Morphologic characteristics of retinal degeneration induced by sodium iodate in mice

Kiuchi, Katsuji; Yoshizawa, Katsuhiko; Shikata, Nobuaki; Moriguchi, Kaei; Tsubura, Airo

doi:10.1076/ceyr.25.6.373.14227

Cited by 128 publications

(113 citation statements)

References 20 publications

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“…In this study, we link the activity of WNT signaling to the tumorigenic potential of ESC-RPCs and provide the experimental evidence for transcriptional factor TCF7 to regulate expression of SOX2 and NESTIN, two important genes actively engaged in the neural development and tumor formation. The tumorigenic and therapeutic effect of transplanted ESC-RPCs is determined in a well-studied sodium iodate-induced (SI-induced) mouse retinal degeneration model (20,21). We also show that the expression of TCF7, SOX2, and NESTIN is closely associated in mouse neonatal retinae.…”

Section: Introductionmentioning

confidence: 74%

WNT signaling determines tumorigenicity and function of ESC-derived retinal progenitors

Cui¹,

Guan²,

Qu³

et al. 2013

J. Clin. Invest.

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Section: Introductionmentioning

confidence: 74%

WNT signaling determines tumorigenicity and function of ESC-derived retinal progenitors

Cui¹,

Guan²,

Qu³

et al. 2013

J. Clin. Invest.

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“…The oxidative stressor sodium iodate (NaIO 3 ) has been used previously to induce selective degeneration of the RPE and consequent retinal degeneration (Ringvold et al 1981;Kiuchi et al 2002;Enzmann et al 2006). Intravenous injection of NaIO 3 into C57/BL6 mice induced disorganization of the RPE layer after 36 h, and subsequently led to the degeneration of photoreceptors.…”

Section: Rpe Inactivation Of Pten In Mice Undergoing Retinal Degeneramentioning

confidence: 99%

“…NaIO 3 injection and RPE lysate preparation C57/BL6 mice (2 to 3 mo) were injected with NaIO 3 solution (30 mg/kg in PBS) into tail veins as described previously (Kiuchi et al 2002;Enzmann et al 2006). Eyes were enucleated and the retina carefully pushed out before treating with dispase (100 U/mL) to isolate RPE cells.…”

Section: Antibodies and Immunohistochemistrymentioning

confidence: 99%

Retinal degeneration triggered by inactivation of PTEN in the retinal pigment epithelium

Kim¹,

Kang²,

Burrola³

et al. 2008

Genes Dev.

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Adhesion between epithelial cells mediates apical-basal polarization, cell proliferation, and survival, and defects in adhesion junctions are associated with abnormalities from degeneration to cancer. We found that the maintenance of specialized adhesions between cells of the retinal pigment epithelium (RPE) requires the phosphatase PTEN. RPE-specific deletion of the mouse pten gene results in RPE cells that fail to maintain basolateral adhesions, undergo an epithelial-to-mesenchymal transition (EMT), and subsequently migrate out of the retina entirely. These events in turn lead to the progressive death of photoreceptors. The C-terminal PSD-95/Dlg/ZO-1 (PDZ)-binding domain of PTEN is essential for the maintenance of RPE cell junctional integrity. Inactivation of PTEN, and loss of its interaction with junctional proteins, are also evident in RPE cells isolated from ccr2 −/− mice and from mice subjected to oxidative damage, both of which display age-related macular degeneration (AMD). Together, these results highlight an essential role for PTEN in normal RPE cell function and in the response of these cells to oxidative stress.[Keywords: PI3K signaling; PTEN; retinal pigment epithelium (RPE); epithelial-to-mesenchymal transition (EMT); age-related macular degeneration (AMD)] Supplemental material is available at http://www.genesdev.org.

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“…On the other hand, the majority of animals did not show an increase but rather a further decrease of their visual function. This might be due to the already initiated apoptosis in the photoreceptors that follows the initial damage of the RPE by NaIO 3 [29] . The impact of the subretinal surgery on the visual function should also be taken into account.…”

Section: Discussionmentioning

confidence: 99%

Bone marrow-derived stem cells differentiate into retinal pigment epithelium-like cells in vitro but are not able to repair retinal degeneration in vivo

Lecaude

Wolf

Abdillahi

et al. 2015

Stem Cell Transl Investig

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The bone marrow (BM) is home to different stem/progenitor populations, including tissue-committed stem cells. In this context, we have cocultured BM-derived stem cells (BMSC) in order to investigate their differentiation capacity towards the retinal pigment epithelial (RPE) lineage in vitro. Furthermore, pre-differentiated BMSC were transplanted into the pharmacologically damaged subretinal space to determine their rescue ability in vivo. BM was harvested from the tibias and femurs of adult GFP + C57BL/6 mice. Differentiated hematopoietic cells were removed by lineage depletion, and CD45 -BMSCs were separated by magnetic activated cell sorting (MACS). To induce differentiation, the cells were then cocultured with murine RPE for 10 days, and retinal markers were assessed using immunohistochemistry (IHC). To induce retinal degeneration, mice were treated with sodium iodate (NaIO 3 ). Seven days later, approx. 60,000 pre-differentiated GFP + BMSC, sorted by FACS, were transplanted subretinally. Optical coherence tomography (OCT) was used to follow the transplants and to quantify the retinal thickness over time. Visual acuity was measured concurrently using the optokinetic reflex (OKR). Finally, IHC was performed to investigate the expression of retina-specific markers in the transplants. CD45-BMSC adopted an RPE-like elongated morphology and showed expression of the RPE markers RPE65 and bestrophin after coculture. After transplantation of CD45 -BMSC, visual acuity increased in individual animals compared to the contralateral control eye, but did not reach baseline levels. Additionally, no significant increase in retinal thickness in the transplanted eye was found. However, the cells were detectable in the subretinal space for up to 28 days and expressed the RPE markers RPE65 and bestrophin. In summary, the BMSC differentiated into RPE-like cells but were not able to restore visual function or rescue retinal morphology after subretinal transplantation.Keywords: retina; degeneration; sodium iodate; transplantation; differentiation; bone marrow-derived stem cells To cite this article: Stéphanie Lecaudé, et al. Bone marrow-derived stem cells differentiate into retinal pigment epithelium-like cells in vitro but are not able to repair retinal degeneration in vivo.

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Morphologic characteristics of retinal degeneration induced by sodium iodate in mice

Abstract: RPE cell necrosis followed by photoreceptor cell apoptosis and the resulting mosaic pattern of the retina phenotypically resembles gyrate atrophy of the choroid and retina.

Cited by 128 publications

References 20 publications

WNT signaling determines tumorigenicity and function of ESC-derived retinal progenitors

WNT signaling determines tumorigenicity and function of ESC-derived retinal progenitors

Retinal degeneration triggered by inactivation of PTEN in the retinal pigment epithelium

Bone marrow-derived stem cells differentiate into retinal pigment epithelium-like cells in vitro but are not able to repair retinal degeneration in vivo

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