Tumor necrosis factor-like weak inducer of apoptosis association with proliferative diabetic retinopathy and promotes proliferation and collagen synthesis in retinal ARPE-19 cells

Chen, D Y; Su, Guanfang

doi:10.4238/gmr.15016920

Cited by 4 publications

(5 citation statements)

References 34 publications

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“…A variety of studies have found critical roles of some signals in the development of DR, including proinflammatory cytokines TNF-α [ 26 ]. Anti-inflammatory drugs prevent the development of DR via the suppression of TNF-α, an independent serum marker for DR [ 27 ]. In our study, the mRNA and protein levels of TNF-α were enhanced in DR RPE cells, which was similar to previous results.…”

Section: Discussionmentioning

confidence: 99%

miRNA-1273g-3p Involvement in Development of Diabetic Retinopathy by Modulating the Autophagy-Lysosome Pathway

2017

Med Sci Monit

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BackgroundDiabetic retinopathy (DR) is one of the most common and serious complications of diabetes mellitus (DM). The autophagy-lysosome pathway (ALP) is one of the main intracellular self-digestive degradation systems. Lysosomal impairment and autophagic dysfunction are early events in the pathogenesis of DR, suggesting autophagy might be a novel therapeutic strategy for DR treatment.Material/MethodsIn our study, we screened a differentially expressed miRNA, miR-1273g-3p, in streptozotocin (STZ)-injected DR rat retinal pigment epithelial (RPE) cells. miR-1273g-3p inhibitor and mimic were employed to treat RPE cells to assess the role of miR-1273g-3p. QRT-PCR and Western blot analysis were performed to examine the function of miR-1273g-3p on ALP-related and DR-related proteins.ResultsmiR-1273g-3p was highly expressed in STZ-induced DM RPE cells. miR-1273g-3p mimic promoted the expression of DR-related MMP-2, MMP-9, and TNF-α proteins, and ALP-related LC3, cathepsin B, and cathepsin L factors, but miR-1273g-3p inhibitor suppressed the levels of these factors.ConclusionsmiR-1273g-3p is involved in the progression of DR by modulating the autophagy-lysosome pathway. These findings provided new evidence of the close relationship between DR and ALP, and reveal a new target for DR therapy.

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Section: Discussionmentioning

confidence: 99%

miRNA-1273g-3p Involvement in Development of Diabetic Retinopathy by Modulating the Autophagy-Lysosome Pathway

2017

Med Sci Monit

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“…Previous studies have identified a potential role for TWEAK/Fn14 in pro-fibrosis in various organs or tissues (52)(53)(54)(55)(56)(57)(58). Chen DY reported TWEAK in proliferative diabetic retinopathy (PDR) and promoted proliferation and collagen synthesis in retinal ARPE-19 cells (59). In our study, the upregulation of TWEAK in TPVR patients, the particularly high AUC value, the most significant positive correlation with HGF, and the correlation with PVR-S led us to propose TWEAK as another candidate target biomarker for the diagnosis of TPVR and for the assessment of PVR severity.…”

Section: Figurementioning

confidence: 99%

Vitreous Olink proteomics reveals inflammatory biomarkers for diagnosis and prognosis of traumatic proliferative vitreoretinopathy

Guo,

Wang,

et al. 2024

Front. Immunol.

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BackgroundThe aim of this study was to identify inflammatory biomarkers in traumatic proliferative vitreoretinopathy (TPVR) patients and further validate the expression curve of particular biomarkers in the rabbit TPVR model.MethodsThe Olink Inflammation Panel was used to compare the differentially expressed proteins (DEPs) in the vitreous of TPVR patients 7–14 days after open globe injury (OGI) (N = 19) and macular hole patients (N = 22), followed by correlation analysis between DEPs and clinical signs, protein–protein interaction (PPI) analysis, area under the receiver operating characteristic curve (AUC) analysis, and function enrichment analysis. A TPVR rabbit model was established and expression levels of candidate interleukin family members (IL-6, IL-7, and IL-33) were measured by enzyme-linked immunosorbent assay (ELISA) at 0, 1, 3, 7, 10, 14, and 28 days after OGI.ResultsForty-eight DEPs were detected between the two groups. Correlation analysis showed that CXCL5, EN-RAGE, IL-7, ADA, CD5, CCL25, CASP8, TWEAK, and IL-33 were significantly correlated with clinical signs including ocular wound characteristics, PVR scoring, PVR recurrence, and final visual acuity (R = 0.467–0.699, p < 0.05), and all with optimal AUC values (0.7344–1). Correlations between DEP analysis and PPI analysis further verified that IL-6, IL-7, IL-8, IL-33, HGF, and CXCL5 were highly interactive (combined score: 0.669–0.983). These DEPs were enriched in novel pathways such as cancer signaling pathway (N = 14, p < 0.000). Vitreous levels of IL-6, IL-7, and IL-33 in the rabbit TPVR model displayed consistency with the trend in Olink data, all exhibiting marked differential expression 1 day following the OGI.ConclusionIL-7, IL-33, EN-RAGE, TWEAK, CXCL5, and CD5 may be potential biomarkers for TPVR pathogenesis and prognosis, and early post-injury may be an ideal time for TPVR intervention targeting interleukin family biomarkers.

