Tissue Barriers最新文献

The protective effects of apelin-13 in HIV-1 tat- induced macrophage infiltration and BBB impairment. apelin-13对HIV-1 tat诱导的巨噬细胞浸润和BBB损伤的保护作用

IF 3.6

Tissue Barriers Pub Date : 2024-09-12 DOI: 10.1080/21688370.2024.2392361

Qi Cao, Wei Zeng, Jingmin Nie, Yongjun Ye, Yanchao Chen

{"title":"The protective effects of apelin-13 in HIV-1 tat- induced macrophage infiltration and BBB impairment.","authors":"Qi Cao, Wei Zeng, Jingmin Nie, Yongjun Ye, Yanchao Chen","doi":"10.1080/21688370.2024.2392361","DOIUrl":"https://doi.org/10.1080/21688370.2024.2392361","url":null,"abstract":"Impairment of the blood - brain barrier (BBB) and subsequent inflammatory responses contribute to the development of human immunodeficiency virus (HIV)-1-associated neurocognitive disorders (HAND). Apelin-13, the most abundant member of the apelin family, acts as the ligand of the angiotensin receptor-like 1 (APJ). However, its pharmacological function in HAND and its underlying mechanism are unknown. In the current study, we report that the presence of HIV-1 Tat reduced the levels of Apelin-13 and APJ in the cortex tissue of mice. Importantly, Apelin-13 preserved BBB integrity against HIV-1 Tat in mice by increasing the expression of the tight junction protein zonula occludens-1 (ZO-1) and occludin. Interestingly, increased macrophage infiltration, indicated by elevated CD68-positive staining was observed in the cortex after stimulation with HIV-1, which was mitigated by the administration of Apelin-13. Correspondingly, Apelin-13 reduced the expression of monocyte chemoattractant protein-1; (MCP-1). An in vitro two-chamber and two-cell trans-well assay demonstrated that HIV-1 Tat challenge significantly promoted macrophage migration, which was notably attenuated by the introduction of Apelin-13. Accordingly, treatment with Apelin-13 restored the HIV-1 Tat-induced reduction of occludin and ZO-1, while preventing the upregulation of MCP-1 in human brain microvascular endothelial cells (HBMVECs). Our results suggest that Apelin-13 may reduce macrophage infiltration into brain tissues and mitigate BBB dysfunction in patients with HAND.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142296509","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

Erk1/2 is not required for endothelial barrier establishment despite its requirement for cAMP-dependent Rac1 activation in heart endothelium. 尽管在心脏内皮中需要依赖 cAMP 的 Rac1 激活，但内皮屏障的建立并不需要 Erk1/2。

IF 3.6

Tissue Barriers Pub Date : 2024-09-04 DOI: 10.1080/21688370.2024.2398875

Sina Moztarzadeh, Hilda Vargas-Robles, Michael Schnoor, Mariya Y Radeva, Jens Waschke, Alexander Garcia-Ponce

{"title":"Erk1/2 is not required for endothelial barrier establishment despite its requirement for cAMP-dependent Rac1 activation in heart endothelium.","authors":"Sina Moztarzadeh, Hilda Vargas-Robles, Michael Schnoor, Mariya Y Radeva, Jens Waschke, Alexander Garcia-Ponce","doi":"10.1080/21688370.2024.2398875","DOIUrl":"https://doi.org/10.1080/21688370.2024.2398875","url":null,"abstract":"The contribution of Erk1/2 to endothelial barrier regulation is convoluted and differs depending on the vascular bed. We explored the effects of Erk1/2 inhibition on endothelial barrier maintenance and its relationship with cAMP-dependent barrier strengthening. Thus, myocardial endothelial cells (MyEnd) were isolated and protein expression, localization and activity of structural and signaling molecules involved in maintenance of endothelial function were investigated by Western blot, immunostainings and G-LISA, respectively. The transendothelial electrical resistance (TEER) from confluent MyEnd monolayers was measured and used as a direct indicator of barrier integrity in vitro. Miles assay was performed to evaluate vascular permeability in vivo. Erk1/2 inhibition with U0126 affected neither the structural organization of adherens or tight junctions nor the protein level of their components, However, TEER drop significantly upon U0126 application, but the effect was transitory as the barrier function recovered 30 min after treatment. Erk1/2 inhibition delayed cAMP-mediated barrier strengthening but did not prevent barrier fortification despite diminishing Rac1 activation. Moreover, Erk1/2 inhibition, induced vascular leakage that could be prevented by local cAMP elevation in vivo. Our data demonstrate that Erk1/2 is required to prevent vascular permeability but is not critical for cAMP-mediated barrier enhancement.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142126822","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

