Tissue Barriers最新文献

Frataxin deficiency and the pathology of Friedreich's Ataxia across tissues.

IF 3.6

Tissue Barriers Pub Date : 2025-02-21 DOI: 10.1080/21688370.2025.2462357

Wesley S Ercanbrack, Mateo Ramirez, Austin Dungan, Ella Gaul, Sarah J Ercanbrack, Rebecca A Wingert

引用次数: 0

β-arrestin 1 and integrin-linked kinase interact in epidermal keratinocytes and regulate cell motility.

IF 3.6

Tissue Barriers Pub Date : 2025-02-13 DOI: 10.1080/21688370.2025.2465048

Hannah Murphy-Marshman, Iordanka A Ivanova, Moshmi Bhattacharya, Lina Dagnino

{"title":"β-arrestin 1 and integrin-linked kinase interact in epidermal keratinocytes and regulate cell motility.","authors":"Hannah Murphy-Marshman, Iordanka A Ivanova, Moshmi Bhattacharya, Lina Dagnino","doi":"10.1080/21688370.2025.2465048","DOIUrl":"https://doi.org/10.1080/21688370.2025.2465048","url":null,"abstract":"Arrestins and integrin-linked kinase (ILK) are important scaffold proteins that regulate myriad cell functions in metazoans. β-arrestins, first identified as critical components in G-protein-coupled receptor (GPCR) signaling pathways, participate in inflammatory, immunomodulatory and tissue repair processes in GPCR-dependent and -independent manners. ILK is a central mediator of signaling cascades elicited by activation of integrins, regulating cell motility, proliferation, and mechanotransduction. In the epidermis, ILK is essential for maintenance of barrier function, hair follicle development, melanocyte colonization and regeneration after injury. In this tissue, β-arrestin 2 mitigates inflammatory processes and development of allergic dermatitis, which also is associated with loss of epidermal barrier function. However, the functional role of β-arrestin 1 in epidermal cells is poorly understood. We now report that β-arrestin 1 directly binds ILK, forming hitherto unidentified protein complexes in epidermal keratinocytes. In the absence of exogenous GPCR ligand stimulation, β-arrestin 1 and ILK are found throughout the cytoplasm in epidermal keratinocytes, and also co-localize to plasma membrane regions associated with cell protrusions. Inactivation of the genes that encode both β-arrestin 1 and 2 attenuates forward cell migration, whereas expression of ILK together with β-arrestin 1 restores cell motility. The cooperative effect of ILK and β-arrestin 1 in promoting directional cell migration may have important implications for epidermal regeneration and reestablishment of barrier function after injury.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2465048"},"PeriodicalIF":3.6,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143411053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Ephrin-Eph signaling: an important regulator of epithelial integrity and barrier function.

IF 3.6

Tissue Barriers Pub Date : 2025-02-08 DOI: 10.1080/21688370.2025.2462855

Mohan Liu, Joseph G Charek, Rodolfo D Vicetti Miguel, Thomas L Cherpes

{"title":"Ephrin-Eph signaling: an important regulator of epithelial integrity and barrier function.","authors":"Mohan Liu, Joseph G Charek, Rodolfo D Vicetti Miguel, Thomas L Cherpes","doi":"10.1080/21688370.2025.2462855","DOIUrl":"10.1080/21688370.2025.2462855","url":null,"abstract":"Eph receptor-interacting proteins (ephrin) ligands and their erythropoietin-producing human hepatocellular (Eph) receptors elicit bidirectional signals that regulate cell migration, angiogenesis, neuronal plasticity, and other developmental processes in the embryo. In adulthood, ephrin-Eph signaling regulates numerous homeostatic events, including epithelial cell proliferation and differentiation. Epithelial surfaces, including those of skin and vagina, are lined by layers of stratified squamous epithelium (SSE) that protect against mechanical stress and microbial pathogen invasion. Ephrin-Eph signaling is known to promote cutaneous epithelial barrier function by regulating the expression of specialized cell-cell adhesion junctions termed desmosomes, but the role of this signaling system in maintaining epithelial integrity and barrier function in the vagina is less explored. This review summarizes current understanding of ephrin-Eph signaling that regulates desmosome expression and barrier function in the skin and considers evidence that suggests ephrin-Eph signaling similarly regulates these processes in vaginal SSE.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2462855"},"PeriodicalIF":3.6,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Size-selective permeation-enhancing modulation of the tight junction by receptor-binding domains of Clostridium perfringens enterotoxin and Clostridium perfringens iota-toxin.

