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 A cell culture condition that induces the mesenchymal-epithelial transition of dedifferentiated porcine retinal pigment epithelial cells. Exp Eye Res. 2018 Aug 07;: Authors: Tian H, Xu JY, Tian Y, Cao Y, Lian C, Ou Q, Wu B, Jin C, Gao F, Wang J, Zhang J, Zhang J, Li W, Lu L, Xu GT Abstract The pathological change of retinal pigment epithelial (RPE) cells is one of the main reasons for the development of age-related macular degeneration (AMD). Thus, cultured RPE cells are a proper cell model for studying the etiology of AMD in vitro. However, such cultured RPE cells easily undergo epithelial-mesenchymal transition (EMT) that results in changes of cellular morphology and functions of the cells. To restore and maintain the mesenchymal-epithelial transition (MET) of the cultured RPE cells, we cultivated dedifferentiated porcine RPE (pRPE) cells and compared their behaviors in four conditions: 1) in cell culture dishes with DMEM/F12 containing FBS (CC dish-FBS), 2) in petri dishes with DMEM/F12 containing FBS (Petri dish-FBS), 3) in cell culture dishes with DMEM/F12 containing N2 and B27 supplements (CC dish-N2B27), and 4) in petri dishes with DMEM/F12 containing N2 and B27 (Petri dish-N2B27). In addition to observing the cell morphology and behavior, RPE specific markers, as well as EMT-related genes and proteins, were examined by immunostaining, quantitative real-time PCR and Western blotting. The results showed that dedifferentiated pRPE cells maintained EMT in CC dish-FBS, Petri dish-FBS and CC dish-N2B27 groups, whereas MET was induced when the dedifferentiated pRPE cells were cultured in Petri dish-N2B27. Such induced pRPE cells showed polygonal morphology with increased expression of RPE-specific markers and decreased EMT-associated markers. Similar results were observed in induced pluripotent stem cell-derived RPE cells. Furthermore, during the re-differentiation of those dedifferentiated pRPE cells, Petri dish-N2B27 reduced the activity of RhoA and induced F-actin rearrangement, which promoted the nuclear exclusion of transcriptional co-activator with PDZ-binding motif (TAZ) and TAZ target molecule zinc finger E-box binding protein (ZEB1), both of which are EMT inducing factors. This study provides a simple and reliable method to reverse dedifferentiated phenotype of pRPE cells into epithelialized phenotype, which is more appropriate for studying AMD in vitro, and suggests that MET of other cell types might be induced by a similar approach. PMID: 30096326 [PubMed - as supplied by publisher]

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