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Professor of Weinberg College of Arts and Sciences and Pathology
Professor of Physiology
Professor of Ophthalmology and Pathology
Owen L. Coon Professor of Molecular Biosciences
Associate Professor of Psychology
Associate Professor of Ophthalmology
Research Professor, Chemistry of Life Process Institute, Research Assistant Professor, Chemistry
Professor of Biomedical Engineering, Professor of Ophthalmology, Feinberg School of Medicine
Professor of Engineering Sciences and Applied Mathematics and (by courtesy) Neurobiology
Professor of Ophthalmology
Assistant Professor of Ophthalmology and Medicine (Rheumatology)
Professor of Biomedical Engineering, Professor of Neurobiology, Professor of Ophthalmology, Director of Northwestern Center for Engineering Education Research
Professor of Pediatrics (Advanced General Pediatrics and Primary Care)
Professor Emeritus of Medicine (Endocrinology)
Professor of Medicine (Nephrology and Hypertension)
Assistant Professor of Neurobiology
Associate Professor of Ophthalmology, Physiology and Weinberg College of Arts and Sciences
Professor of Neurobiology
Professor of Psychology
Professor of Ophthalmology
Professor of Biomedical Engineering, Professor of Ophthalmology, Feinberg School of Medicine
Yongling Zhu Lab
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.
- 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
- Sercan Deniz: Postdoc fellow
- Andrew Jo: Graduate student
Vijay P. Sarthy Lab
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
Phone 312- 503-3031
Tsutomu Kume Lab
Cardiovascular development is at the center of all the work that goes on in the Kume lab. The cardiovascular system is the first functional unit to form during embryonic development and is essential for the growth and nurturing of other developing organs. Failure to form the cardiovascular system often leads to embryonic lethality and inherited disorders of the cardiovascular system are quite common in humans. The causes and underlying developmental mechanisms of these disorders, however, are poorly understood. A particular emphasis in our laboratory has recently been the study of cardiovascular signaling pathways and transcriptional regulation in physiological and pathological settings using mice as animal models, as well as embryonic stem (ES) cells as an in vitro differentiation system. The ultimate goal of our research is to provide new insights into the mechanisms that lead to the development of therapeutic strategies designed to treat clinically relevant conditions of pathological neovascularization.
View Dr. Kume's publications on PubMed.
For more information, visit the faculty profile for Tsutomu Kume, PhD.
Contact Dr. Kume at 312-503-0623 or the Kume Lab at 312-503-3008.
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.
Steven DeVries Lab
Parallel processing is one of the key strategies used by the visual system. In the mammalian retina, the responses of the cone photoreceptor inputs are temporally uniform when stimulated with equivalent lights. However, the retinal ganglion cell outputs can be grouped into 30 to 35 different classes based on the temporal properties of their light responses, morphology and central targets. Our goal is to characterize the processing in the parallel retinal networks that leads to these different responses. We study retinal processing by using a very basic approach: We isolate the excitatory “skeleton” of the retina — the cones, bipolar cells and ganglion cells — and systematically determine how signals are modified at each synapse by recording from pairs of pre- and post-synaptic neurons in a retinal slices and whole mounts. In the outer retina, we record from cone and bipolar cell pairs; whereas, in the inner retina, our goal is to optogenetically stimulate bipolar cells and record from identified postsynaptic ganglion cells. In collaboration with the Zhu lab, we identify and functionally probe the connects between bipolar and ganglion cells by using a retrograde rabies virus tracer that is introduced into ganglion cells at their axon terminals.
For more information, visit the faculty profile for Steven H. DeVries, MD, PhD.
- Saszik, S. & DeVries, S. H. (2012). A mammalian retinal bipolar cell uses both graded changes in membrane potential and all-or-nothing Na+ spikes to encode light. Journal of Neuroscience. 32, 297-307.
- Sher, A. & DeVries, S.H. (2012). A non-canonical pathway for mammalian blue-green color vision. Nature Neuroscience 15, 952-953.