IF 3.6

Tissue Barriers Pub Date : 2025-02-05 DOI: 10.1080/21688370.2025.2459963

Keisuke Tachibana, Sayaka Sugimura, Shuko Sakimura, Lin Bai, Hiroshi Aoyama, Hiroyuki Takeda, Yuki Niwa, Masahiro Nagahama, Masuo Kondoh

{"title":"Size-selective permeation-enhancing modulation of the tight junction by receptor-binding domains of Clostridium perfringens enterotoxin and Clostridium perfringens iota-toxin.","authors":"Keisuke Tachibana, Sayaka Sugimura, Shuko Sakimura, Lin Bai, Hiroshi Aoyama, Hiroyuki Takeda, Yuki Niwa, Masahiro Nagahama, Masuo Kondoh","doi":"10.1080/21688370.2025.2459963","DOIUrl":"https://doi.org/10.1080/21688370.2025.2459963","url":null,"abstract":"Modulation of claudin-based bicellular tight junction (TJ) and angulin-based tricellular TJ seals has been shown to enhance mucosal permeation of macromolecules, by using the receptor-binding fragments of Clostridium perfringens enterotoxin (C-CPE194, C-CPEmt, and C-CPEm19) and Clostridium perfringens iota-toxin (angubindin-1) as claudin modulators and an angulin modulator, respectively. Here, we compared the activity of these modulators on the TJ in human intestinal Caco-2 cells. All the claudin modulators loosened TJ integrity more potently compared to angubindin-1 with the order of potency being C-CPEm19 > C-CPE194 > C-CPEmt, and results for permeation enhancement were similar. Treatment with C-CPEmt and C-CPE194 at 100 µg/mL for 48 h enhanced the permeation of dextran sized 20 kDa and 70 kDa, respectively. Treatment with C-CPEm19 at 30 µg/mL for 48 h enhanced permeation of dextran with a molecular mass of up to 150 kDa. Furthermore, co-treatment of bicellular TJ modulators, such as C-CPEmt, C-CPE194, and C-CPEm19, and tricellular TJ modulators, such as angubindin-1, showed additive TJ-loosening and permeation-enhancing activities compared with individual treatments; specifically, C-CPEm19 and angubindin-1 co-treatment increased permeation of large molecules (70 kDa and 150 kDa). These findings indicate that TJ modulators may be used as size-selective permeation enhancers.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2459963"},"PeriodicalIF":3.6,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143256837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Fistula in Crohn's disease: classification, pathogenesis, and treatment options.

IF 3.6

Tissue Barriers Pub Date : 2025-01-31 DOI: 10.1080/21688370.2025.2458784

Kimia Basiji, Nesa Kazemifard, Maryam Farmani, Kasra Jahankhani, Shaghayegh Baradaran Ghavami, Amir Fallahnia, Hesameddin Eghlimi, Adil Mir

