Faculty Profile

Dr. Wei Liu, Ph.D.

Wei Liu, Ph.D.

Assistant Professor, Department of Ophthalmology & Visual Sciences

Assistant Professor, Department of Genetics

Areas of Research: To model human retinal development and disease using human pluripotent stem cells and mice via molecular, cellular, and genetic approaches. CRISPR/Cas9-mediated gene editing, microscopy, and genome-wide studies are performed.

Professional Interests

Retinal Development, Stem Cell-based Modeling and Retinal Repair

  • Molecular mechanisms of retinal development
  • Mouse genetics
  • Stem cell-based modeling of retinal development in normal and diseased conditions; retinal repair

The retina is a light-sensitive layer of tissue at the back of the eye.  In retina, rod and cone photoreceptors are the cells that detect light and convert it to an electrical signal. This signal is relayed to bipolar cells and then to ganglion cells whose axons transmit this signal to the brain. In this signal processing, horizontal cells and amacrine cells play essential roles. The photoreceptors are metabolically active and are nourished by a layer of support cells – the retinal pigment epithelium (RPE). The retina is fed by both retinal and the choroidal vasculature, which is within and underneath the retina, respectively.

Photoreceptors are vulnerable to progressive dysfunction and death (photoreceptor degeneration) due to inherited and acquired conditions. For example, in the “dry” form age-related macular degeneration (AMD), which is highly prevalent in the elderly and makes up to nearly 90 percent of patients of AMD, RPE and photoreceptors in the macular region growingly become degenerated. Since photoreceptors have no intrinsic capability to regenerate, this cell loss will lead to permanent impairment and loss of central, high-acuity vision, causing substantial burden for affected persons and society.

Stem cell-based retinal repair represents as an emerging strategy in the treatment of the so far incurable photoreceptor degeneration, the convergent end point in variety of retinal diseases. As evidence for its significance, National Eye Institute has initiated an Audacious Goal: “to regenerate the neurons and neural connections in the eye and visual system”…“ to save and restore their vision”. One of the challenges in this initiative is the efficient generation of healthy and safe donor cells from pluripotent stem cells for cell transplant. Related to this stem cell-based treatment, patient-derived induced pluripotent cells provide an unprecedented tool for disease-modeling and drug discovery.

Molecular dissection of retinal development in model systems provides a foundation for stem cell-based retinal repair. In my lab, we utilize genetic engineered mouse models to investigate the molecular mechanisms of retinal development. We also employ human embryonic stem cells to model retinal development and to generate donor cells for retinal repair.

Current projects in my lab:

1) To elucidate the regulatory pathways that control the proliferation and differentiation of retinal progenitor cells

2) To determine the molecular mechanisms that control photoreceptor cell differentiation

3) To model retinal development with human embryonic stem cells for the purpose of retinal repair

The outcomes of our studies are expected to unravel the regulatory pathways for retinal cell differentiation and contribute to stem cell-based retinal repair in the endeavor of saving and restoring vision.          


NIH-funded positions are available for highly self-motivated postdoctoral research fellow/graduate student.

Selected Publications

  1. Liu W, Cvekl A (2017) Six3 in a small population of progenitors at E8.5 is required for neuroretinal specification via regulating cell signaling and survival in mice. Developmental Biology. http://dx.doi.org/10.1016/j.ydbio.2017.05.026.        Corresponding author. 
  2. Albert Lowe, Raven Harris, Punita Bhansali, Ales Cvekl, Wei Liu. Intercellular adhesion-dependent cell survival and ROCK-regulated actomyosin-driven forces mediate self-formation of a retinal organoid. Stem Cell Reports (2016), http://dx.doi.org/0.1016/j.stemcr.2016.03.011.
  3. Liu W, LagutinO, SwindellE, JamrichM and OliverG. Neuroretina specification in mouse embryos requires Six3-mediated suppression of Wnt8b in the anterior neural plate. J of Clin Invest,120: 3568-77, 2010.
  4. Liu W. Focus on Molecules: Wnt8b: A suppressor of early eye and retinal progenitor formation. Exp Eye Res 2011 Jan 8. [Epub ahead of print].
  5. Liu W, Lagutin OV, Mende M, Streit A and Oliver G. Six3 activation of Pax6 expression is essential for mammalian lens induction and specification. EMBO J 25: 5383-5395, 2006.
  6. Geng X, Speirs C, Lagutin O, Inbal A, Liu W, Solnica-Krezel L, Jeong Y, Epstein DJ, Oliver G. Haploinsufficiency of Six3 fails to activate Sonic hedgehog expression in the ventral forebrain and causes holoprosencephaly. Dev Cell15: 236-247, 2008.
  7. Geng X, Lavado A, Lagutin OV, Liu W, Oliver, G. Expression of Six3 Opposite Strand (Six3OS) during mouse embryonic development. Gene Expression Patterns7: 252-257, 2006.

Research Images

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Albert Einstein College of Medicine
Jack and Pearl Resnick Campus
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Research Information