RNCR3 knockdown inhibits diabetes mellitus-induced retinal reactive gliosis

Liu, Chang; Li, Chaopeng; Wang, Jia-Jian; Shan, K. Y.; Liu, Xin; Yan, Biao

doi:10.1016/j.bbrc.2016.09.032

Cited by 39 publications

(40 citation statements)

References 26 publications

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“…When the damage is extensive or intense, MGCs may stay activated even after the stimuli have disappeared. This process of persistent gliosis is considered an indicator of a bad prognosis for retinal recovery (Liu et al., ). Simultaneously, in the injured retina, MGCs participate in the inflammatory response through the secretion of cytokines and other mediators to the extracellular space and the vitreous cavity.…”

Section: Introductionmentioning

confidence: 99%

A journey into the retina: Müller glia commanding survival and death

Subirada

Paz

Ridano

et al. 2018

Eur J of Neuroscience

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Müller glial cells (MGCs) are known to participate actively in retinal development and to contribute to homoeostasis through many intracellular mechanisms. As there are no homologous cells in other neuronal tissues, it is certain that retinal health depends on MGCs. These macroglial cells are located at the centre of the columnar subunit and have a great ability to interact with neurons, astrocytes, microglia and endothelial cells in order to modulate different events. Several investigations have focused their attention on the role of MGCs in diabetic retinopathy, a progressive pathology where several insults coexist. As expected, data suggest that MGCs display different responses according to the severity of the stimulus, and therefore trigger distinct events throughout the course of the disease. Here, we describe physiological functions of MGCs and their participation in inflammation, gliosis, synthesis and secretion of trophic and antioxidant factors in the diabetic retina. We invite the reader to consider the protective/deleterious role of MGCs in the early and late stages of the disease. In the light of the results, we open up the discussion around and ask the question: Is it possible that the modulation of a single cell type could improve or even re-establish retinal function after an injury?

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Section: Introductionmentioning

confidence: 99%

A journey into the retina: Müller glia commanding survival and death

Subirada

Paz

Ridano

et al. 2018

Eur J of Neuroscience

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“…RNCR3 participates in the retinal development and neuronal and oligodendrocyte differentiation. It is also up-regulated in RF/6A cell line and the retina of diabetic mice, similarly to some interleukins and inflammatory factors like VEGF and TNFα (Liu et al, 2016;Rapicavoli et al, 2010).…”

Section: Diabetic Retinopathymentioning

confidence: 91%

Circular and long non-coding RNAs and their role in ophthalmologic diseases

et al. 2018

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Long non-coding RNAs are >200-nucleotide-long RNA molecules which lack or have limited protein-coding potential. They can regulate protein formation through several different mechanisms. Similarly, circular RNAs are reported to play a critical role in post-transcriptional gene regulation. Changes in the expression pattern of these molecules are known to underlie various diseases, including cancer, cardiovascular, neurological and immunological disorders (Rinn & Chang, 2012; Sun & Kraus, 2015). Recent studies suggest that they are differentially expressed both in healthy ocular tissues as well as in eye pathologies, such as neovascularization, proliferative vitreoretinopathy, glaucoma, cataract, ocular malignancy or even strabismus (Li et al., 2016). Aetiology of ocular diseases is multifactorial and combines genetic and environmental factors, including epigenetic and non-coding RNAs. In addition, disorders like diabetic retinopathy or age-related macular degeneration lack biomarkers for early detection as well as effective treatment methods that would allow controlling the disease progression at its early stages. The newly discovered non-coding RNAs seem to be the ideal candidates for novel molecular markers and therapeutic strategies. In this review, we summarized the current knowledge about gene expression regulators – long non-coding and circular RNA molecules in eye diseases.

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“…metabolic injury in course of diabetic retinopathy. 11 Retinal reactive gliosis could be sustained with knockdown of retinal noncoding RNA 3 (RNCR3) and ceasing the function of RNCR3 results in reduction of viability and proliferation with diminished expression of GFAP and vimentin of Müller cells in vitro as well decrease of various cytokines that are drivers of retinal neurodegeneration in diabetes mellitus. 10,11 As a proof of non neoplastic nature, MRG was shown to be polyclonal in nature in analysis of tumor clonality using a human androgen receptor assay in case of a 32-year-old woman with bilateral microphthalmia.…”

Section: Molecular Backgroundmentioning

confidence: 99%

“…11 Retinal reactive gliosis could be sustained with knockdown of retinal noncoding RNA 3 (RNCR3) and ceasing the function of RNCR3 results in reduction of viability and proliferation with diminished expression of GFAP and vimentin of Müller cells in vitro as well decrease of various cytokines that are drivers of retinal neurodegeneration in diabetes mellitus. 10,11 As a proof of non neoplastic nature, MRG was shown to be polyclonal in nature in analysis of tumor clonality using a human androgen receptor assay in case of a 32-year-old woman with bilateral microphthalmia. 22 The lesion classically was composed of spindle cells with delicate fi brillary cytoplasm and glial fi brillary acidic protein and neuron-specifi c enolase and partly S-100 protein positivity consistent with mainly non-atypical astrocytes with atrophic residues of retinal epithelium and sclera at the margins of the lesion.…”

Section: Molecular Backgroundmentioning

confidence: 99%

“…1,10 Müller cells contain intermediate fi laments, so they are both positive for vimentin and partially for glial fi brillary acidic protein (GFAP). 11 Besides all supporting properties of glia, Müller cells are a special type of retinal glial cells, which are also characterized by capability of streaming of various wavelength of light to the correct photoreceptor cells via fi ber optic cables. 6 In retina, there are also ganglion cells that serve as cellular intermediaries (or intermediate stations) of signaling on optic tract.…”

Section: Introductionmentioning

confidence: 99%

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Review on Retinal Gliosis Illustrated with a Series of Massive Glioses and Focal Nodular Gliosis Cases in Regard to Potential Pitfalls of Ocular Reactive Tumor-like Lesions of this Type

Wincewicz¹,

Urbaniak-Wasik²,

Urbaniak³

et al. 2018

Folia Medica

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This paper presents a review on retinal gliosis illustrated by series of three cases of patients (a 39-year-old man and a 35-year-old woman with massive retinal gliosis (MRG) and a 51-year-old man with truly focal nodular gliosis of retina) with intraocular tumor-like masses and loss of vision, who recently suffered from painful inflammation of eyeball and who classically had a history of remote ocular trauma, onset of blindness early in lifetime or gradual but progressive loss of sight. The diagnosis of this pathological entity is given for the lesions that are composed of GFAP strongly positive, elongated, fusiform cells consistent with fibrillary astrocytes. As illustrated in cases from our pathological practice, PAS gave positive patchy disseminated reaction in form of cellular densely purplish granules in minority of cells representing glycogen storing. This feature could be consistent with PAS-positive Müller cells that also constitute retinal gliosis as one of cellular components of normal retina that is induced to reactive proliferation. Thus, the paper presents histological background and differential diagnosis of the entity.

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RNCR3 knockdown inhibits diabetes mellitus-induced retinal reactive gliosis

Cited by 39 publications

References 26 publications

A journey into the retina: Müller glia commanding survival and death

A journey into the retina: Müller glia commanding survival and death

Circular and long non-coding RNAs and their role in ophthalmologic diseases

Review on Retinal Gliosis Illustrated with a Series of Massive Glioses and Focal Nodular Gliosis Cases in Regard to Potential Pitfalls of Ocular Reactive Tumor-like Lesions of this Type

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