GLIA Reasearch Laboratory

Debasish Sinha, Ph.D.
Jennifer Salvitti Davis, M.D. Chair in Ophthalmology Research
Professor of Ophthalmology, Cell Biology and Developmental Biology
University of Pittsburgh School of Medicine
Adjunct Faculty, Ophthalmology, The Johns Hopkins University School of Medicine

Laboratory Personnel

Christopher Fitting, Research Technician

Stacey Hose, BA Laboratory Manager

Peng Shang, PhD, Postdoctoral Associate

Meysam Yazdankhah, PhD, Postdoctoral Associate

Nadezda Stepicheva, PhD, Postdoctoral Scholar

Sayan Ghosh, PhD, Postdoctoral Associate

Haitao Liu, PhD, Postdoctoral Associate

Research Interests

Our laboratory is interested in understanding the role of glia and glia-like cells (retinal pigmented epithelium) in ocular health and disease.  We use genetically engineered mouse and spontaneous mutant rat models as tools to decipher functions of these cells in health and disease.  The diseases we focus on are (1) Persistent Fetal Vasculature (PFV) and (2) Age-related Macular Degeneration (AMD).


Selected Publications

Original articles

  1.  Zigler JS Jr.  et al. Mutation in the bA3/A1-crystallin gene impairs phagosome degradation in the retinal pigmented epithelium of the rat.   (2011), Journal of Cell Science. 124: 523-531.
  2. Valapala M et al. Impaired endolysosomal function disrupts Notch signaling in optic nerve astrocytes. Nature Communications. (2013), 4:1629. doi: 10.1038/ ncomms2624.
  3. Valapala M et al. Lysosomal-mediated waste clearance in retinal pigmented epithelial cells is regulated by CRYBA1/bA3/A1-crystallin via V-ATPase-MTORC1 signaling.  Autophagy.  (2014), 10 (3): 480-496.
  4. Valapala M et al.  Increased Lipocalin-2 in the retinal pigment epithelium of Cryba1 cKO mice is associated with a chronic inflammatory response. Aging Cell. (2014), 13(6): 1091-4.
  5. Valapala M et al.  bA3/A1-crystallin is a critical mediator of STAT3 signaling in optic nerve astrocytes.  2015, Scientific Reports. 5:8755. doi: 10.1038/srep08755.
  6. Shang P et al. The amino acid transporter SLC36A4 regulates the amino acid pool in retinal pigmented epithelial cells and mediates the mechanistic target of rapamycin, complex 1 signaling. Aging Cell.(2017), 16 (2): 349-359.
  7. Ghosh S et al. Activating AKT2/NFkB/LCN-2 axis elicits inflammatory response in age-related macular degeneration. The Journal of Pathology. (2017), 241(5): 583-588.
  8. Wang J et al. ATAC-Seq analysis reveals a widespread decrease of chromatin accessibility in age-related macular degeneration. Nature Communications.  (2018), 9(1):1364. doi: 10.1038/s41467-018-03856-y.
  9. Yazdankhah M et al. Modulating EGFR/MTORC1/Autophagy as a potential therapy for Persistent Fetal Vasculature (PFV) disease.  (2019), Autophagy, In Press.
  10.  Ghosh S et al.  Neutrophils homing into the retina trigger pathology in early age-related macular degeneration.  (2019), Communications Biology, In Press.


Invited Review articles 

  1. Whitcup SM et al. The role of the immune response in age-related macular degeneration.   International Journal of Inflammation, (2013); 2013, 348092.
  2. Zigler, Jr. JS et al. bA3/A1-crystallin: more than a lens protein.  Progress in Retinal and Eye Research. (2015) 44C: 62-85.
  3. Zigler, Jr. JS et al.  bA3/A1-crystallin and persistent fetal vasculature (PFV)   disease of the eye.   BBA-General Subjects. (2016) 1860 (Pt. B): 287-298.
  4. Sinha D et al. Lysosomes: regulators of autophagy in the retinal pigmented epithelium.  Experimental Eye Research. (2016) 144: 46-53.
  5. Ferrington D et al. Potential defects in RPE in proteolysis and AMD pathology.  Progress in Retinal and Eye Research. (2016); 51: 69-89.


Contact Information

Debasish Sinha, PhD
Children’s Hospital of Pittsburgh of UPMC
One Children’s Hospital Drive
4401 Penn Avenue
John G. Rangos Sr. Research Center of University of Pittsburgh School of Medicine
3rd Floor, Bays 5 & 6
Pittsburgh, PA 15224
C: (410)-707-8621