by studying both genetic and epigenetic changes that occur during retinoblastoma progression in human retinoblastoma tumors and in retinoblastoma model systems. Defining these changes is particularly valuable for the purposes of identifying novel targets for chemotherapeutic interventions.


See Dr. Laurie's publications in PubMed.

Lab Staff

Graduate Students

Vanessa Montoya


Dr. Laurie

Justin B. Starren Lab

Research Description

My current research focuses on new ways to make health care computing more useful. This includes developing intuitive, novel Human Computer Interfaces (HCI) for health care, including working on the design of graphical icons for clinical applications, addressing data overload for clinicians and issues in affective computing. A related line of research is developing methods for the integration of clinic research computing into clinical care.

For more information, visit the faculty profile of Justin Starren, MD/PhD.


View Dr. Starren's publications at PubMed


Email Dr. Starren

Jeremy Lavine Lab

Research Description

My research lab focuses on translational, basic science projects that aim to develop new therapeutics for ocular angiogenesis independent of vascular endothelial growth factor (VEGF). Neovascular age-related macular degeneration (nAMD) is the leading cause of visual impairment in the developed world. Currently, humanized anti-VEGF antibodies are the gold standard for the treatment of nAMD. Patients currently undergo frequent (up to monthly) injections of anti-VEGF antibodies into the vitreous cavity. The average patient achieves 1-2 lines of visual acuity gain, but 15% of patients still lose vision despite maximal anti-VEGF therapy. Although 15% appears small, given the high prevalence of nAMD, this amounts to 2.5 million patients worldwide. For these poorly responsive patients, there is a clear unmet need for alternative, VEGF-independent therapeutic options.

Macrophage recruitment is central in nAMD pathogenesis. Choroidal neovascularization (CNV) is the pathological hallmark of nAMD. In human histopathology studies of excised CNV membranes, macrophages are readily apparent. In mice, nAMD is modeled by laser-induced injury, which causes CNV membrane formation. Laser-induced CNV formation is robustly inhibited by chemical or genetic macrophage depletion. Based upon these accepted dogma, intravitreal steroids were attempted for nAMD treatment and are unfortunately ineffective. I hypothesize that steroids anti-inflammatory properties are too broad and specific anti-macrophage therapies are necessary. Furthermore, macrophages are highly plastic and heterogenous populations, including pro-inflammatory, pro-restorative, pro-fibrotic, and pro-angiogenic subtypes. My lab’s focus is to identify macrophage heterogeneity in CNV, delineate pro-angiogenic macrophage subtypes, and attempt to develop therapies against pro-angiogenic macrophages for nAMD.

For more information, visit the faculty profile for Dr. Lavine.

Selected Publications

  • A. Lavine, Y. Sang, S. Wang, M.S. Ip, N. Sheibani. “Attenuation of choroidal neovascularization by beta(2)-adrenoreceptor antagonism” (2013) JAMA Ophthalmology, 131(3):376-382. (PMID: 23303344)
  • Nourinia, M. Rezaei Kanavi, A. Kaharkaboudi, S.I. Taghavi, S.J. Aldavood, S.R. Darjatmoko, S. Wang, Z. Gurel, J.A. Lavine, S. Safi, H. Ahmadieh, N. Daftarian, N. Sheibani. “Ocular safety of intravitreal propranolol and its efficacy in attenuation of choroidal neovascularization.” (2015) Investigative Ophthalmology and Visual Science, 56: 8228-8235. (PMID: 26720475)
  • A. Lavine, M. Farnoodian, S. Wang, S.R. Darjatmoko, L.S. Wright, D.G. Gamm, M.S. Ip, N. Sheibani. “beta2-Adrenergic receptor antagonism attenuates CNV through inhibition of VEGF and IL-6 expression” (2017) Investigative Ophthalmology and Visual Sciences, 58 (1): 299-308. (PMID: 28114591)
  • M. Hendrick, J. A. Lavine, A. Domalpally, A.D. Kulkarni, M.S. Ip. “Propranolol for proliferative diabetic retinopathy.” (2018) OSLI Retina, 49 (1): 35-40. (PMID: 29304264).
  • A. Lavine, A.D. Singh, A. Sharma, K. Baynes, C.Y. Lowder, S.K. Srivastava. “Ultra-Widefield Multimodal Imaging in Primary Central Nervous System Lymphoma with Ophthalmic Involvement.” (2018) Retina, Epub ahead of print. (PMID 30044267)

Contact Dr. Lavine

Lab Phone: 312-503-0487

Amani Fawzi Lab

Research Description

Fawzi’s research lab is focused on translational approaches to age-related macular degeneration, ischemic retinal diseases and neurodegenerative diseases with a special focus on functional retinal imaging and image-guided interventions.

For more information, visit the faculty profile for Amani A. Fawzi, MD.

Selected Publications

  • Soetikno BT, Beckmann L, Zhang X, Fawzi AA, Zhang HF. Visible-light optical coherence tomography oximetry based on circumpapillary scan and graph-search segmentation. Biomed Opt Express. 2018 Jul 10;9(8):3640-3652.
  • Treister AD, Nesper PL, Fayed AE, Gill MK, Mirza RG, Fawzi AA. Prevalence of subclinical CNV and choriocapillaris nonperfusion in fellow eyes of unilateral exudative AMD on OCT angiography. Transl Vis Sci Technol. 2018 Oct 1;7(5):19.
  • Ashraf M, Nesper PL, Jampol LM, Yu F, Fawzi AA. Statistical model of optical coherence tomography angiography parameters that correlate with severity of diabetic retinopathy. Invest Ophthalmol Vis Sci. 2018 Aug 1;59(10):4292-4298.
  • Lajko M, Cardona HJ, Taylor JM, Farrow KN, Fawzi AA. Photoreceptor oxidative stress in hyperoxia-induced proliferative retinopathy accelerates rd8 degeneration. PLoS One. 2017 Jul 3;12(7):e0180384.
  • Lajko M, Cardona HJ, Taylor JM, Shah RS, Farrow KN, Fawzi AA. Hyperoxia-induced proliferative retinopathy: Early interruption of retinal vascular development with severe and irreversible neovascular disruption. PLoS One, 2016, 11(11): e0166886.

Lab Staff

  • Suzie Lee
  • Tom Tedeschi

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