Protection of tight junction between RPE cells with tissue factor targeting peptide

Zou, Xiulan; Wang, Guan‐Feng; Li, Dandan; Chen, Jing-Xia; Zhang, Chunli; Yu, Yong-Zhen; Zhou, Wenjie; Zou, Yao; Rao, Benqiang

doi:10.18240/ijo.2018.10.04

Cited by 7 publications

(5 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Specifically, ARPE-19 cells, in response to oxidative stress or inflammation, induced by the addition of H 2 O 2 or LPS, revealed partial loss and damage of their junctional integrity. This is in line with previous studies whereby exposure of ARPE-19 cells to the same stress inducers resulted in reduced expression of ZO-1 protein, more disorganized tight junctions with breaks in peripheral staining [36,44,45]. Additionally, our results demonstrated that application of N and ND to the media counteracted these morphological changes.…”

Section: Discussionsupporting

confidence: 93%

Anti-Inflammatory and Anti-Oxidative Synergistic Effect of Vitamin D and Nutritional Complex on Retinal Pigment Epithelial and Endothelial Cell Lines against Age-Related Macular Degeneration

et al. 2021

View full text Add to dashboard Cite

Age-related macular degeneration (AMD) is a multifactorial disease of the retina featured by dysfunction of retinal pigmented epithelial (RPE) and loss of photoreceptor cells under oxidative stress and inflammatory conditions. Vitamin D and antioxidants have beneficial effects against retinal degenerative diseases, such as AMD. We investigated the impact of associating vitamin D (ND) with a nutritional antioxidant complex (Nutrof Total®; N) on oxidative stress and inflammation-like induced conditions by H2O2 and LPS, respectively, in human retinal epithelial (ARPE-19) and human retinal endothelial (HREC) cells. Application of either N or ND treatments to H2O2-induced media in ARPE-19 cells counteracted late apoptosis, attenuated oxidative DNA damage, and increased cell proliferation. Significant reduction in the expression levels of MCP1, IL-8, and IL6 cytokines was observed following application of either N or ND treatments under LPS-induced conditions in ARPE-19 cells and in MCP-1 and IL12p70 cytokine levels in HREC cells. ND and not N revealed significant downregulation of IFNγ in ARPE-19 cells, and of IL-6 and IL-18 in HREC cells. In conclusion, adding vitamin D to Nutrof Total® protects in a synergistic way against oxidative and inflammatory stress-induced conditions in retinal epithelial and endothelial cells.

show abstract

Section: Discussionsupporting

confidence: 93%

Anti-Inflammatory and Anti-Oxidative Synergistic Effect of Vitamin D and Nutritional Complex on Retinal Pigment Epithelial and Endothelial Cell Lines against Age-Related Macular Degeneration

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Moreover, several studies demonstrated that some retinal diseases such as AMD are characterized by the abnormal expression and irregular distribution of tight junction proteins in RPE cells ( Du et al, 2013 ). Hence, it is well known that LPS affects the epithelial integrity ( Zheng et al, 2018 ; He et al, 2019 ), reducing the expression of ZO-1 protein and diminishing TEER values, in ARPE-19 cell monolayers ( Chen et al, 2017 ; Zou et al, 2018 ; Hernandez et al, 2021 ). In this study, we confirmed that the LPS insult reduced the ARPE-19 monolayer integrity, as shown by instrumental (TEER measurements), spectroscopic (NaF permeability assays), and immunocytochemistry analyses.…”

Section: Discussionmentioning

confidence: 99%

Caffeine Protects Against Retinal Inflammation

et al. 2022

View full text Add to dashboard Cite

Caffeine, one of the most consumed central nervous system (CNS) stimulants, is an antagonist of A1 and A2A adenosine receptors. In this study, we investigated the potential protective effects of this methylxanthine in the retinal tissue. We tested caffeine by using in vitro and in vivo paradigms of retinal inflammation. Human retinal pigment epithelial cells (ARPE-19) were exposed to lipopolysaccharide (LPS) with or without caffeine. This latter was able to reduce the inflammatory response in ARPE-19 cells exposed to LPS, attenuating the release of IL-1β, IL-6, and TNF-α and the nuclear translocation of p-NFκB. Additionally, caffeine treatment restored the integrity of the ARPE-19 monolayer assessed by transepithelial electrical resistance (TEER) and the sodium fluorescein permeability test. Finally, the ischemia reperfusion (I/R) injury model was used in C57BL/6J mice to induce retinal inflammation and investigate the effects of caffeine treatment. Mouse eyes were treated topically with caffeine, and a pattern electroretinogram (PERG) was used to assess the retinal ganglion cell (RGC) function; furthermore, we evaluated the levels of IL-6 and BDNF in the retina. Retinal BDNF dropped significantly (p < 0.05) in the I/R group compared to the control group (normal mice); on the contrary, caffeine treatment maintained physiological levels of BDNF in the retina of I/R eyes. Caffeine was also able to reduce IL-6 mRNA levels in the retina of I/R eyes. In conclusion, these findings suggest that caffeine is a good candidate to counteract inflammation in retinal diseases.

show abstract

“…Manu studies have shown that bioactive peptides can improve the intestinal barrier and that bioactive peptides can regulate the expression of ZO-1 and MUC-2. Zou has researched the protective function of the intestinal tight junction with tissue factor-related peptides ( 44 ). The effect of shrimp peptide on the intestinal barrier of cyclophosphamide-treated mice was detected, and the results revealed the peptide could increase tight-junction-associated proteins ( 45 ).…”

Section: Discussionmentioning

confidence: 99%

Protective effects and potential mechanisms of fermented egg-milk peptides on the damaged intestinal barrier

et al. 2022

View full text Add to dashboard Cite

IntroductionFermented egg-milk peptides (FEMPs) could enhance the colon-intestinal barrier and upgrade the expression of zonula occludens-1 and mucin 2. Besides, the underlying biological mechanism and the targets FEMPs could regulate were analyzed in our study.MethodsHerein, the immunofluorescence technique and western blot were utilized to evaluate the repair of the intestinal barrier. Network pharmacology analysis and bioinformatics methods were performed to investigate the targets and pathways affected by FEMPs.Results and discussionAnimal experiments showed that FEMPs could restore intestinal damage and enhance the expression of two key proteins. The pharmacological results revealed that FEMPs could regulate targets related to kinase activity, such as AKT, CASP, RAF, and GSK. The above targets could interact with each other. GO analysis indicated that the targets regulated by FEMPs could participate in the kinase activity of the metabolic process. KEGG enrichment revealed that the core targets were enriched in pathways related to cell apoptosis and other important procedures. Molecular docking demonstrated that FEMPs could bind to the key target AKT via hydrogen bond interactions. Our study combined the experiment in vivo with the method in silico and investigated the interaction between peptides and targets in a pattern of multi-targets and multi-pathways, which offered a new perspective on the functional validation and potential application of bioactive peptides.

show abstract

Protection of tight junction between RPE cells with tissue factor targeting peptide

Cited by 7 publications

References 26 publications

Anti-Inflammatory and Anti-Oxidative Synergistic Effect of Vitamin D and Nutritional Complex on Retinal Pigment Epithelial and Endothelial Cell Lines against Age-Related Macular Degeneration

Anti-Inflammatory and Anti-Oxidative Synergistic Effect of Vitamin D and Nutritional Complex on Retinal Pigment Epithelial and Endothelial Cell Lines against Age-Related Macular Degeneration

Caffeine Protects Against Retinal Inflammation

Protective effects and potential mechanisms of fermented egg-milk peptides on the damaged intestinal barrier

Contact Info

Product

Resources

About