MicroRNA-126 Reduces Blood-Retina Barrier Breakdown via the Regulation of VCAM-1 and BCL2L11 in Ischemic Retinopathy

Bai, Xueshi; Luo, Junpeng; Zhang, Xiaofeng; Han, Jingjing; Wang, Zhaoyue; Miao, J.; Bai, Yanyan

doi:10.1159/000454716

Cited by 18 publications

(14 citation statements)

References 49 publications

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“…We could find miR‐126 as one of the glomerular endothelial cell‐specific miRs in our screening. Well in line with this finding, miR‐126 was already described as an endothelial cell‐specific miR that governs vascular integrity in other tissue …”

Section: Discussionsupporting

confidence: 54%

Identification of cell and disease specific microRNAs in glomerular pathologies

Müller-Deile

Dannenberg

Liu

et al. 2019

J Cellular Molecular Medi

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MicroRNAs (miRs) are small non‐coding RNAs that regulate gene expression in physiological processes as well as in diseases. Currently miRs are already used to find novel mechanisms involved in diseases and in the future, they might serve as diagnostic markers. To identify miRs that play a role in glomerular diseases urinary miR‐screenings are a frequently used tool. However, miRs that are detected in the urine might simply be filtered from the blood stream and could have been produced anywhere in the body, so they might be completely unrelated to the diseases. We performed a combined miR‐screening in pooled urine samples from patients with different glomerular diseases as well as in cultured human podocytes, human mesangial cells, human glomerular endothelial cells and human tubular cells. The miR‐screening in renal cells was done in untreated conditions and after stimulation with TGF‐β. A merge of the detected regulated miRs led us to identify disease‐specific, cell type‐specific and cell stress‐induced miRs. Most miRs were down‐regulated following the stimulation with TGF‐β in all cell types. Up‐regulation of miRs after TGF‐β was cell type‐specific for most miRs. Furthermore, urinary miRs from patients with different glomerular diseases could be assigned to the different renal cell types. Most miRs were specifically regulated in one disease. Only miR‐155 was up‐regulated in all disease urines compared to control and therefore seems to be rather unspecific. In conclusion, a combined urinary and cell miR‐screening can improve the interpretation of screening results. These data are useful to identify novel miRs potentially involved in glomerular diseases.

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Section: Discussionsupporting

confidence: 54%

Identification of cell and disease specific microRNAs in glomerular pathologies

Müller-Deile

Dannenberg

Liu

et al. 2019

J Cellular Molecular Medi

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show abstract

“…We could identify miR-126 as one of the glomerular endothelial cell-specific miRs in our screening. Well in line with this finding, miR-126 was already described as an endothelial cell-specific miR that governs vascular integrity in other tissue [20][21][22][23].…”

Section: Discussionsupporting

confidence: 56%

Identification of Cell-and Disease-Specific Micro RNAs in Glomerular Pathologies

Müller-Deile¹,

Dannenberg²,

P³

et al. 2017

J Mol Genet Med

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Background: MicroRNAs (miRs) are small non-coding RNAs that regulate gene expression in physiological processes as well as in diseases. Currently miRs are already used to find novel mechanisms involved in diseases and in the future, they might serve as diagnostic markers. To identify miRs that play a role in glomerular diseases urinary miR-screenings are a frequently used tool. However, miRs that are detected in the urine might simply be filtered from the blood stream and could have been produced anywhere in the body, so they might be completely unrelated to the diseases. Methods:We performed a combined miR-screening in pooled urine samples from patients with different glomerular diseases as well as in cultured human podocytes, human mesangial cells, human glomerular endothelial cells, and human tubular cells. The miR-screening in renal cells was done in untreated conditions and after stimulation with TGF-β.Results: A merge of the detected regulated miRs led us to identify disease-specific, cell type-specific and cell stress-induced miRs. Further, urinary miRs from patients with different glomerular diseases could be assigned to the different renal cell types. Conclusion:Thus, a combined urinary and cell miR-screening can improve the interpretation of screening results. These data are useful to identify novel miRs potentially involved in glomerular diseases.

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“…On the contrary, AhR activation via TCDD preserved BRB integrity, thereby reducing vascular leakage. BRB breakdown was further proven to be associated with apoptosis of retinal cells ( 47 ). In our study, AhR knockout increases cell apoptosis in mice of EAU, while AhR activation with TCDD inhibits apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Aryl Hydrocarbon Receptor Regulates Apoptosis and Inflammation in a Murine Model of Experimental Autoimmune Uveitis

Huang

Liang

et al. 2018

Front. Immunol.

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Uveitis is characterized as a common cause of blindness worldwide. Aryl hydrocarbon receptor (AhR), a ligand-activated nuclear receptor, has been implicated to play a role in human uveitis, although the exact mechanisms remain poorly understood. The purpose of this study was to enhance our knowledge concerning the role of AhR during intraocular inflammation. We immunized wild-type and AhR-knockout C57BL/6J mice with IRBP651–670 to induce experimental autoimmune uveitis (EAU). Disease severity was evaluated with both clinical and histopathological grading. Blood–retinal barrier (BRB) integrity was tested by Evans blue and tight junction proteins qualifications. Apoptosis was measured using TdT-mediated dUTP nick end labeling staining. Macrophage/microglia activation and polarization were studied by immunofluorescence and Western blot. Following EAU induction, AhR−/− mice had more severe clinical and histopathological manifestations of uveitis than AhR+/+ mice. Increased vascular permeability and apoptotic cells were observed in AhR−/− EAU mice when compared with AhR+/+ EAU mice. In addition, AhR−/− EAU mice showed evidence of a significantly increased macrophage/microglia cells and a stronger polarization from the M2 to the M1 phenotype as compared to AhR+/+ EAU mice. The levels of pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β were increased in AhR−/− EAU mice, which was associated with the activation of NF-κB and signal transducers and activators of transcription (STAT) pathways. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), an agonist of AhR, caused a significant decrease in the clinical and histopathological manifestations, preserved BRB integrity, reduced apoptotic cells, inhibited macrophage/microglia activation, and shifted their polarization from M1 toward M2. Moreover, decreased expression of pro-inflammatory cytokines including TNF-α, IL-6, and IL-1β and inhibition of NF-κB and STAT pathways were found in EAU mice following TCDD treatment. In conclusion, AhR activation with TCDD exhibits an immunomodulatory effect by reducing BRB breakdown, inhibiting retinal cell apoptosis, and reducing pro-inflammatory cytokine expression during EAU. The underlying mechanism may involve the modulation of macrophages/microglia polarization and the downregulation of NF-κB and STAT pathways.

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MicroRNA-126 Reduces Blood-Retina Barrier Breakdown via the Regulation of VCAM-1 and BCL2L11 in Ischemic Retinopathy

Cited by 18 publications

References 49 publications

Identification of cell and disease specific microRNAs in glomerular pathologies

Identification of cell and disease specific microRNAs in glomerular pathologies

Identification of Cell-and Disease-Specific Micro RNAs in Glomerular Pathologies

Aryl Hydrocarbon Receptor Regulates Apoptosis and Inflammation in a Murine Model of Experimental Autoimmune Uveitis

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