{"title":"Fistula in Crohn's disease: classification, pathogenesis, and treatment options.","authors":"Kimia Basiji, Nesa Kazemifard, Maryam Farmani, Kasra Jahankhani, Shaghayegh Baradaran Ghavami, Amir Fallahnia, Hesameddin Eghlimi, Adil Mir","doi":"10.1080/21688370.2025.2458784","DOIUrl":"https://doi.org/10.1080/21688370.2025.2458784","url":null,"abstract":"Crohn's disease is a form of inflammation that affects the gastrointestinal (GI) tract. It is characterized by persistent inflammation in the gut, which can lead to the formation of abnormal connections called fistulas. These fistulas can occur between the GI tract and the abdominal cavity, adjacent organs, or the skin. The most prevalent type of fistula in Crohn's disease patients is the perianal fistula, which forms between the rectum and the skin near the anus. Although the exact cause of fistula formation is not fully understood, research suggests that factors such as epithelial to mesenchymal transition, matrix metalloproteinase, immune system dysregulation, and microbiota may contribute to their development. There is currently no definitive treatment for fistula closure, but options include surgery, endoscopic procedures, antibiotics, biologic agents, and immunosuppressive drugs. These treatments can be used alone or in combination. However, recurrence is a significant challenge that needs to be addressed in the case of fistula treatment. This review provides an overview of the common types of fistulas, their characteristics, the main factors and mechanisms of fistula formation, and available therapeutic options.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2458784"},"PeriodicalIF":3.6,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143068209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cell-cell crosstalk in the pathogenesis of acute lung injury and acute respiratory distress syndrome. 细胞-细胞串扰在急性肺损伤和急性呼吸窘迫综合征发病机制中的作用。

IF 3.6

Tissue Barriers Pub Date : 2025-01-11 DOI: 10.1080/21688370.2025.2452082

Zhenzhen Zhu, Ying Zhang, Huan Chen, Huali Zhang

引用次数: 0

Claudins in vulvar cancer - from epithelial barrier to potential tumor-agnostic cancer therapy. 外阴癌中的cladin -从上皮屏障到潜在的肿瘤不可知的癌症治疗。

IF 3.6

Tissue Barriers Pub Date : 2024-12-25 DOI: 10.1080/21688370.2024.2444724

Gilbert Georg Klamminger, Annick Bitterlich, Meletios P Nigdelis, Martin Ertz, Kim Yoo-Jin, Annette Hasenburg, Mathias Wagner

引用次数: 0

Treatment with TNFα and lipolysis-stimulated lipoprotein receptor (LSR) antibody in the presence of HDAC inhibitors promotes apoptosis in human salivary duct adenocarcinoma. 在HDAC抑制剂存在的情况下，用TNFα和脂肪酶刺激脂蛋白受体（LSR）抗体治疗可促进人唾液管腺癌的细胞凋亡。

IF 3.6

Tissue Barriers Pub Date : 2024-12-16 DOI: 10.1080/21688370.2024.2437215

Soshi Nishida, Takumi Konno, Takayuki Kohno, Masahiko Ohyanagi, Masaya Nakano, Kizuku Ohwada, Kazufumi Obata, Takuya Kakuki, Akito Kakiuchi, Makoto Kurose, Kenichi Takano, Takashi Kojima