Multiciliated cell development and ciliary resorption at the mammalian choroid plexus. 哺乳动物脉络丛的多缘细胞发育和睫状体吸收

IF 3.6

Tissue Barriers Pub Date : 2024-09-04 DOI: 10.1080/21688370.2024.2399990

Ashini Kaushik, Rebecca A Wingert

引用次数: 0

Oncostatin M promotes epithelial barrier dysfunction in patients with eosinophilic chronic rhinosinusitis with nasal polyps. Oncostatin M 可促进嗜酸性粒细胞慢性鼻炎伴鼻息肉患者的上皮屏障功能障碍。

IF 3.6

Tissue Barriers Pub Date : 2024-09-03 DOI: 10.1080/21688370.2024.2399235

Bao-Feng Wang, Ying-Ying Wang, Hai Lin, Yun-Lan Yi

{"title":"Oncostatin M promotes epithelial barrier dysfunction in patients with eosinophilic chronic rhinosinusitis with nasal polyps.","authors":"Bao-Feng Wang, Ying-Ying Wang, Hai Lin, Yun-Lan Yi","doi":"10.1080/21688370.2024.2399235","DOIUrl":"https://doi.org/10.1080/21688370.2024.2399235","url":null,"abstract":"Background: Oncostatin M (OSM) may be involved in the promotion of mucosal epithelial barrier dysfunction in patients with eosinophilic chronic rhinosinusitis with nasal polyps (Eos CRSwNP) by inducing matrix metalloproteinase (MMP) -1 and -7. The aim was to evaluate the roles and mechanisms of action of OSM on MMP-1 and -7 synthesis from nasal epithelial cells (NECs).Methods: OSM, OSM receptor (OSMR), MMP-1 and -7 expression was evaluated in nasal mucosa or primary NECs from scrapings by quantitative polymerase chain reaction (qPCR), immunofluorescence and immunohistochemistry. OSM and other cytokines were used to stimulate air-liquid interface (ALI) cultured NECs. qPCR, enzyme-linked immunosorbent assay (ELISA) and immunofluorescence were used to evaluate the expression of OSMR, MMP-1, -7 and occludin in NECs.Results: Elevated levels of OSMRβ, MMP-1 and -7 were found in the tissues and scraped NECs of Eos CRSwNP in comparison to them obtained from the inferior turbinate (IT) and control subjects. The levels of OSM and OSMRβ mRNA in tissues were positively correlated with the levels of MMP-1 and -7. OSM stimulation of NECs increased the expression of MMP-1 and -7, and the responses were suppressed by a STAT3 inhibitor, and a PI3K inhibitor respectively. In parallel studies, we found that stimulation with OSM disrupted the localization of occludin, a tight junction protein in NECs. The response was suppressed by a pan-MMP inhibitor.Conclusion: OSM induces the synthesis and release of MMP-1 and -7 in NECs. Furthermore, MMP-1 and -7 promote mucosal epithelial barrier dysfunction in patients with Eos CRSwNP.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142120751","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

Epithelial barrier dysfunction and microbial dysbiosis: exploring the pathogenesis and therapeutic strategies for Crohn's disease. 上皮屏障功能障碍和微生物菌群失调：探索克罗恩病的发病机制和治疗策略。

IF 3.6

Tissue Barriers Pub Date : 2024-08-26 DOI: 10.1080/21688370.2024.2390705

Tunç Akkoç

{"title":"Epithelial barrier dysfunction and microbial dysbiosis: exploring the pathogenesis and therapeutic strategies for Crohn's disease.","authors":"Tunç Akkoç","doi":"10.1080/21688370.2024.2390705","DOIUrl":"https://doi.org/10.1080/21688370.2024.2390705","url":null,"abstract":"Crohn's disease (CD), a chronic gastrointestinal inflammatory disease, is becoming more widespread worldwide. Crohn's disease is caused by gut microbiota changes, genetics, environmental stresses, and immunological responses. Current treatments attempt to achieve long-term remission and avoid complications, delaying disease progression. Immunosuppressive measures and combination medicines should be started early for high-risk patients. These medicines monitor inflammatory indicators and adjust as needed. The epithelial barrier helps defend against physical, chemical, and immunological threats. When tissues' protective barrier breaks down, the microbiome may reach the layer underneath. Unbalanced microbial populations and inflammation impair healing and adjustment. Inflammatory cells infiltrating sensitive tissues aggravate the damage and inflammation. This approach promotes chronic inflammatory diseases. The epithelial barrier hypothesis states that hereditary and environmental variables cause epithelial tissue inflammation. This review focuses on how epithelial barrier break-down and microbial dysbiosis cause Crohn's disease and current advances in understanding the epithelial barrier, immune system, and microbiome. Additionally, investigate treatments that restore barrier integrity and promote microbial balance. Overall, it stresses the role of epithelial barrier failure and microbial dysbiosis in Crohn's disease development and discusses current advances in understanding the barrier, immunological responses, and microbiota.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142056638","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

