PIPages
Labs

James Hurley

University of Washington, WA·Biochemistry

Photoreceptors, the light-sensing cells of the retina, burn glucose remarkably fast, drawing about half of their energy from aerobic glycolysis, a quick but inefficient way of breaking down sugar. All of that glucose must first cross the retinal pigment epithelium (RPE), the cell layer that sits between the outer retina and the blood supply.

Fields

Biochemistry

Physiology

Medicine & Clinical Research

Topics

retina

photoreceptors

aerobic glycolysis

Grants
3 known grants, through Aug 2029

What they work on

  1. Determine how daily cycles shape glycogen metabolism, the stored-sugar reserve, in RPE/choroid tissue, using ex vivo and in vivo measurements of metabolic flux and energy stores.
  2. Identify diurnal influences on fatty acid metabolism in the retinal pigment epithelium and how stored fat contributes to outer retina homeostasis.
  3. Test how mutations that cause photoreceptor degeneration, or that disrupt the RPE's engulfment of shed photoreceptor material, change stored glycogen and fat.
  4. Identify the biochemical changes that make glycolytic intermediates upstream of pyruvate kinase accumulate in degenerated retinas.
  5. Measure metabolic flux in living mice infused with carbon-13 labeled fuels through a jugular vein catheter, to test whether retina and RPE/choroid trade fuels in the intact eye as explant studies suggest.
  6. Analyze how disrupting specific metabolic enzymes in the RPE, using knockout mice, alters metabolic interactions with the retina.
  7. Complete metabolic analysis of mouse models engineered to slow photoreceptor degeneration by enhancing glycolysis in rod photoreceptors while suppressing it in the RPE.
  8. Operate a shared molecular and cellular biology core providing vision scientists with Sanger sequencing, quantitative real-time PCR, ultracentrifugation, spectrophotometry and cell culture facilities, plus technical training.

More about the research

Work in this lab treats retina and RPE as a shared metabolic ecosystem and asks how breakdowns in that partnership, from genetics, environment or aging, lead to vision loss.

Why it matters

Deficiencies in how the retinal pigment epithelium transports and recycles fuel contribute to vision loss from inherited retinal degenerations, environmental insults and aging. Mapping how retina and RPE share glucose and stored fuels, and how daily cycles affect them, could point toward metabolism-based strategies that make photoreceptors more resilient to stress and may apply across several forms of retinal degeneration.

Known grants

From NIH and NSF research grants. Labs often have other funding we can't see.

Determinants of Rod and Cone Response Characteristics

NIH · Jul 1986 – Aug 2029

Control of Photoreceptor Metabolism

NIH · Sep 2007 – Nov 2028

Molecular and Cellular Biology Module

NIH · Jun 1997 – Aug 2026

Closest labs

Jianhai Du

West Virginia University, WV·Biochemistry

Trace how retinal pigment epithelium cells use the amino acid proline as fuel alongside glucose, using tracer methods and mass spectrometry.

Tylor Lewis

University of Alabama at Birmingham, AL·Neuroscience·Early-career

Comprehensively characterize retinal degeneration in global ADAM9 knockout mice, focusing on the interface between photoreceptor outer segments and the retinal pigment epithelium.

Nancy Philp

Thomas Jefferson University, PA·Neuroscience

Test whether the retinal pigment epithelium keeps some glucose for its own biosynthetic and phagocytic activities, using RPE-iΔGlut1 mice that lack the glucose transporter GLUT1 in the RPE.

The school

University of Washington: 81 labs on PI Pages, $1.7B a year on research, 694 research doctorates a year.

More about University of Washington

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