Tight Junctions in Cell Proliferation

Díaz-Coránguez, Mónica; Liu, Xuwen; Antonetti, David A.

doi:10.3390/ijms20235972

Cited by 62 publications

(42 citation statements)

References 188 publications

(210 reference statements)

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“…The TAMP (TJ-associated MARVEL protein) family members include occludin (MarvelD1), tricellulin (MarvelD2), and MarvelD3 [19,20]. They contain a conserved four-transmembrane MARVEL (Mal and related proteins for vesicle trafficking and membrane link) domain [21].…”

Section: Tight Junctions (Tjs)mentioning

confidence: 99%

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Tight Junctions of the Outer Blood Retina Barrier

Naylor

Hopkins

Hudson

et al. 2019

IJMS

123

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The outer blood retina barrier (oBRB) formed by the retinal pigment epithelium (RPE) is critical for maintaining retinal homeostasis. Critical to this modified neuro-epithelial barrier is the presence of the tight junction structure that is formed at the apical periphery of contacting cells. This tight junction complex mediates size-selective passive diffusion of solutes to and from the outer segments of the retina. Unlike other epithelial cells, the apical surface of the RPE is in direct contact with neural tissue and it is centrally involved in the daily phagocytosis of the effete tips of photoreceptor cells. While much is known about the intracellular trafficking of material within the RPE, less is known about the role of the tight junction complexes in health and diseased states. Here, we provide a succinct overview of the molecular composition of the RPE tight junction complex in addition to highlighting some of the most common retinopathies that involve a dysregulation of RPE integrity

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Section: Tight Junctions (Tjs)mentioning

confidence: 99%

“…They contain a conserved four-transmembrane MARVEL (Mal and related proteins for vesicle trafficking and membrane link) domain [21]. Occludin, tricellulin, and marvelD3 have both redundant and unique contributions to epithelial function [19,20]. Occludin was the first transmembrane protein identified in the TJ.…”

Section: Tight Junctions (Tjs)mentioning

confidence: 99%

Tight Junctions of the Outer Blood Retina Barrier

Naylor

Hopkins

Hudson

et al. 2019

IJMS

123

View full text Add to dashboard Cite

show abstract

“…Epithelial cells establish tight junctions (TJs) at the lateral membrane between neighboring cells. The TJs are involved in the regulation of cell proliferation, polarization, differentiation, and polarity [ 10 , 11 ]. In addition, they rigorously regulate the paracellular flux of solutes and ions.…”

Section: Introductionmentioning

confidence: 99%

Down-Regulation of Claudin-2 Expression by Cyanidin-3-Glucoside Enhances Sensitivity to Anticancer Drugs in the Spheroid of Human Lung Adenocarcinoma A549 Cells

Eguchi

Matsunaga

Onuma

et al. 2021

IJMS

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Claudin-2 (CLDN2), an integral membrane protein located at tight junctions, is abnormally expressed in human lung adenocarcinoma tissues, and is linked to drug resistance in human lung adenocarcinoma A549 cells. CLDN2 may be a target for the prevention of lung adenocarcinoma, but there are few compounds which can reduce CLDN2 expression. We found that cyanidin-3-glucoside (C3G), the anthocyanin with two hydroxyl groups on the B-ring, and cyanidin significantly reduce the protein level of CLDN2 in A549 cells. In contrast, pelargonidin-3-glucoside (P3G), the anthocyanin with one hydroxyl group on the B-ring, had no effect. These results suggest that cyanidin and the hydroxyl group at the 3-position on the B-ring play an important role in the reduction of CLDN2 expression. The phosphorylation of Akt, an activator of CLDN2 expression at the transcriptional level, was inhibited by C3G, but not by P3G. The endocytosis and lysosomal degradation are suggested to be involved in the C3G-induced decrease in CLDN2 protein expression. C3G increased the phosphorylation of p38 and the p38 inhibitor SB203580 rescued the C3G-induced decrease in CLDN2 expression. In addition, SB203580 rescued the protein stability of CLDN2. C3G may reduce CLDN2 expression at the transcriptional and post-translational steps mediated by inhibiting Akt and activating p38, respectively. C3G enhanced the accumulation and cytotoxicity of doxorubicin (DXR) in the spheroid models. The percentages of apoptotic and necrotic cells induced by DXR were increased by C3G. Our data suggest that C3G-rich foods can prevent the chemoresistance of lung adenocarcinoma A549 cells through the reduction of CLDN2 expression.

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“…Rap1 and Ras are all the downstream of ERK signaling as well as a part of MAPK signaling pathway [50], which can manipulate the transdifferentiation of BMSCs into IPCs by targeting FOS [51] to nally effect proliferation and differentiation of cells [52]. Cell junction and cell adhesion molecules can form a barrier with selection of small molecules, water and proteins to in and out cells to regulate cell differentiation [53,54]. Under a nonadherent state during induction, cells exhibit similar protein expression pattern and intercellular junctions with organs in vivo [55], which means that cells could in uence other cells via paracrine factors like EGF, VEGF, etc.…”

Section: Discussionmentioning

confidence: 99%

Transcriptome Analysis of the Transdifferentiation of canine BMSCs into Insulin Producing Cells

WANG

Dai

Zou

et al. 2020

Preprint

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Background Bone marrow mesenchymal stem cells are a potential resource for the clinical therapy of certain diseases. Canine, as a companion animal, living in the same space with human, is an ideal new model for human diseases research. Because of the high prevalence of diabetes, alternative transplantation islets resource (i.e. insulin producing cells) for diabetes treatment will be in urgent need, which makes our research on the transdifferentiation of Bone marrow mesenchymal stem cells into insulin producing cells become more important.Result In this study, we completed the transdifferentiation process and achieved the transcriptome profiling of five samples with two biological duplicates, namely, “BMSCs”, “islets”, “stage1”, “stage2” and “stage3”, and the latter three samples were achieved on the second, fifth and eighth day of induction. A total of 11,530 differentially expressed transcripts were revealed in the profiling data. The enrichment analysis of differentially expressed genes revealed several signaling pathways that are essential for regulating proliferation and transdifferentiation, including focal adhesion, ECM–receptor interaction, tight junction, protein digestion and absorption, and the Rap1 signaling pathway. Meanwhile, the obtained protein–protein interaction network and functional identification indicating involvement of three genes, SSTR2, RPS6KA6, and VIP could act as a foundation for further research.Conclusion In conclusion, to the best of our knowledge, this is the first survey of the transdifferentiation of canine BMSCs into insulin-producing cells according with the timeline using next-generation sequencing technology. The three key genes we pick out may regulate decisive genes during the development of transdifferentiation.

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Tight Junctions in Cell Proliferation

Cited by 62 publications

References 188 publications

Tight Junctions of the Outer Blood Retina Barrier

Tight Junctions of the Outer Blood Retina Barrier

Down-Regulation of Claudin-2 Expression by Cyanidin-3-Glucoside Enhances Sensitivity to Anticancer Drugs in the Spheroid of Human Lung Adenocarcinoma A549 Cells

Transcriptome Analysis of the Transdifferentiation of canine BMSCs into Insulin Producing Cells

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