Tissue Barriers最新文献_第3页

HIV1-Nef perturbs the integrity of blood testis barrier in rat model. 在大鼠模型中，HIV1-Nef干扰了血睾屏障的完整性。

IF 3.6

Tissue Barriers Pub Date : 2025-01-02 Epub Date: 2024-05-22 DOI: 10.1080/21688370.2024.2357406

Deependra Singh, Saurabh Kumar, Rajnikant Mishra, Anjali, R K Tripathi, Monika Sachdev

{"title":"HIV1-Nef perturbs the integrity of blood testis barrier in rat model.","authors":"Deependra Singh, Saurabh Kumar, Rajnikant Mishra, Anjali, R K Tripathi, Monika Sachdev","doi":"10.1080/21688370.2024.2357406","DOIUrl":"10.1080/21688370.2024.2357406","url":null,"abstract":"The blood-testis barrier is a specialized feature within the mammalian testis, located in close proximity to the basement membrane of seminiferous tubules. This barrier serves to divide the seminiferous epithelium into distinct basal and adluminal (apical) compartments. The selectivity of the BTB to foreign particles makes it a safe haven for the virus, and the high affinity of HIV for testis might lead to the vertical transmission of the virus. In the present study, recombinant HIV1-Nef (rNef) protein was injected intravenously to examine the effect of rNef on BTB. SD male rats received 250 µg and 500 µg of rNef along with 2% Evans blue dye within 1 ml through the tail vein. After 1 hour of perfusion, the animals were sacrificed for analysis. The dye migration assay and ELISA confirmed a significant impairment in the blood-testis barrier (BTB) and the manifestation of rNef in testes tissues, respectively. Moreover, a decline in the expression of tight junction proteins, including ZO1 and Occludin, was observed during rNef-induced BTB disruption. Overall, our findings demonstrated that rNef induces BTB disruption through various signaling events. At the site of ectoplasmic specialization of the seminiferous epithelium, the localization of cadherins was found to be disrupted, making the testis a vulnerable site. In conclusion, rNef perturbs the integrity of the blood-testis barrier in rat models; hence, it can also serve as a suitable model for studying the dynamics of the blood-testis barrier.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2357406"},"PeriodicalIF":3.6,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11970733/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141082380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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

Understanding the mechanisms of Streptococcus pneumoniae in penetrating the blood-brain barrier: insights into bacterial binding with central nervous system host receptors. 了解肺炎链球菌穿透血脑屏障的机制：细菌与中枢神经系统宿主受体结合的见解。

IF 3.6

Tissue Barriers Pub Date : 2024-12-04 DOI: 10.1080/21688370.2024.2434764

Mazen M Jamil Al-Obaidi, Muzna Saif Khalfan Al Siyabi, AbdulRahman Muthanna, Mohd Nasir Mohd Desa

{"title":"Understanding the mechanisms of Streptococcus pneumoniae in penetrating the blood-brain barrier: insights into bacterial binding with central nervous system host receptors.","authors":"Mazen M Jamil Al-Obaidi, Muzna Saif Khalfan Al Siyabi, AbdulRahman Muthanna, Mohd Nasir Mohd Desa","doi":"10.1080/21688370.2024.2434764","DOIUrl":"10.1080/21688370.2024.2434764","url":null,"abstract":"This review investigates the pathogenic processes through which Streptococcus pneumoniae crosses the blood-brain barrier (BBB) to cause meningitis, with a focus on the interaction with host receptors in the central nervous system (CNS). S. pneumoniae a primary cause of bacterial meningitis, utilizes unique receptor-mediated pathways to infiltrate the BBB. The bacterial interaction with the platelet-activating factor receptor (PAFR) and the polymeric immunoglobulin receptor (pIgR) is looked at in this study. The goal is to understand how this interaction helps the bacterium move across the BBB and cause infection in the CNS. We examine the functions of cellular and molecular participants at the endothelium level, such as cytokines, chemokines, and matrix metalloproteinases (MMP), which have a role in the development of the disease. This study consolidates data from multiple studies, providing a thorough summary of the interactions between S. pneumoniae and the BBB. It also explores potential treatment targets that could reduce the significant illness and death rates associated with pneumococcal meningitis.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2434764"},"PeriodicalIF":3.6,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142772697","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