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“…The expression of Fn14 was increased in the hearts of transaortic constriction mice, and treatment with the Fn14 antagonist L524-0366 reduces macrophage infiltration and fibrosis (Unudurthi et al, 2020). In a chronic GVHD murine model, neutralizing anti-TWEAK mAb significantly reduced proteinuria and downregulated T A B L E 2 TWEAK/Fn14 pathway mediates fibrosis in various organs Chen and Su (2016) Abbreviations: AP-1, activator protein 1; CCL2, C-C motif chemokine ligand 2; ECM, extracellular matrix; EGF, epidermal growth factor; EGFR, epidermal growth factor receptor; EMT, epithelial-mesenchymal transition; ERK, extracellular-signal-regulated kinase; Fn14, fibroblast growth factor-inducible 14; IL-13, interleukin-13; MAL, myelin and lymphocyte; MAPK, mitogen-activated protein kinase; MMP, matrix metalloproteinase; MRTF-A, myocardin-related transcription factor A; NF-κB, nuclear factor-κB; PKG, protein kinase G; SOCS1, suppression of cytokine signaling 1; STAT3, signal transducer and activator of transcription 3; TGF-β1, transforming growth factor β1; TIMP, tissue inhibitor of metalloproteinase; VCAM-1, vascular cell adhesion molecule-1;…”

Section: In Vivo Studies Of Targeted Therapymentioning

confidence: 99%

“…TWEAK was also found to be involved in the pathogenesis of proliferative diabetic retinopathy (PDR). The expression levels of TWEAK and Fn14 were higher in the vitreous fluid of patients with PDR than those without PDR, and TWEAK promoted the proliferation and collagen synthesis of retinal cells (D. Y. Chen & Su, 2016).…”

Section: Tweak/fn14 Activation Contributes To Fibrosis In Various Dis...mentioning

confidence: 99%

“…The expression levels of TWEAK and Fn14 were higher in the vitreous fluid of patients with PDR than those without PDR, and TWEAK promoted the proliferation and collagen synthesis of retinal cells (D. Y. Chen & Su, 2016). TWEAK/Fn14 signaling participates in fibrosis through multiple mechanisms, including maintaining chronic inflammation, activating myofibroblasts, secreting profibrotic cytokines and ECM, and regulating enzymes related to ECM accumulation.…”

Section: Other Fibrosismentioning

confidence: 99%

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TWEAK/Fn14 axis is an important player in fibrosis

Zhang

Zeng

Xia

2020

Journal Cellular Physiology

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Fibrosis is a common pathological condition associated with abnormal repair after tissue injury. However, the etiology and molecular mechanisms of fibrosis are still not well‐understood. Tumor necrosis factor (TNF)‐like weak inducer of apoptosis (TWEAK) belongs to the TNF superfamily and acts by binding to its receptor, fibroblast growth factor‐inducible 14 (Fn14), thereby activating a variety of intracellular signal transduction pathways in various types of cells. Besides promoting the expression of growth factors, activation of TWEAK/Fn14 signaling after tissue injury can promote the expression of pro‐inflammatory cytokines, which trigger the immune response, thereby exacerbating the injury. Severe or repetitive injury leads to a dysregulated tissue repair process, in which the TWEAK/Fn14 axis promotes the activation and proliferation of myofibroblasts, induces the secretion of the extracellular matrix, and regulates profibrotic mediators to further perpetuate and sustain the fibrotic process. In this review, we summarize the available experimental evidence on the underlying molecular mechanisms by which the TWEAK/Fn14 pathway mediates the development and progression of fibrosis. In addition, we discuss the therapeutic potential of the TWEAK/Fn14 pathway in fibrosis‐associated diseases based on evidence derived from multiple models and cells from injured tissue and fibrotic tissue.

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Tumor necrosis factor-like weak inducer of apoptosis association with proliferative diabetic retinopathy and promotes proliferation and collagen synthesis in retinal ARPE-19 cells

Cited by 4 publications

References 34 publications

miRNA-1273g-3p Involvement in Development of Diabetic Retinopathy by Modulating the Autophagy-Lysosome Pathway

miRNA-1273g-3p Involvement in Development of Diabetic Retinopathy by Modulating the Autophagy-Lysosome Pathway

Vitreous Olink proteomics reveals inflammatory biomarkers for diagnosis and prognosis of traumatic proliferative vitreoretinopathy

TWEAK/Fn14 axis is an important player in fibrosis

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