Download ARVO 2015 Annual Meeting Abstracts 463 The Choroid: Connecting

ARVO 2015 Annual Meeting Abstracts
463 The Choroid: Connecting vision to the lifeblood Minisymposium
Wednesday, May 06, 2015 3:45 PM–5:30 PM
2B/3B Mile High Blrm Minisymposium
Program #/Board # Range: 4814–4819
Organizing Section: Retinal Cell Biology
Program Number: 4814
Presentation Time: 3:45 PM–4:02 PM
Overview of the choroid in health, aging and disease
Gerard A. Lutty. Johns Hopkins Univ School of Medicine, Baltimore,
MD.
Presentation Description: The human choroid has a unique lobular
capillary system, the choriocapillaris (CC), which lies immediately
posterior to Bruchs membrane and RPE, providing oxygen and
nutrients to RPE and photoreceptors. The CC is fenestrated,
predominantly but not completely on the retinal side. Posterior to
CC are intermediate blood vessels in Sattler’s layer and then large
choroidal vessels in Haller’s layer near lamina fuscha, the border
of choroid and sclera. Choroid is a highly pigmented tissue with
melanocytes interspersed throughout the stroma with ganglion cells
and the inflammatory cells of choroid, mast cells and macrophages.
We have assessed the viability of choroidal vessels using enzyme
histochemistry to stain for endogenous alkaline phosphatase activity,
a marker for the choroidal vasculature (McLeod et al, IOVS, 1994).
Although transport from the CC is tightly regulated by fenestrations
and caveolae, we have observed an accumulation of serum proteins
(ex: CRP and albumin) in choroid during aging and disease states.
The human choroid is severely affected by age-related macular
degeneration (AMD). Blood flow is reduced in the submacular
choroid and Haller’s layer vessels often have atherosclerotic changes.
The CC atrophies in both wet and dry AMD. In wet AMD, the loss
occurs before loss of RPE, perhaps resulting in RPE hypoxia and
upregulation of hypoxia-inducible growth factors like VEGF. In
dry AMD, the loss of CC is secondary to loss of RPE (McLeod
et al, IOVS, 2009). In addition, the entire choroid thins in AMD.
The choroid is also affected by diabetes, a process called diabetic
choroidopathy. CC occlusion and death are evident and often
accompanied by intraluminal polymorphonuclear leukocytes. There
are deposits on Bruchs membrane similar to basal laminar deposits
observed in early AMD. We have also documented intrachoroidal
neovascularization as well as CNV in and on Bruchs membrane;
this occurs beyond the equator in most subjects. In conclusion,
the choroid and its vasculature is vital for the survival of RPE and
photoreceptors. It is dysfunctional in AMD and diabetes.
Commercial Relationships: Gerard A. Lutty, None
Support: NIH-NEI RO1-016151 (GL), NIH-NEI P21-EY01765
(Wilmer
Program Number: 4815
Presentation Time: 4:02 PM–4:19 PM
Assessing blood flow in the choroid in health, aging and disease
Jeffrey Kiel. Ophthalmology, UT Health Science Center at San
Antonio, San Antonio, TX.
Presentation Description: Although the choroid is tantalizingly
close to the surface of the eye, measurement of choroidal blood flow
is extremely difficult. Conspiring against simple approaches are
the inaccessible locations of the multiple arterial inputs and venous
outputs within the bony orbit, the light scattering and absorbing
properties of the enveloping retinal pigment epithelium and sclera,
and the need to preserve the normal IOP and not damage the ocular
parenchyma. This talk will provide a brief description of some of
the more common choroidal blood flow measuring techniques, their
strengths and weaknesses, and where the technology appears to be
heading.
Commercial Relationships: Jeffrey Kiel, None
Support: NIH EY09702, van Heuven Endowment
Program Number: 4816
Presentation Time: 4:19 PM–4:36 PM
Myeloid cells in the normal aging choroid and their potential role
in homeostasis and disease
Paul G. McMenamin. Monash University, Victoria, Australia,
Melbourne, VIC, Australia.