- Lindstrom, S.H., Ryan, D.G., Shi, J. & DeVries, S.H. (2014). Kainate receptor subunit diversity underlying response diversity in retinal Off bipolar cells. Journal of Physiology, 592, 1457-1477.
- Zhu, Y., Xu, J., Hauswirth, W.W., & DeVries, S.H. (2014). Genetically targeted binary labeling of retinal neurons. Journal of Neuroscience 34, 7845-7861.
- Grabner, C.P., Ratliff, C.P., Light, A.C. & DeVries, S.H. (2016). Mechanism of high frequency signaling at a depressing ribbon synapse. Neuron 91, 133-145.
- Jun Shi
- Eric Schwartz
- Sercan Deniz
Robert Lavker Lab
The Lavker laboratory focuses on the biology of epithelial stem cells and the roles of microRNAs (miRNAs) in regulating epithelial homeostasis. In collaboration with Tung-Tien Sun (NYU Medical School), the lab identified and characterized stem cells of the epidermis, hair follicle and corneal epithelium. We have demonstrated that the hair follicle stem cells (located in the bulge region of the follicle) are pluripotent; capable of forming the hair shaft as well as the epidermis. Collectively, these studies have been of major importance for their implications regarding tissue regeneration, hair follicle growth, and carcinogenesis.
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.
Recently, the lab has 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.
We have also demonstrated that miR-31 targets FIH-1 to positively regulate corneal epithelial glycogen metabolism, which results in the accumulation of glycogen. Increased glucose in the form of glycogen may be a mechanism by which the corneal epithelium is able to withstand periods of hypoxia during eyelid closure or extended contact lens wear. Thus miR-31 may function as a novel means if protecting the corneal epithelium from hypoxic stress.
Most recently, the laboratory has defined the microRNA expression patterns of the stem cell-enriched limbal basal cells and has begun to identify targets that are unique to the limbal epithelium. This should lead to an understanding of how miRNAs regulate epithelial stem cells.
For publication information and more, see the Lab faculty’s profiles:
Contact Lavker Lab
Contact the Lavker 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.
Richard Longnecker Lab
Research in the Longnecker laboratory focuses on herpes simplex virus (HSV) and Epstein-Barr virus (EBV). These viruses typically cause self-limiting disease within the human population but both can be associated with serious complications. EBV is associated with variety of hematopoietic cancers such as African Burkitt lymphoma, Hodgkin Lymphoma and adult T-cell leukemia. EBV-associated lymphoproliferative disease occurs in individuals with congenital or acquired cellular immune deficiencies. The two notable epithelial diseases associated with EBV infection are nasopharyngeal cancer and oral hairy leukoplakia. Similar to EBV, HSV latent infections are very common in humans. HSV typically does not cause severe disease but is associated with localized mucocutaneous lesions, but in some cases can cause meningitis and encephalitis. The Longnecker laboratory focuses on several aspects of EBV and HSV replication and pathogenesis. First, the molecular basis EBV transformation and how it relates to cancer is being investigated. The laboratory is currently screening selective inhibitors that may be beneficial in EBV-associated cancers such as Hodgkin lymphoma, Burkitt lymphoma and proliferative disorders that occur in HIV/AIDS and transplant patients. Second, the laboratory is investigating herpesvirus latency in the human host and pathogenesis associated with infections in humans. In this regard, the laboratory is developing animal models for EBV and HSV infections. Finally, the laboratory is investigating the function of herpesvirus encoded proteins and the cellular receptors that are important for infection both using in vivo culture models as well as animal models. Ultimately, studies by the Longnecker laboratory may provide insight for the development of novel therapeutics for the treatment of herpesvirus infections in humans and better understanding of the herpesvirus life cycle in the human host
For lab information and more, see Dr. Longnecker's faculty profile
See Dr. Longnecker's publications on PubMed.
Contact Dr. Longnecker at 312-503-0467 or the lab at 312-503-0468 or 312-503-9783.
Nikia Laurie Lab
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.
Justin B. Starren Lab
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.
View Dr. Starren's publications at PubMed
Jeremy Lavine Lab
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.
- 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
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.
- 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.
- Suzie Lee
- Tom Tedeschi