{"title":"Treatment with TNFα and lipolysis-stimulated lipoprotein receptor (LSR) antibody in the presence of HDAC inhibitors promotes apoptosis in human salivary duct adenocarcinoma.","authors":"Soshi Nishida, Takumi Konno, Takayuki Kohno, Masahiko Ohyanagi, Masaya Nakano, Kizuku Ohwada, Kazufumi Obata, Takuya Kakuki, Akito Kakiuchi, Makoto Kurose, Kenichi Takano, Takashi Kojima","doi":"10.1080/21688370.2024.2437215","DOIUrl":"https://doi.org/10.1080/21688370.2024.2437215","url":null,"abstract":"Lipolysis-stimulated lipoprotein receptor (LSR), a lipid metabolism-related factor localized in tricellular tight junctions (tTJs), plays an important role in maintaining the epithelial homeostasis. LSR is highly expressed in well-differentiated cancers, and its expression decreases during malignancy. The LSR antibody inhibits cell growth and promotes apoptosis in some cancers. Histone deacetylases (HDACs) are thought to play a crucial role in carcinogenesis, and HDAC inhibitors promote differentiation and prevent cell proliferation and migration in cancers. HDAC inhibitors together with TNFα also induce apoptosis via TNFα-related apoptosis-inducing ligand (TRAIL) in some cancers. In this study, we investigated the apoptosis signaling induced by an anti-LSR antibody in human salivary duct adenocarcinoma (SDC) cell line A253, compared to TRAIL-induced apoptosis. A253 cells were treated with human recombinant TNFα with or without HDAC inhibitor trichostatin A (TSA) and quisinostat (JNJ-26481585). Treatment using TNFα with HDAC inhibitors markedly induced apoptosis in A253 cells and the anti-TNFα antibody prevented the induced apoptosis. A253 cells were treated with an antibody against the extracellular N-terminal domain of human LSR (LSR-N-ab) with or without HDAC inhibitors. Treatment with HDAC inhibitors induced LSR expression in the membranes of A253 cells. Treatment using LSR-N-ab with HDAC inhibitors markedly promoted apoptosis in A253 cells. The tricellular signaling pathway JNK inhibitor SP600125 and Hippo pathway MST1/2 inhibitor XMU-MP-1 prevented the apoptosis induced by treatment using TNFα or LSR-N-ab with HDAC inhibitors. Our findings indicated that treatment with TNFα or LSR-N-ab with HDAC inhibitors might be useful in the therapy for human SDC by enhancing apoptosis.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2437215"},"PeriodicalIF":3.6,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142830086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction. 修正。

IF 3.6

Tissue Barriers Pub Date : 2024-12-11 DOI: 10.1080/21688370.2024.2440987

引用次数: 0

Unfolded protein response modulates the effects of GHRH antagonists in experimental models of in vivo and in vitro lung injury. 未折叠蛋白反应调节GHRH拮抗剂在体内和体外肺损伤实验模型中的作用。

IF 3.6

Tissue Barriers Pub Date : 2024-12-09 DOI: 10.1080/21688370.2024.2438974

Saikat Fakir, Khadeja-Tul Kubra, Mohammad Shohel Akhter, Mohammad Afaz Uddin, Md Matiur Rahman Sarker, Agnieszka Siejka, Nektarios Barabutis

{"title":"Unfolded protein response modulates the effects of GHRH antagonists in experimental models of in vivo and in vitro lung injury.","authors":"Saikat Fakir, Khadeja-Tul Kubra, Mohammad Shohel Akhter, Mohammad Afaz Uddin, Md Matiur Rahman Sarker, Agnieszka Siejka, Nektarios Barabutis","doi":"10.1080/21688370.2024.2438974","DOIUrl":"10.1080/21688370.2024.2438974","url":null,"abstract":"The development of efficient targeted therapies to ameliorate endothelial disorders is of the utmost need, as evident by the devastating outcomes of the recent pandemic. Recent findings suggest that unfolded protein response (UPR) modulates barrier function. In the current study, we reveal that the aforementioned highly conservative mechanism is involved in the protective effects of growth hormone-releasing hormone antagonists (GHRHAnt) in lung injury, both in vivo and in vitro. In bovine pulmonary artery endothelial cells, UPR suppression counteracted the protective effects of GHRHAnt in lipopolysaccharide (LPS)-induced endothelial hyperpermeability. In mouse lungs, UPR activation enhanced the beneficial effects of GHRHAnt against LPS-induced acute lung injury. Our observations - which are focused on lung endothelial cells and tissues - enhance our knowledge on the mechanisms mediating the barrier function and contribute to the development of novel therapies toward sepsis, direct and indirect lung injury. The effects of UPR modulation on the effects of GHRHAnt in other tissues are unknown, and they are the subject of future investigations.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2438974"},"PeriodicalIF":3.6,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142802360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0