{"title":"The correlation between fecal microbiota profiles and intracellular junction genes expression in young Iranian patients with celiac disease.","authors":"Mohadeseh Mahmoudi Ghehsareh, Nastaran Asri, Fahimeh Sadat Gholam-Mostafaei, Hamidreza Houri, Flora Forouzesh, Shokoufeh Ahmadipour, Somayeh Jahani-Sherafat, Mohammad Rostami-Nejad, Pasquale Mansueto, Aurelio Seidita","doi":"10.1080/21688370.2024.2347766","DOIUrl":"https://doi.org/10.1080/21688370.2024.2347766","url":null,"abstract":"<p><p>Celiac disease (CD) is characterized by the disruption of the intestinal barrier integrity and alterations in the microbiota composition. This study aimed to evaluate the changes in the fecal microbiota profile and mRNA expressions of intracellular junction-related genes in pediatric patients with CD compared to healthy controls (HCs). Thirty treated CD patients, 10 active CD, and 40 HCs were recruited. Peripheral blood (PB) and fecal samples were collected. Microbiota analysis was performed using quantitative real-time PCR (qPCR) test. The mRNA expressions of ZO-1, occludin, β-catenin, E-cadherin, and COX-2 were also evaluated. In active and treated CD patients, the PB expression levels of ZO-1 (<i>p</i> = 0.04 and 0.002, respectively) and β-catenin (<i>p</i> = 0.006 and 0.02, respectively) were lower than in HCs. PB Occludin's level was upregulated in both active and treated CD patients compared to HCs (<i>p</i> = 0.04 and 0.02, respectively). However, PB E-cadherin and COX-2 expression levels and fecal mRNA expressions of ZO-1, occludin, and COX-2 did not differ significantly between cases and HCs (P˃0.05). Active CD patients had a higher relative abundance of the <i>Firmicutes</i> (<i>p</i> = 0.04) and <i>Actinobacteria</i> (<i>p</i> = 0.03) phyla compared to treated subjects. The relative abundance of <i>Veillonella</i> (<i>p</i> = 0.04) and <i>Staphylococcus</i> (<i>p</i> = 0.01) genera was lower in active patients in comparison to HCs. Researchers should explore the precise impact of the gut microbiome on the molecules and mechanisms involved in intestinal damage of CD. Special attention should be given to <i>Bifidobacteria</i> and Enterobacteriaceae, as they have shown a significant correlation with the expression of tight junction-related genes.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2347766"},"PeriodicalIF":3.1,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140870223","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}
Tissue BarriersPub Date : 2024-04-29DOI: 10.1080/21688370.2024.2347070
Abdullah Alhumaid, Fang Liu, Shengshuai Shan, Eissa Jafari, Nadia Nourin, Payaningal R Somanath, S Priya Narayanan
{"title":"Spermine oxidase inhibitor, MDL 72527, reduced neovascularization, vascular permeability, and acrolein-conjugated proteins in a mouse model of ischemic retinopathy.","authors":"Abdullah Alhumaid, Fang Liu, Shengshuai Shan, Eissa Jafari, Nadia Nourin, Payaningal R Somanath, S Priya Narayanan","doi":"10.1080/21688370.2024.2347070","DOIUrl":"10.1080/21688370.2024.2347070","url":null,"abstract":"<p><p>Disruptions in polyamine metabolism have been identified as contributing factors to various central nervous system disorders. Our laboratory has previously highlighted the crucial role of polyamine oxidation in retinal disease models, specifically noting elevated levels of spermine oxidase (SMOX) in inner retinal neurons. Our prior research demonstrated that inhibiting SMOX with MDL 72527 protected against vascular injury and microglial activation induced by hyperoxia in the retina. However, the effects of SMOX inhibition on retinal neovascularization and vascular permeability, along with the underlying molecular mechanisms of vascular protection, remain incompletely understood. In this study, we utilized the oxygen-induced retinopathy (OIR) model to explore the impact of SMOX inhibition on retinal neovascularization, vascular permeability, and the molecular mechanisms underlying MDL 72527-mediated vasoprotection in the OIR retina. Our findings indicate that inhibiting SMOX with MDL 72527 mitigated vaso-obliteration and neovascularization in the OIR retina. Additionally, it reduced OIR-induced vascular permeability and Claudin-5 expression, suppressed acrolein-conjugated protein levels, and downregulated P38/ERK1/2/STAT3 signaling. Furthermore, our results revealed that treatment with BSA-Acrolein conjugates significantly decreased the viability of human retinal endothelial cells (HRECs) and activated P38 signaling. These observations contribute valuable insights into the potential therapeutic benefits of SMOX inhibition by MDL 72527 in ischemic retinopathy.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2347070"},"PeriodicalIF":3.1,"publicationDate":"2024-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140851564","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}