Ulcerative colitis: the healing power of macrophages. 溃疡性结肠炎：巨噬细胞的治愈能力

IF 3.6

Tissue Barriers Pub Date : 2024-08-10 DOI: 10.1080/21688370.2024.2390218

Nesa Kazemifard, Nafiseh Golestani, Kasra Jahankhani, Maryam Farmani, Shaghayegh Baradaran Ghavami

{"title":"Ulcerative colitis: the healing power of macrophages.","authors":"Nesa Kazemifard, Nafiseh Golestani, Kasra Jahankhani, Maryam Farmani, Shaghayegh Baradaran Ghavami","doi":"10.1080/21688370.2024.2390218","DOIUrl":"https://doi.org/10.1080/21688370.2024.2390218","url":null,"abstract":"Ulcerative colitis (UC) is a chronic and debilitating disorder that falls under the broad category of inflammatory bowel disease (IBD). Therefore, affects the colon and rectum, resulting in inflammation and ulcers in the lining of these organs. Over the years, there has been a significant shift in the management of UC. The focus has moved from achieving symptom-free daily living to attaining mucosal healing. Mucosal healing means completely restoring the colon and rectum's lining, significantly reducing the risk of complications and relapse. Macrophages are a crucial component of the immune system that play a vital role in the regeneration and repair of colonic ulcers. These immune cells are responsible for production of a variety of cytokines and growth factors that facilitate tissue repair. Macrophages are responsible for maintaining a balance between inflammation and healing. When this balance is disrupted, it can lead to chronic inflammation and tissue damage, exacerbating UC symptoms. Thus, this review aims to investigate the contribution of macrophages to mucosal repair and remission maintenance in UC patients.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141914132","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

Claudin-12: guardian of the tissue barrier or friend of tumor cells. Claudin-12：组织屏障的守护者或肿瘤细胞的朋友。

IF 3.6

Tissue Barriers Pub Date : 2024-08-01 DOI: 10.1080/21688370.2024.2387408

Desislava Apostolova, Georgi Apostolov, Dzhemal Moten, Tsvetelina Batsalova, Balik Dzhambazov

{"title":"Claudin-12: guardian of the tissue barrier or friend of tumor cells.","authors":"Desislava Apostolova, Georgi Apostolov, Dzhemal Moten, Tsvetelina Batsalova, Balik Dzhambazov","doi":"10.1080/21688370.2024.2387408","DOIUrl":"https://doi.org/10.1080/21688370.2024.2387408","url":null,"abstract":"Tight junctions (TJs) are an important component of cellular connectivity. Claudin family proteins, as a constituent of TJs, determine their barrier properties, cell polarity and paracellular permeability. Claudin-12 is an atypical member of the claudin family, as it belongs to the group of non-classical claudins that lack a PDZ-binding domain. It has been shown that claudin-12 is involved in paracellular Ca2+ transients and it is present in normal and hyperplastic tissues in addition to neoplastic tissues. Dysregulation of claudin-12 expression has been reported in various cancers, suggesting that this protein may play an important role in cancer cell migration, invasion, and metastasis. Some studies have shown that claudin-12 gene functions as a tumor suppressor, but others have reported that overexpression of claudin-12 significantly increases the metastatic properties of various tumor cells. Investigating this dual role of claudin-12 is of utmost importance and should therefore be studied in detail. The aim of this review is to provide an overview of the information available to date on claudin-12, including its structure, expression in various tissues and substances that may affect it, with a final focus on its role in cancer.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141861026","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

The impact of diabetes mellitus on blood-tissue barrier regulation and vascular complications: Is the lung different from other organs? 糖尿病对血液-组织屏障调节和血管并发症的影响：肺与其他器官是否不同？

