Macular Degeneration Stem Cell Treatment

Macular Degeneration and Stem Cell Therapy

What is Macular Degeneration?

Macular Degeneration and Stem Cell Therapy

Macular Degeneration and Stem Cell Therapy

Macular Degeneration or Age Related Macular Degeneration (AMD,ARMD) is a eyesight condition which mostly affects older people. AMD results in a loss of vision in the center of the visual field (the macula) because of damage or wear to the retina.

AMD can occur in either a wet or dry types. AMD is a major cause of visual impairment in people of 50 years age or more. AMD can make it difficult or impossible to read or to be able to recognize faces, although enough peripheral vision can remain to allow normal daily life.
Although some macular dystrophies that younger people get are referred to as macular degeneration, the term generally refers to age-related macular degeneration.


Stemming vision loss with stem cells.

J Clin Invest. 2010 Sep 1;120(9):3012-21

Authors: Marchetti V, Krohne TU, Friedlander DF, Friedlander M

Dramatic advances in the field of stem cell research have raised the possibility of using these cells to treat a variety of diseases. The eye is an excellent target organ for such cell-based therapeutics due to its ready accessibility, the prevalence of vasculo- and neurodegenerative diseases affecting vision, and the availability of animal models to demonstrate proof of concept. In fact, stem cell therapies have already been applied to the treatment of disease affecting the ocular surface, leading to preservation of vision. Diseases in the back of the eye, such as macular degeneration, diabetic retinopathy, and inherited retinal degenerations, present greater challenges, but rapidly emerging stem cell technologies hold the promise of autologous grafts to stabilize vision loss through cellular replacement or paracrine rescue effects.

PMID: 20811157 [PubMed - indexed for MEDLINE]

Related Articles Laminin modification subretinal bio-scaffold remodels retinal pigment epithelium-driven microenvironment in vitro and in vivo. Oncotarget. 2016 Oct 04;7(40):64631-64648 Authors: Peng CH, Chuang JH, Wang ML, Jhan YY, Chien KH, Chung YC, Hung KH, Chang CC, Lee CK, Tseng WL, Hwang DK, Hsu CH, Lin TC, Chiou SH, Chen SJ Abstract Advanced age-related macular degeneration (AMD) may lead to geographic atrophy or fibrovascular scar at macular, dysfunctional retinal microenvironment, and cause profound visual loss. Recent clinical trials have implied the potential application of pluripotent cell-differentiated retinal pigment epithelial cells (dRPEs) and membranous scaffolds implantation in repairing the degenerated retina in AMD. However, the efficacy of implanted membrane in immobilization and supporting the viability and functions of dRPEs, as well as maintaining the retinal microenvironment is still unclear. Herein we generated a biomimetic scaffold mimicking subretinal Bruch's basement from plasma modified polydimethylsiloxane (PDMS) sheet with laminin coating (PDMS-PmL), and investigated its potential functions to provide a subretinal environment for dRPE-monolayer grown on it. Firstly, compared to non-modified PDMS, PDMS-PmL enhanced the attachment, proliferation, polarization, and maturation of dRPEs. Second, PDMS-PmL increased the polarized tight junction, PEDF secretion, melanosome pigment deposit, and phagocytotic-ability of dRPEs. Third, PDMS-PmL was able to carry a dRPEs/photoreceptor-precursors multilayer retina tissue. Finally, the in vivo subretinal implantation of PDMS-PmL in porcine eyes showed well-biocompatibility up to 2-year follow-up. Notably, multifocal ERGs at 2-year follow-up revealed well preservation of macular function in PDMS-PmL, but not PDMS, transplanted porcine eyes. Trophic PEDF secretion of macular retina in PDMS-PmL group was also maintained to preserve retinal microenvironment in PDMS-PmL eyes at 2 year. Taken together, these data indicated that PDMS-PmL is able to sustain the physiological morphology and functions of polarized RPE monolayer, suggesting its potential of rescuing macular degeneration in vivo. PMID: 27564261 [PubMed - indexed for MEDLINE]
Related Articles Gene Delivery of Calreticulin Anti-Angiogenic Domain Attenuates the Development of Choroidal Neovascularization in Rats. Hum Gene Ther. 2017 May;28(5):403-414 Authors: Bee YS, Tu L, Sheu SJ, Lin HC, Tang JH, Wang JH, Prea SM, Dusting GJ, Wu DC, Zhong J, Bui BV, Tai MH, Liu GS Abstract Choroidal neovascularization (CNV) is a common pathological feature in neovascular age-related macular degeneration, which is the leading cause of vision loss among elderly populations in developed countries. This study evaluated the effect of a novel endogenous inhibitor of angiogenesis, calreticulin anti-angiogenic domain (CAD), subconjunctivally delivered by an adenoviral vector (Ad-CAD) in a rat model of laser-induced CNV. CAD was expressed in Ad-CAD-infected cells and inhibited the angiogenic activity in human umbilical vein endothelial cells in vitro. CAD expression was also found in various ocular tissues after in vivo subconjunctival Ad-CAD injection. Via bioluminescence imaging it is shown that a single subconjunctival injection of Ad-luciferase induced the expression of the transgene in the injected eyes within 24 h, which lasted for at least 112 days. Forty-two days after subconjunctival injection of Ad-CAD, retinal structure and function were unaffected, as measured using optical coherence tomography and electroretinography, respectively. After laser injury, subconjunctival Ad-CAD gene delivery significantly inhibited CNV lesions as measured via choroid flat-mounts (51% reduction at 21 days; p < 0.001), as well as by fundus fluorescein angiography (19.3%, 28.2%, 31%, and 27.5% reductions at days 21, 28, 35, and 42, respectively; p < 0.05) in rats. The data suggest that subconjunctival Ad-CAD gene therapy could effectively inhibit laser-induced CNV and might be an attractive therapeutic approach for the management of choroidal neovascularization. PMID: 28363247 [PubMed - indexed for MEDLINE]

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