Exploring fatty acid effects in celiac disease: potential therapeutic avenues. 探索脂肪酸在乳糜泻中的作用：潜在的治疗途径。

IF 3.6

Tissue Barriers Pub Date : 2024-12-03 DOI: 10.1080/21688370.2024.2435552

Sajjad Bakhtiari, Nastaran Asri, Abdolrahim Nikzamir, Shokoufeh Ahmadipour, Mohammad Rostami-Nejad, Carolina Ciacci

{"title":"Exploring fatty acid effects in celiac disease: potential therapeutic avenues.","authors":"Sajjad Bakhtiari, Nastaran Asri, Abdolrahim Nikzamir, Shokoufeh Ahmadipour, Mohammad Rostami-Nejad, Carolina Ciacci","doi":"10.1080/21688370.2024.2435552","DOIUrl":"https://doi.org/10.1080/21688370.2024.2435552","url":null,"abstract":"Background: Fatty acids (FAs) play pivotal roles in modulating inflammatory pathways in celiac disease (CD). The present study explored the relationship between serum FAs levels and the expression of both pro- and anti-inflammatory cytokines in adult and pediatric patients with CD.Methods: Serum FA levels in 20 treated CD patients (11 children, 9 adults) and 20 healthy controls (10 children, 10 adults) were analyzed using gas chromatography. Cytokine gene expression (IL-6, TNF-α, IL-10, IL-12, TGFβ, NF-κB) was assessed through quantitative real-time PCR.Results: Myristoleic acid levels decreased in children with CD (p = 0.03) but increased in adults (p = 0.04). Elevated IL-6 mRNA expression was found in both pediatric (p = 0.01) and adult (p = 0.04) groups. TNF-α expression was significantly higher in adults (p = 0.01). In children, IL-10 mRNA levels positively correlated with palmitic acid (p = 0.01, r = 0.73), and TGF-β correlated with myristoleic acid (p = 0.03, r = 0.63). In adults, IL-10 positively correlated with dihomo-gamma-linolenic acid (p = 0.04, r = 0.68) and negatively with linoleic acid (p = 0.02, r = -0.72). These age-related differences may reflect variations in disease duration, metabolic and developmental factors, dietary intake, and gut microbiota composition.Conclusion: These findings suggest that FAs could be therapeutic targets for improving CD management across different age groups.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2435552"},"PeriodicalIF":3.6,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142772751","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

Mechanical stiffness across skin layers in human: a pilot study. 人体跨皮肤层的机械刚度：一项初步研究。

IF 3.6

Tissue Barriers Pub Date : 2024-12-03 DOI: 10.1080/21688370.2024.2437220

Wan-Yu Chi, Hao-Wei Huang, Gang-Hui Lee, Criselda Jean G Cruz, Michael W Hughes, Ming-Jer Tang, Shyh-Jou Shieh, Chao-Chun Yang

引用次数: 0

Metabolic alterations of endothelial cells under transient and persistent hypoxia: study using a 3D microvessels-on-chip model. 内皮细胞在短暂和持续缺氧条件下的代谢变化：利用三维芯片微血管模型进行的研究。