Presentation Description: The choroid of the normal human eye,
and of the laboratory mammals that have been studied, is extremely
richly endowed with populations of cells which are of myeloid
origin. These appear to consist of a mixture of conventional tissue
macrophages and Dendritic cells. Whilst much is known from
laboratory animal studies of the origin, turnover, phenotype and
function of their close neigbours, the retinal microglia, the myeloid
cells of the choroid have been less intensively studied despite the
pathological processes at the retinal-choroidal interface being
the potential site of changes that lead to both dry and wet AMD.
The anatomical differences between the eye of a nocturnal rodent
and a diurnal primate (man) with a macula combined with the
heavily pigmented nature of choroid tissue has hampered research
in this area as has the difficulty in obtaining normal and diseased
human tissue. Following a review of the background knowledge of
macrophages and Dendritic cells in animal studies new data on the
immunophenotypic characterisation of myeloid cells in the aging and
diseased human choroid will be discussed.
Commercial Relationships: Paul G. McMenamin, None
Support: NH&MRC, Rebecca Cooper Foundation, Ophthalmic
Research Institute of Australia
Program Number: 4817
Presentation Time: 4:36 PM–4:53 PM
Molecular changes in the choroid in aging and AMD
Robert F. Mullins. 1Ophthalmology and Visual Sciences, University
of Iowa, Iowa City, IA; 2Stephen A. Wynn Institute for Vision
Research, Iowa City, IA.
Presentation Description: In this presentation we will review the
molecular and biochemical events that occur in the aging choroid,
including gene expression changes and choriocapillaris endothelial
cell dedifferentiation. We will especially focus on the complement
membrane attack complex (MAC) at the level of the choriocapillaris
in aging and AMD, and what is known about impact of MAC injury
to choroidal endothelial cells. Changes in normal aging, such as loss
of CD34 expression, will be contrasted to changes in early AMD,
such as increased MAC, vascular dropout, and increased abundance
of “ghost” vessels. Finally, we will discuss the translational
implications of these studies.
Commercial Relationships: Robert F. Mullins, None
Support: NIH Grant EY024605, Research to Prevent Blindness, the
Elmer and Sylvia Sramek Charitable Foundation, and the Martin and
Ruth Carver Chair in Ocular Cell Biology
Program Number: 4818
Presentation Time: 4:53 PM–5:10 PM
Molecular Basis of Choroidal Neovascularization
Bela Anand-Apte. 1Cole Eye Institute, Cleveland, OH;
2
Ophthalmology, Cleveland Clinic Lerner College of MedicineCWRU, Cleveland, OH.
Presentation Description: A historical perspective and current status
of research on choroidal neovascularization will be presented.
©2015, Copyright by the Association for Research in Vision and Ophthalmology, Inc., all rights reserved. Go to iovs.org to access the version of record. For permission
to reproduce any abstract, contact the ARVO Office at [email protected].
ARVO 2015 Annual Meeting Abstracts
Commercial Relationships: Bela Anand-Apte, None
Support: NIH Grant EY020861, EY022768, FFB Center grant,
Research to Prevent Blindness Challenge Grant
Program Number: 4819
Presentation Time: 5:10 PM–5:27 PM
New approaches to imaging the choroid in health and disease
John S. Werner. University of California, Davis, Sacramento, CA.
Presentation Description: We have developed a noninvasive,
OCT-based, phase-variance method for depth-resolved imaging
of the microcirculation of the human chorioretinal complex. This
presentation will describe technical challenges and solutions for
creating three-dimensional perfusion maps that may be segmented
to reveal the individual layers of the choroid. Examples from normal
as well as diseased eyes will be compared to retinal images of the
same subjects acquired with fluorescein angiography and indocyanine
green angiography. The en face, depth-resolved, projection view
of the data produces two-dimensional vascular perfusion maps
of specific layers or groups of layers in the chorioretinal complex
without the risks associated with injection of fluorophores.
Commercial Relationships: John S. Werner, None
Support: NIH Grant EY024239
©2015, Copyright by the Association for Research in Vision and Ophthalmology, Inc., all rights reserved. Go to iovs.org to access the version of record. For permission
to reproduce any abstract, contact the ARVO Office at [email protected].