Transplantation of CX3CL1-expressing Mesenchymal Stem Cells Provides Neuroprotective and Immunomodulatory Effects in a Rat Model of Retinal Degeneration

Huang, Libin; Xu, Wei; Xu, Guo

doi:10.3109/09273948.2013.791925

Cited by 22 publications

(13 citation statements)

References 46 publications

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“…In this sense, under oxidative and ischemia/reperfusion conditions and in the absence of CX3CR1, uncontrolled retinal inflammation results in extensive retinal degeneration , and it has been suggested that CX3CL1 can exert a protective effect on the lightinjured retina (Huang et al, 2013a). On the other hand, the expression of fractalkine was found to be significantly upregulated after exposure to light, and was located mainly at the photoreceptors (Zhang et al, 2012a).…”

Section: Microglia In Degenerating Diseasesmentioning

confidence: 98%

Cellular responses following retinal injuries and therapeutic approaches for neurodegenerative diseases

Cuenca

Fernández‐Sánchez

Campello

et al. 2014

Progress in Retinal and Eye Research

353

394

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Section: Microglia In Degenerating Diseasesmentioning

confidence: 98%

Cellular responses following retinal injuries and therapeutic approaches for neurodegenerative diseases

Cuenca

Fernández‐Sánchez

Campello

et al. 2014

Progress in Retinal and Eye Research

353

394

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“…111,112 This has also been accomplished by altering MSC gene expression prior to transplantation. 113,114 …”

Section: Therapeutic Potential Of Mesenchymal Stem Cellsmentioning

confidence: 99%

Extrinsic and Intrinsic Mechanisms by Which Mesenchymal Stem Cells Suppress the Immune System

et al. 2016

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Mesenchymal stem cells (MSCs) are a group of fibroblast-like multipotent mesenchymal stromal cells that have the ability to differentiate into osteoblasts, adipocytes, and chondrocytes. Recent studies have demonstrated that MSCs possess a unique ability to exert suppressive and regulatory effects on both adaptive and innate immunity in an autologous and allogeneic manner. A vital step in stem cell transplantation is overcoming the potential graft-versus-host disease, which is a limiting factor to transplantation success. Given that MSCs attain powerful differentiation capabilities and also present immunosuppressive properties, which enable them to survive host immune rejection, MSCs are of great interest. Due to their ability to differentiate into different cell types and to suppress and modulate the immune system, MSCs are being developed for treating a plethora of diseases, including immune disorders. Moreover, in recent years, MSCs have been genetically engineered to treat and sometimes even cure some diseases, and the use of MSCs for cell therapy presents new perspectives for overcoming tissue rejection. In this review, we discuss the potential extrinsic and intrinsic mechanisms that underlie MSCs’ unique ability to modulate inflammation, and both innate and adaptive immunity.

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“…Very recent data show, however, protective effects of the fractalkine protein on retinal structure and function. This is supported by the analysis of light-injured rat retinas with transplanted mesenchymal stem cells engineered to secrete CX3CL1 [76]. Here the CX3CL1-expressing mesenchymal stem cells inhibited apoptosis of the retinal cells and microglial activation.…”

Section: Discussionmentioning

confidence: 83%

CX3CL1 (Fractalkine) Protein Expression in Normal and Degenerating Mouse Retina: In Vivo Studies

2014

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We aimed to investigate fractalkine (CX3CL1) protein expression in wild type (wt) retina and its alterations during retinal degeneration in mouse model (rd10) of retinitis pigmentosa. Forms of retinal protein CX3CL1, total protein and mRNA levels of CX3CL1 were analyzed at postnatal days (P) 5, 10, 14, 22, 30, 45, and 60 by Western blotting and real-time PCR. Cellular sources of CX3CL1 were investigated by in situ hybridization histochemistry (ISH) and using transgenic (CX3CL1cherry) mice. The immunoblots revealed that in both, wt and rd10 retinas, a membrane integrated ∼100 kDa CX3CL1 form and a cleaved ∼85 kDa CX3CL1 form were present at P5. At P10, accumulation of another presumably intra-neuronal ∼95 kDa form and a decrease in the ∼85-kDa form were observed. From P14, a ∼95 kDa form became principal in wt retina, while in rd10 retinas a soluble ∼85 kDa form increased at P45 and P60. In comparison, retinas of rd10 mice had significantly lower levels of total CX3CL1 protein (from P10 onwards) and lower CX3CL1 mRNA levels (from P14), even before the onset of primary rod degeneration. ISH and mCherry reporter fluorescence showed neurons in the inner retina layers as principal sites of CX3CL1 synthesis both in wt and rd10 retinas. In conclusion, our results demonstrate that CX3CL1 has a distinctive course of expression and functional regulation in rd10 retina starting at P10. The biological activity of CX3CL1 is regulated by conversion of a membrane integrated to a soluble form during neurogenesis and in response to pathologic changes in the adult retinal milieu. Viable mature neurons in the inner retina likely exhibit a dynamic intracellular storage depot of CX3CL1.

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Transplantation of CX3CL1-expressing Mesenchymal Stem Cells Provides Neuroprotective and Immunomodulatory Effects in a Rat Model of Retinal Degeneration

Abstract: CX3CL1-MSCs subretinal transplantation may enhance protective effect against light-induced retinal degeneration.

Cited by 22 publications

References 46 publications

Cellular responses following retinal injuries and therapeutic approaches for neurodegenerative diseases

Cellular responses following retinal injuries and therapeutic approaches for neurodegenerative diseases

Extrinsic and Intrinsic Mechanisms by Which Mesenchymal Stem Cells Suppress the Immune System

CX3CL1 (Fractalkine) Protein Expression in Normal and Degenerating Mouse Retina: In Vivo Studies

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