IF 3.6

Tissue Barriers Pub Date : 2024-07-29 DOI: 10.1080/21688370.2024.2386183

Abdulaziz H Alanazi, Mohamed S Selim, Manyasreeprapti R Yendamuri, Duo Zhang, S Priya Narayanan, Payaningal R Somanath

{"title":"The impact of diabetes mellitus on blood-tissue barrier regulation and vascular complications: Is the lung different from other organs?","authors":"Abdulaziz H Alanazi, Mohamed S Selim, Manyasreeprapti R Yendamuri, Duo Zhang, S Priya Narayanan, Payaningal R Somanath","doi":"10.1080/21688370.2024.2386183","DOIUrl":"https://doi.org/10.1080/21688370.2024.2386183","url":null,"abstract":"Diabetes Mellitus presents a formidable challenge as one of the most prevalent and complex chronic diseases, exerting significant strain on both patients and the world economy. It is recognized as a common comorbidity among severely ill individuals, often leading to a myriad of micro- and macro-vascular complications. Despite extensive research dissecting the pathophysiology and molecular mechanisms underlying vascular complications of diabetes, relatively little attention has been paid to potential lung-related complications. This review aims to illuminate the impact of diabetes on prevalent respiratory diseases, including chronic obstructive pulmonary disease (COPD), acute respiratory distress syndrome (ARDS), idiopathic pulmonary fibrosis (IPF), tuberculosis (TB), pneumonia infections, and asthma, and compare the vascular complications with other vascular beds. Additionally, we explore the primary mechanistic pathways contributing to these complications, such as the expression modulation of blood-tissue-barrier proteins, resulting in increased paracellular and transcellular permeability, and compromised immune responses rendering diabetes patients more susceptible to infections. The activation of inflammatory pathways leading to cellular injury and hastening the onset of these respiratory complications is also discussed.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141789129","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

Canadine inhibits epithelial mesenchymal transformation of HPV-negative cervical cancer. Canadine抑制HPV-阴性宫颈癌症的上皮-间质转化。

IF 3.6

Tissue Barriers Pub Date : 2024-07-02 Epub Date: 2023-10-11 DOI: 10.1080/21688370.2023.2256641

Yan Ma, Qian-Qian Yang, Dong-Mei Gu, Xiao Yuan, Yu-Hong Wang, Ling-Chuan Guo

{"title":"Canadine inhibits epithelial mesenchymal transformation of HPV-negative cervical cancer.","authors":"Yan Ma, Qian-Qian Yang, Dong-Mei Gu, Xiao Yuan, Yu-Hong Wang, Ling-Chuan Guo","doi":"10.1080/21688370.2023.2256641","DOIUrl":"10.1080/21688370.2023.2256641","url":null,"abstract":"Although the majority of the population will be protected due to the advent and widespread use of the HPV vaccine, the treatment of cervical cancer for all causes, including HPV-negative cervical cancer, is still worthy of further research. The focal point of this study was Canadine's inhibition of epithelial-mesenchymal transformation (EMT) in cervical cancer. Immunoblotting, wound healing and tumor invasion experiments showed that low concentration of Canadine could inhibit the EMT process, proliferation and migration of HT-3 cells (HPV-negative cell line). Combined with GEO database, it was found that the expression levels of several genes highly expressed in cervical tumor tissues could be inhibited by Canadine, especially MAGEA3. Further experiments confirmed that the inhibition of Canadine on MAGEA3 protein increased with time. The small interference and overexpression plasmid of MAGEA3 were designed and verified. In HT-3 cells, when MAGEA3 levels were directly decreased, mesenchymal phenotypic markers were decreased and epithelial phenotypic markers were increased. The opposite result was obtained by overexpression of MAGEA3. In addition, the inhibition of EMT due to the reduction of endogenous MAGEA3 by Canadine was also offset by the overexpression of exogenous MAGEA3. The study concludes that Canadine inhibits EMT of cervical cancer by inhibiting MAGEA3.","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11262239/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41214120","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

Curative role of natural PPARγ agonist in non-alcoholic fatty liver disease (NAFLD). 天然 PPARγ 激动剂对非酒精性脂肪肝（NAFLD）的治疗作用。

IF 3.6

Tissue Barriers Pub Date : 2024-07-02 Epub Date: 2023-12-05 DOI: 10.1080/21688370.2023.2289830

Swati Singh, Anit Kumar, Suruchi Gupta, Rohini Agrawal

引用次数: 0