Mesenchymal marker expression is elevated in Müller cells exposed to high glucose and in animal models of diabetic retinopathy

Zhou, Ti; Che, Di; Lan, Yuqing; Fang, Zhiheng; Xie, Jinye; Gong, Hai Jun; Li, Chaoyang; Feng, Juan; Hong, Honghai; Qi, Weiwei; Ma, Caiqi; Yang, Zhonghan; Cai, Wei; Zhong, Jun; Xing, Jian; Yang, Xia; Gao, Guoquan

doi:10.18632/oncotarget.13945

Cited by 29 publications

(22 citation statements)

References 35 publications

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“…Gliotic altered Müller cells have increased GFAP immunoreactivity under pathological conditions [ 23 ]. We further investigated the expression level of the GFAP protein in the TAA-injected rats by immunohistochemistry.…”

Section: Resultsmentioning

confidence: 99%

“…Gliotic alterations of Müller cells include cellular hypertrophy and proliferation [ 33 ]. Upregulation of GFAP is known to be a very sensitive early indicator of retinal stress [ 23 ]. In the present study, we showed that GFAP was highly expressed in the retinas of the TAA-injected rats with hepatic retinopathy, indicating a predominant Müller cell gliosis.…”

Section: Discussionmentioning

confidence: 99%

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Aloin Inhibits Müller Cells Swelling in a Rat Model of Thioacetamide-Induced Hepatic Retinopathy

Jung

Kim

2018

Molecules

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Swelling of retinal Müller cells is implicated in retinal edema and neuronal degeneration. Müller cell swelling is observed in patients with liver failure and is referred to as hepatic retinopathy. In the present study, we evaluated the effects of aloin, an anthraquinone-C-glycoside present in various Aloe species, on Müller cell dysfunction in a rat model of thioacetamide (TAA)-induced hepatic retinopathy. Experimental hepatic retinopathy was induced by three injections of TAA (200 mg/kg/day, intraperitoneal injection) for 3 days in rats. After the last injection of TAA, aloin (50 and 100 mg/kg) was orally gavaged for 5 days. The effects of aloin on the liver injury, serum ammonia levels, Müller cell swelling, glial fibrillary acidic protein (GFAP) expression, and gene expression of Kir4.1 and aquaporin-4 were examined. TAA-injected rats exhibited liver failure and hyperammonemia. In the TAA-injected rats, Müller cell bodies were highly enlarged, and GFAP, an indicator of retinal stress, was highly expressed in the retinas, indicating a predominant Müller cell gliosis. However, administration of aloin suppressed liver injury as well as Müller cell swelling through the normalization of Kir4.1 and aquaporin-4 channels, which play a key role in potassium and water transport in Müller cells. These results indicate that aloin may be helpful to protect retinal injury associated with liver failure.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Aloin Inhibits Müller Cells Swelling in a Rat Model of Thioacetamide-Induced Hepatic Retinopathy

Jung

Kim

2018

Molecules

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“…Hyperglycemia promotes release of (1) growth factors, such as vascular endothelial growth factor (VEGF) and pigment epithelium-derived factor (PEDF), and (2) cytokines and chemokines including interleukin-1β (IL-β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and chemokine ligand-2 (CCL2)[52,55–61] [62–64]. In vitro studies have provided ample evidence that Müller cells are a potential source for growth factors and cytokines when stimulated with elevated glucose levels.…”

Section: Release Of Growth Factors and Pro-/anti-inflammatory Cytokinmentioning

confidence: 99%

Müller cells and diabetic retinopathy

2017

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Müller cells are one of the primary glial cell types found in the retina and play a significant role in maintaining retinal function and health. Since Müller cells are the only cell type to span the entire width of the retina and have contact to almost every cell type in the retina they are uniquely positioned to perform a wide variety of functions necessary to maintaining retinal homeostasis. In the healthy retina, Müller cells recycle neurotransmitters, prevent glutamate toxicity, redistribute ions by spatial buffering, participate in the retinoid cycle, and regulate nutrient supplies by multiple mechanisms. Any disturbance to the retinal environment is going to influence proper Müller cell function and well being which in turn will affect the entire retina. This is evident in a disease like diabetic retinopathy where Müller cells contribute to neuronal dysfunction, the production of pro-angiogenic factors leading to neovascularization, the set up of a chronic inflammatory retinal environment, and eventual cell death. In this review, we highlight the importance of Müller cells in maintaining a healthy and functioning retina and discuss various pathological events of diabetic retinopathy in which Müller cells seem to play a crucial role. The beneficial and detrimental effects of cytokine and growth factor production by Müller cells on the microvasculature and retinal neuronal tissue will be outlined. Understanding Müller cell functions within the retina and restoring such function in diabetic retinopathy should become a cornerstone for developing effective therapies to treat diabetic retinopathy.

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“…Moreover, the oral administration of an inhibitor of aldose reductase (sorbinil) prevented gliotic changes. An increase in retinal vimentin expression was observed in STZ‐induced diabetic rats, in MGCs cell cultured under high glucose conditions and in epiretinal membranes of diabetic patients (Zhou et al., ).…”

Section: Gliosismentioning

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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Mesenchymal marker expression is elevated in Müller cells exposed to high glucose and in animal models of diabetic retinopathy

Abstract: ABSTRACT

Cited by 29 publications

References 35 publications

Aloin Inhibits Müller Cells Swelling in a Rat Model of Thioacetamide-Induced Hepatic Retinopathy

Aloin Inhibits Müller Cells Swelling in a Rat Model of Thioacetamide-Induced Hepatic Retinopathy

Müller cells and diabetic retinopathy

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

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