Moran Eye Center

The Ambati Laboratory

Ocular Angiogenesis and Corneal Research

Photo of Bala Ambati, M.D.

Dr. Bala Ambati devotes a significant portion of his time to research endeavors investigating the molecular mechanisms of angiogenesis, the growth of new blood vessels, in the cornea. His laboratory group has solved the long-outstanding mystery of what keeps the cornea normally free of blood vessels, identifying the protein sVEGFR-1 as the prime mediator of this essential requirement for clear vision. His team has applied this knowledge in developing novel inhibitors targeting the key mediator of angiogenesis, VEGF, specifically sequestering this linchpin molecule within cells, complementing the existing anti-VEGF arsenal.

Dr. Ambati hopes to build collaborative research programmes within Moran and on-campus with a view towards continued development of anti-angiogenic agents, understanding the mechanisms of alternative splicing controlling sVEGFR-1, and advancing drug delivery to the eye. With respect to clinical research, Dr. Ambati is committed to constant analysis of results of cornea transplants, LASIK, cataract extraction, and other anterior segment procedures with a view towards optimization of patient outcomes.

Research Bio:

As a physician-investigator, Dr. Ambati is experienced in cornea transplants, cataract extraction, keratoprosthesis (artificial cornea), LASIK, and other complex procedures of the cornea and anterior segment of the eye. Dr. Ambati devotes a significant portion of his time to research endeavors investigating the molecular mechanisms of angiogenesis, the growth of new blood vessels, in the cornea. Photo of Bala Ambati, M.D. His laboratory group has solved the long-outstanding mystery of what keeps the cornea normally free of blood vessels, identifying the protein sVEGFR-1 as the prime mediator of this essential requirement for clear vision. His team has applied this knowledge in developing novel inhibitors targeting the key mediator of angiogenesis, VEGF, specifically sequestering this linchpin molecule within cells, complementing the existing anti-VEGF arsenal. Dr. Ambati hopes to build collaborative research programmes within Moran and on-campus with a view towards continued development of anti-angiogenic agents, understanding the mechanisms of alternative splicing controlling sVEGFR-1, and advancing drug delivery to the eye. Dr. Ambati's laboratory published a key paper in Nature in 2006 defining the basis of the cornea's natural avascularity, which was selected as a 2006 Signaling Breakthrough of the Year by Science. With respect to clinical research, Dr. Ambati is committed to constant analysis of results of cornea transplants, LASIK, cataract extraction, and other anterior segment procedures with a view towards optimization of patient outcomes.

Funding Sources: National Eye Institute; Veterans Administration MERIT

Education:
B.A., Biology - 1991, New York University
Doctor of Medicine - 1995, Mount Sinai School of Medicine
Internal Medicine Residency - 1997, Beth Israel Medical School
Ophthalmology Residency - 2001, Massachusetts Eye & Ear Infirmary
PhD - Cell Biology, Medical College of Georgia, 2008 Fellowships:
Cornea & Refractive Surgery - 2002, Duke University

Certifications:
American Board of Internal Medicine
American Board of Ophthalmology - 2003

Academic Appointments:
Associate Professor of Ophthalmology and Visual Sciences & Director of Corneal Research - University of Utah School of Medicine

A sample of major publications from the Ambati Laboratory:

  1. Ambati BK, Nozaki M, Singh N, Sakurai E, Jani P, et al. (2006) Corneal avascularity is due to soluble VEGFR-1. Nature. 443: 993-7
  2. Hammond S, Puri A, Ambati BK (2004) Quality of vision after LASIK. Curr Opin Ophth. 15: 328-32
  3. Jani P, Singh N, Jenkins C, Yun M, Raghava S, Kompella U, Ambati BK (2007) Nanoparticles sustain extended-release of Flt intraceptors in the cornea and can inhibit injury-induced corneal angiogenesis. Invest Ophthal Vis Sci. 48: 2030-6
  4. Singh, N, Jani P, Suthar T, Amin S, Ambati BK. (2006) Flt-1 intraceptors induces the unfolded protein response, apoptotic factors, and regression of murine injury-induced corneal neovascularization. Inv Ophth Vis Sci. 47: 4787-93.
  5. Singh N, Amin S, Richter E, Jani P, Dong Z, Wang J, Kaur R, Ambati BK (2005) Flt intraceptors inhibit hypoxia-induced VEGF secretion and injury-induced corneal neovascularization. Inv Ophth Vis Sci. 2005; 46: 1647-52
  6. Ambati BK, Higgins E, Hu G, Gupta N, et al. (2005). Outcomes of LASIK complications requiring surgical intervention. Ophthalmology; 112: 2052-3
  7. Chandrasekaran V, Ambati J, Ambati BK, Taylor WE (2007) Molecular docking and analysis of interactions between VEGF and SPARC. J Mol Graph Model. 26: 775-82
  8. Singh N, Higgins E, Suthar T, Jani P, Ambati BK. (2007) A unique homologous siRNA targeting VEGF inhibits and regresses injury-induced corneal neovascularization. Cornea. 26(1):65-72
  9. Singh N, Macnamara E, Rashid S, Kontos CD, Ambati BK (2005) Systemic soluble Tie2 expression inhibits and regresses corneal neovascularization. Biochem Biophys Res Commun. 2005; 332:194-9.

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