IF 3.6

Tissue Barriers Pub Date : 2024-11-25 DOI: 10.1080/21688370.2024.2431416

Kanchana Pandian, Anton Jan van Zonneveld, Amy Harms, Thomas Hankemeier

{"title":"Metabolic alterations of endothelial cells under transient and persistent hypoxia: study using a 3D microvessels-on-chip model.","authors":"Kanchana Pandian, Anton Jan van Zonneveld, Amy Harms, Thomas Hankemeier","doi":"10.1080/21688370.2024.2431416","DOIUrl":"https://doi.org/10.1080/21688370.2024.2431416","url":null,"abstract":"Numerous signaling pathways are activated during hypoxia to facilitate angiogenesis, promoting interactions among endothelial cells and initiating downstream signaling cascades. Although the pivotal role of the nitric oxide (NO) response pathway is well-established, the involvement of arginine-specific metabolism and bioactive lipid mechanisms in 3D flow-activated in vitro models remains less understood. In this study, we explored the levels of arginine-specific metabolites and bioactive lipids in human coronary artery endothelial cells (HCAECs) under both transient and persistent hypoxia. We compared targeted metabolite levels between a 2D static culture model and a 3D microvessels-on-chip model. Notably, we observed robust regulation of NO metabolites in both transient and persistent hypoxic conditions. In the 2D model under transient hypoxia, metabolic readouts of bioactive lipids revealed increased oxidative stress markers, a phenomenon not observed in the 3D microvessels. Furthermore, we made a novel discovery that the responses of bioactive lipids were regulated by hypoxia inducible factor-1α (HIF-1α) in the 2D cell culture model and partially by HIF-1α and flow-induced shear stress in the 3D microvessels. Immunostaining confirmed the HIF-1α-induced regulation under both hypoxic conditions. Real-time oxygen measurements in the 3D microvessels using an oxygen probe validated that oxygen levels were maintained in the 3D model. Overall, our findings underscore the critical regulatory roles of HIF-1α and shear stress in NO metabolites and bioactive lipids in both 2D and 3D cell culture models.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2431416"},"PeriodicalIF":3.6,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142711053","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

Dengue virus NS1 hits hard at the barrier integrity of human cerebral microvascular endothelial cells via cellular microRNA dysregulations. 登革病毒 NS1 通过细胞微 RNA 失调重创人脑微血管内皮细胞的屏障完整性。

IF 3.6

Tissue Barriers Pub Date : 2024-11-07 DOI: 10.1080/21688370.2024.2424628

Apoorva, Atul Kumar, Sunit K Singh

{"title":"Dengue virus NS1 hits hard at the barrier integrity of human cerebral microvascular endothelial cells via cellular microRNA dysregulations.","authors":"Apoorva, Atul Kumar, Sunit K Singh","doi":"10.1080/21688370.2024.2424628","DOIUrl":"https://doi.org/10.1080/21688370.2024.2424628","url":null,"abstract":"Dengue virus (DENV) infections are commonly reported in the tropical and subtropical regions of the world. DENV is reported to exploit various strategies to cross the blood-brain barrier. The NS1 protein of DENV plays an important role in viral neuropathogenesis, resulting in endothelial hyperpermeability and cytokine-induced vascular leak. miRNAs are short non-coding RNAs that play an important role in post-transcriptional gene regulations. However, no comprehensive information about the involvement of miRNAs in DENV-NS1-mediated neuropathogenesis has been explored to date. We observed that DENV-NS1 significantly alters the cellular miRNome of human cerebral microvascular endothelial cells in a bystander fashion. Subsequent target prediction and pathway enrichment analysis indicated that these microRNAs and their corresponding target genes are involved in pathways associated with blood-brain barrier dysfunction such as \"Adherens junction\" and \"Tight junction\". Additionally, several miRNA-mRNA pairs were also found to be involved in cellular signaling pathways related to cytokine production, for instance, \"Jak-STAT signaling pathway\", \"Chemokine signaling pathway\", \"IL-17 signaling pathway\", \"NF-κB signaling pathway\", and \"Viral protein interaction with cytokine and cytokine receptor\". The dysregulated production of inflammatory cytokines is reported to compromise BBB permeability. This study is the first report to demonstrate that DENV-NS1-mediated miRNA perturbations are crucial in compromising endothelial barrier integrity. It also offers insights into potential therapeutic targets to mitigate DENV-NS1-induced vascular permeability and inflammation.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2424628"},"PeriodicalIF":3.6,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142606629","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