Stefanie Wohl

Dr. Stefanie Wohl
SUNY College of Optometry
33 West 42nd Street
New York, NY 10036
Lab Website

The Role of microRNAs in Retinal Glia FunctionMy laboratory studies the neural retina at the cellular and molecular level. The cells we are interested in and focus on are called glia cells, more precisely Müller glia. Müller glia are the predominant glia in the neural retina and named after Professor Heinrich Müller (described in 1851). Glia cells per se are known as the support cells in the central nervous system but have a variety of other functions including maintaining the homeostasis of the tissue but also protection after injury or disease.

In mammals, including humans, the central nervous system i.e., the brain (including the retina) and the spinal cord, does not regenerate after injury or disease. We know that glia, as part of their protective function, undergo morphological changes to create a barrier and a non-permissive environment for regeneration. This glial response, called gliosis, is a very complex process and includes a variety of factors and mechanisms which are not fully understood.

Molecules known to play in role in Müller glia development and function are microRNAs. microRNAs are small molecules present in every cell of the body that act as translational repressors. That means mRNA (transcribed from DNA) is not translated into protein. About 1000 different microRNAs have been identified so far and it is known that they have a huge impact in development, independent from tissue origin and cell type. However, their expression pattern can vary between different cell types, developmental stages (maturation of a cell) as well as physiological and pathophysiological conditions. For the latter, there is increasing evidence that microRNAs play an important role in various diseases and can be used as a biomarker for certain diseases.

In my laboratory, we investigate the role of microRNAs in the glial response to injury/disease. The focus lies on Müller glia but will also include other glia types such as astrocytes and microglia. Specific approaches are

  1. Transgenic models to visualize and isolate the different kind of glia
  2. Cell and tissue culture to study cellular and molecular changes in glia
  3. microRNA profiling and RNA analyses
  4. Techniques to overexpress or inhibit microRNAs and alter protein expression

Investigating the impact of microRNAs in the different phases of glial activation after injury and/or disease will give us a better understanding of the underlying mechanisms of gliosis in order to develop strategies to minimize the inhibitory nature of this process. The long-term goal is to develop new approaches and therapies to attenuate the glial response after damage which might allow regeneration of the central nervous system including the neural retina.

  • Friedrich Schiller University of Jena, Germany, BS, 2001, Biology
  • Friedrich Schiller University of Jena, Germany, MS, 2005, Biology, Major: Zoology, Minors: Neurobiology, Genetics
  • Friedrich Schiller University of Jena, Germany, PhD, 2011, Biology (Neurobiology/ Ophthalmology)
  • University of Washington, Department of Biological Structure, Seattle, WA, Postdoc, 2012-2017, Neuroscience/ Ophthalmology/ Molecular Biology

  • 2004-2005, Student Research Assistant (undergraduate), Clinic of Neurology, Jena University Hospital, Jena, Germany
  • 2005-2006, Research Associate (Ph.D. student/ biologist), Friedrich Schiller University of Jena (FSU), Jena University Hospital, Clinic of Neurology, Jena, Germany
  • 2007-2009, Research Associate (Ph.D. student/ biologist), Hans-Berger Department of Neurology, Jena, University Hospital, Jena, Germany
  • 2009-2011, Research Associate (Ph.D. student/ biologist), Private University of Witten/Herdecke, Witten, Germany; Department of Neurology and guest student the Hans Berger Department of Neurology, Jena University Hospital, Jena, Germany
  • 2012-2017, Postdoctoral Research Scientist, Department of Biological Structure, University of Washington, Seattle, WA
  • 2017-2018, Acting Instructor, Department of Biological Structure, University of Washington, Seattle, WA
  • Since Sep. 2018, Assistant Professor, Department of Biological and Vision Sciences, State University of New York, College of Optometry, New York, NY

  • 2011: “summa cum laude” doctoral degree
  • 2012: Novartis Travel Award to attend ISER meeting
  • 2014-2016: Scholarship from the German Research Foundation (Deutsche Forschungsgemeinschaft – DFG, Wo2010/1-1), postdoctoral training)
  • 2018: The New York State Empire Innovator Grant

  • 2018-2021: The New York State Empire Innovator Grant

  • Schultz, R., Krug, M., Precht, M., Wohl, S. G., Witte, O.W., Schmeer, C., 2018: Frataxin overexpression in Müller cells protects retinal ganglion cells in a mouse model of ischemia/reperfusion injury in vivo. Scientific Reports 8, doi:10.1038/s41598-018-22887-5.
  • Wohl, S. G., Jorstad, N. L., Levine, E., and Reh, T.A., 2017: Müller glial microRNAs are required for the maintenance of glial homeostasis and retinal architecture. Nature Communications, 8(1):1603. DOI: 10.1038/s41467-017-01624-y.
  • Jorstad, N. L., Wilken, M. S., Grimes, W. N., Wohl, S. G., VandenBosch L., Yoshimatsu T., Wong R. O., Rieke F., and Reh, T.A., 2017: Stimulation of functional neuronal regeneration from Müller glia in adult mice. Nature 548, 103-107, DOI: 10.1038/nature23283.
  • Wohl, S. G. and Reh, T.A., 2016. The microRNAs expression profile of mouse Müller glia in vivo and in vitro. Scientific Reports 6, 35423; doi 10.1038/srep35423.
  • Wohl, S. G. and Reh, T.A., 2016. miR-124-9-9* potentiates Ascl1-induced reprogramming of cultured Müller glia. Glia 64, 743-762.
  • Wohl, S. G., Schmeer, C. W., and Isenmann, S., 2012. Neurogenic potential of stem/progenitor-like cells in the adult mammalian eye. Progress in Retinal and Eye Research 31, 213-242.
  • Schmeer, C. W., Wohl, S. G., and Isenmann, S., 2012. Cell-replacement therapy and neural repair in the retina. Cell and Tissue Research 349, 363-374.
  • Wohl, S. G., Schmeer, C. W., Friese, T., Witte, O. W., and Isenmann, S., 2011. In situ dividing and phagocytosing retinal microglia express Nestin, Vimentin, and NG2 in vivo. PLoSOne 6, e22408.
  • Wohl, S. G., Schmeer, C. W., Witte, O. W., and Isenmann, S., 2010. Proliferative response of microglia and macrophages in the adult mouse eye after optic nerve lesion. Investigative Ophthalmology & Visual Science 51, 2686-2696.
  • Wohl, S. G., Schmeer, C. W., Kretz, A., Witte, O. W., and Isenmann, S., 2009. Optic nerve lesion increases cell proliferation and Nestin expression in the adult mouse eye in vivo. Experimental Neurology 219, 175-186.