Epo inhibits the fibrosis and migration of Müller glial cells induced by TGF-β and high glucose

Luo, Wentao; Hu, Liumei; Li, Weiye; Xu, Guo‐Tong; Xu, Ling; Zhang, Conghui; Wang, Fang

doi:10.1007/s00417-016-3290-5

Cited by 21 publications

(12 citation statements)

References 59 publications

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“…We therefore examined whether hyperglycemia was sufficient for increasing mesenchymal marker levels in retinal Müller cells. As was the case in a previous study [29], we found that high glucose conditions increased α-SMA, fibronectin, and connective tissue growth factor (CTGF) levels in Müller cells. Furthermore, we found that high glucose conditions also increased N-cadherin, β-catenin, Vimentin, and Snail levels (Figure 4).…”

Section: Discussionsupporting

confidence: 83%

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

Zhou¹,

Che²,

Lan

et al. 2016

Oncotarget

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Section: Discussionsupporting

confidence: 83%

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

Zhou¹,

Che²,

Lan

et al. 2016

Oncotarget

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“…Li et al [34] also found that oxidative stress is the main reason for the decrease of EPO expression in aging of rats. In addition to the inhibition of oxidative stress and inflammation, EPO can also inhibit fibrosis of renal tubular epithelial cells by inhibiting EMT, where EPO downregulates the expression of TGF-β, α-SMA, fibronectin, and connective tissue growth factor [35]. However, many original research studies showed that soluble EPOR levels may contribute to erythropoietin resistance in ESRD and that soluble EPOR production may be mediated by proinflammatory cytokines [36].…”

Section: Discussionmentioning

confidence: 99%

Siwu Granules and Erythropoietin Synergistically Ameliorated Anemia in Adenine-Induced Chronic Renal Failure Rats

Wan

Shi

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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Objective. Renal anemia in patients with end-stage chronic kidney disease is closely related to the deterioration of cardiac function, renal function, and quality of life. This study involved adenine-induced renal anemic rat models and evaluated the treatment effect of Siwu granules and/or erythropoietin (EPO). Methods. Fifty SD rats were randomly divided into 5 groups: control, model, Siwu, EPO, and Siwu plus EPO groups. The expression levels of NO, MDA, SOD, CAT, IL-6, TNF-α, EPO, EPOR, α-SMA, and TGF-β1 were detected in rats after 8 weeks of treatment with Siwu granules and/or EPO. Results. After modeling, 47 rats entered the stage of treatment. Siwu plus EPO treatment significantly increased the rat hemoglobin content (p<0.05) and reduced blood urea nitrogen (p<0.05) and serum creatinine (p<0.001). Compared with the control group, the expression of EPO and EPOR in the kidney of rats with renal failure was significantly decreased (p<0.05). Moreover, the Siwu plus EPO group improved the level of oxidative stress in rats with chronic renal failure and reduced the expression of inflammatory factors. The expression of α-SMA and TGF-β1 in rats with renal failure was higher, but there was no expression in the control group. Conclusion. Combined treatment of Siwu granules with EPO increased the expression of EPO and EPOR in the renal tissues and inhibited oxidative stress and inflammatory factors, improving the renal function and anemia.

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“…Transforming growth factor-b induces the differentiation of these cells into a fibroblast-like phenotype and promotes their migration. 7,8 Characteristic cytokine profiles for the differentiation of fibroblasts and retinal glia are unknown, but we assume activated fibroblasts as a source, but not so evidently Müller glia cells, in the chronic phase of ERM formation. The cytokine profiles in our study are commensurate with an activation of fibrotic and inflammatory processes, which are associated with elevated levels of IL-6, IL-4, IL-1b, TNF-a, IL-10, IL-2, and INF-c (among others).…”

Section: Discussionmentioning

confidence: 99%

“…1,2,5 Müller glial cells are known to activate fibroblasts and to promote fibrotic changes within the eye, such as proliferative vitreoretinopathy (PVR) 3,6 and the formation of epiretinal membranes (ERMs). 7,8 Epiretinal membranes are characterized by the growth of fibrocellular tissue along the inner limiting membrane (ILM), which can lead to metamorphopsia and visual loss. The most frequently encountered, so-called idiopathic ERMs, are not linked to any other ocular disease process and their pathogenesis remains unidentified.…”

mentioning

confidence: 99%

Vitreal Cytokine Profile Differences Between Eyes With Epiretinal Membranes or Macular Holes

Zandi

Tappeiner

Pfister

et al. 2016

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. Cytokines play an important role in cell signaling in inflammatory and repair processes, also within the posterior segment of the eye. These molecules are thus implicated in the pathophysiology of several vitreoretinal diseases. In the present study, we compared vitreal cytokine profiles in patients with idiopathic epiretinal membranes (ERMs) and idiopathic full-thickness macular holes (MHs) without epiretinal membranes.METHODS. Native vitreal humor was collected during elective pars plana vitrectomy for the treatment of macular pathologies (group 1: ERM; group 2: MH) from patients without any other ocular or systemic disease. The concentrations of 43 chemokines and cytokines were measured in parallel by multiplex beads analysis. Intergroup comparisons were conducted using the Mann-Whitney U test and Bonferroni's correction, at a level of significance of P < 0.0012. RESULTS.Vitreal samples from 31 patients with ERMs (group 1) and from 30 with MHs (group 2) were analyzed. For 12 of the tested cytokines (GM-CSF, MCP-1, MIF, CCL15, CCL20, CCL17, CX3CL1, CXCL10, CXCL16, and TGF-b-1, -2, and -3), no intergroup differences were revealed; for the other 31, the concentrations were higher in the ERM than in the MH group (P < 0.0012 in each case).CONCLUSIONS. The vitreal levels of 72% of the tested cytokines were higher in ERM than in MH. This indicates that even in the absence of clinical markers, activation of inflammatory and profibrotic mechanisms is implicated in the progression of ERMs. Although frequently used as such in the past, eyes with ERMs should be considered with caution as a healthy control group.

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Epo inhibits the fibrosis and migration of Müller glial cells induced by TGF-β and high glucose

Abstract: High glucose together with TGF-β promote MGCs to exhibit a fibroblast-like phenotype and develop a greater migratory ability. These changes can be inhibited by Epo, which therefore may contribute to the controlling of epiretinal membrane formation.

Cited by 21 publications

References 59 publications

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

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

Siwu Granules and Erythropoietin Synergistically Ameliorated Anemia in Adenine-Induced Chronic Renal Failure Rats

Vitreal Cytokine Profile Differences Between Eyes With Epiretinal Membranes or Macular Holes

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