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The Role of Tight Junction Proteins in Health and Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 30 July 2024 | Viewed by 2430

Special Issue Editor


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Guest Editor
Department of Parasitology and Genetics, College of Medicine, Kosin University, Busan 49104, Republic of Korea
Interests: molecular function of tight junction proteins; CRISPR Cas 9 gene knock out; functional genomics of human endogenous retrovirus
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Tight junction proteins are critical to the integrity and selective permeability of epithelial and endothelial barriers in various tissues and organs, creating tight seals between adjacent cells, controlling the passage of ions, molecules, and pathogens across cell layers. Tight junctions also contribute to tissue homeostasis, nutrient absorption, and immune response regulation in the human body. However, dysregulation of these proteins can lead to a range of diseases: increased permeability may result in inflammatory disorders, autoimmune diseases, and infections, while excessive tightness may hinder nutrient absorption or promote tumor metastasis. Understanding the role of tight junction proteins in health and disease is vital to the development of targeted therapies to address various pathological conditions related to their dysfunction.

Dr. Hee-Jae Cha
Guest Editor

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Keywords

  • tight junction protein
  • health
  • disease
  • selective permeability
  • cancer

Published Papers (2 papers)

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18 pages, 1462 KiB  
Article
Functional Analysis of Membrane-Associated Scaffolding Tight Junction (TJ) Proteins in Tumorigenic Characteristics of B16-F10 Mouse Melanoma Cells
by Eun-Ji Ko, Do-Ye Kim, Min-Hye Kim, Hyojin An, Jeongtae Kim, Jee-Yeong Jeong, Kyoung Seob Song and Hee-Jae Cha
Int. J. Mol. Sci. 2024, 25(2), 833; https://doi.org/10.3390/ijms25020833 - 9 Jan 2024
Viewed by 1020
Abstract
Tight junction (TJ) proteins (Tjps), Tjp1 and Tjp2, are tight junction-associated scaffold proteins that bind to the transmembrane proteins of tight junctions and the underlying cytoskeleton. In this study, we first analyzed the tumorigenic characteristics of B16-F10 melanoma cells, including cell proliferation, migration, [...] Read more.
Tight junction (TJ) proteins (Tjps), Tjp1 and Tjp2, are tight junction-associated scaffold proteins that bind to the transmembrane proteins of tight junctions and the underlying cytoskeleton. In this study, we first analyzed the tumorigenic characteristics of B16-F10 melanoma cells, including cell proliferation, migration, invasion, metastatic potential, and the expression patterns of related proteins, after the CRISPR–Cas9-mediated knockout (KO) of Tjp genes. The proliferation of Tjp1 and Tjp2 KO cells significantly increased in vitro. Other tumorigenic characteristics, including migration and invasion, were significantly enhanced in Tjp1 and Tjp2 KO cells. Zonula occludens (ZO)-associated protein Claudin-1 (CLDN-1), which is a major component of tight junctions and functions in controlling cell-to-cell adhesion, was decreased in Tjp KO cells. Additionally, Tjp KO significantly stimulated tumor growth and metastasis in an in vivo mouse model. We performed a transcriptome analysis using next-generation sequencing (NGS) to elucidate the key genes involved in the mechanisms of action of Tjp1 and Tjp2. Among the various genes affected by Tjp KO-, cell cycle-, cell migration-, angiogenesis-, and cell–cell adhesion-related genes were significantly altered. In particular, we found that the Ninjurin-1 (Ninj1) and Catenin alpha-1 (Ctnna1) genes, which are known to play fundamental roles in Tjps, were significantly downregulated in Tjp KO cells. In summary, tumorigenic characteristics, including cell proliferation, migration, invasion, tumor growth, and metastatic potential, were significantly increased in Tjp1 and Tjp2 KO cells, and the knockout of Tjp genes significantly affected the expression of related proteins. Full article
(This article belongs to the Special Issue The Role of Tight Junction Proteins in Health and Disease)
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13 pages, 8583 KiB  
Article
Effect of Polycan, a β-Glucan from Aureobasidium pullulans SM-2001, on Inflammatory Response and Intestinal Barrier Function in DSS-Induced Ulcerative Colitis
by Hyun Ju Do, Young-Suk Kim and Tae Woo Oh
Int. J. Mol. Sci. 2023, 24(19), 14773; https://doi.org/10.3390/ijms241914773 - 30 Sep 2023
Cited by 1 | Viewed by 1099
Abstract
Ulcerative colitis (UC), a subtype of inflammatory bowel disease, is a chronic gastrointestinal inflammatory disease with unclear etiology and pathophysiology. Herein, we determined the effects of extracellular polysaccharides purified from Aureobasidium pullulans SM-2001 (Polycan) on tight junction protein expression, inflammation, and apoptosis in [...] Read more.
Ulcerative colitis (UC), a subtype of inflammatory bowel disease, is a chronic gastrointestinal inflammatory disease with unclear etiology and pathophysiology. Herein, we determined the effects of extracellular polysaccharides purified from Aureobasidium pullulans SM-2001 (Polycan) on tight junction protein expression, inflammation, and apoptosis in a dextran sodium sulfate (DSS)-induced acute colitis model. Fifty mice were divided into normal, DSS, DSS + Polycan 250 mg/kg (Polycan 250), DSS + Polycan 500 mg/kg (Polycan 500), and DSS + 5-aminosalicylic acid 100 mg/kg (5-ASA) groups. Their body weights, colon lengths, histological changes in colon tissue, and tight junction function were observed. Results showed that Polycan 250, Polycan 500, and 5-ASA significantly inhibited body weight loss compared with DSS. Similar to 5-ASA, Polycan 500 exhibited preventive effects on colon length shortening and histological changes in colon tissues. Polycan inhibited the DSS-induced decrease in fluorescein isothiocyanate-dextran permeability and myeloperoxidase activity. Moreover, Polycan significantly recovered serum cytokine (e.g., tumor necrosis factor-α, interleukin (IL)-6, and IL-1β) or mRNA expression in colon tissue compared with DSS. Polycan also inhibited apoptosis by reducing caspase-3 activity and the Bcl-2 associated X/B-cell lymphoma 2 (Bcl-2) ratio. Additionally, DSS treatment significantly reduced microbial abundance and diversity, but the administration of Polycan reversed this effect. Collectively, Polycan protected intestinal barrier function and inhibited inflammation and apoptosis in DSS-induced colitis. Full article
(This article belongs to the Special Issue The Role of Tight Junction Proteins in Health and Disease)
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