Tissue BarriersPub Date : 2024-04-02Epub Date: 2023-06-20DOI: 10.1080/21688370.2023.2222628
Brittany E Watson, Julia A Miles, Melissa A Moss
{"title":"Human <i>in vitro</i> blood barrier models: architectures and applications.","authors":"Brittany E Watson, Julia A Miles, Melissa A Moss","doi":"10.1080/21688370.2023.2222628","DOIUrl":"10.1080/21688370.2023.2222628","url":null,"abstract":"<p><p>Blood barriers serve as key points of transport for essential molecules as well as lines of defense to protect against toxins. <i>In vitro</i> modeling of these barriers is common practice in the study of their physiology and related diseases. This review describes a common method of using an adaptable, low cost, semipermeable, suspended membrane to experimentally model three blood barriers in the human body: the blood-brain barrier (BBB), the gut-blood barrier (GBB), and the air-blood barrier (ABB). The GBB and ABB both protect from the outside environment, while the BBB protects the central nervous system from potential neurotoxic agents in the blood. These barriers share several commonalities, including the formation of tight junctions, polarized cellular monolayers, and circulatory system contact. Cell architectures used to mimic barrier anatomy as well as applications to study function, dysfunction, and response provide an overview of the versatility enabled by these cultural systems.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2222628"},"PeriodicalIF":3.6,"publicationDate":"2024-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11042067/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9669494","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}
Tissue BarriersPub Date : 2024-04-02Epub Date: 2023-06-09DOI: 10.1080/21688370.2023.2221632
J Ponmozhi, S Dhinakaran, Dorottya Kocsis, Kristóf Iván, Franciska Erdő
{"title":"Models for barrier understanding in health and disease in lab-on-a-chips.","authors":"J Ponmozhi, S Dhinakaran, Dorottya Kocsis, Kristóf Iván, Franciska Erdő","doi":"10.1080/21688370.2023.2221632","DOIUrl":"10.1080/21688370.2023.2221632","url":null,"abstract":"<p><p>The maintenance of body homeostasis relies heavily on physiological barriers. Dysfunction of these barriers can lead to various pathological processes, including increased exposure to toxic materials and microorganisms. Various methods exist to investigate barrier function in vivo and in vitro. To investigate barrier function in a highly reproducible manner, ethically, and high throughput, researchers have turned to non-animal techniques and micro-scale technologies. In this comprehensive review, the authors summarize the current applications of organ-on-a-chip microfluidic devices in the study of physiological barriers. The review covers the blood-brain barrier, ocular barriers, dermal barrier, respiratory barriers, intestinal, hepatobiliary, and renal/bladder barriers under both healthy and pathological conditions. The article then briefly presents placental/vaginal, and tumour/multi-organ barriers in organ-on-a-chip devices. Finally, the review discusses Computational Fluid Dynamics in microfluidic systems that integrate biological barriers. This article provides a concise yet informative overview of the current state-of-the-art in barrier studies using microfluidic devices.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2221632"},"PeriodicalIF":3.1,"publicationDate":"2024-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11042069/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9967899","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}
Tissue BarriersPub Date : 2024-04-02Epub Date: 2023-07-12DOI: 10.1080/21688370.2023.2232245
Nektarios Barabutis, Mohammad S Akhter
{"title":"Unfolded protein response suppression potentiates LPS-induced barrier dysfunction and inflammation in bovine pulmonary artery endothelial cells.","authors":"Nektarios Barabutis, Mohammad S Akhter","doi":"10.1080/21688370.2023.2232245","DOIUrl":"10.1080/21688370.2023.2232245","url":null,"abstract":"<p><p>The development of novel strategies to counteract diseases related to barrier dysfunction is a priority, since sepsis and acute respiratory distress syndrome are still associated with high mortality rates. In the present study, we focus on the effects of the unfolded protein response suppressor (UPR) 4-Phenylbutyrate (4-PBA) in Lipopolysaccharides (LPS)-induced endothelial injury, to investigate the effects of that compound in the corresponding damage. 4-PBA suppressed binding immunoglobulin protein (BiP) - a UPR activation marker - and potentiated LPS - induced signal transducer and activator of transcription 3 (STAT3) and extracellular signal‑regulated protein kinase (ERK) 1/2 activation. In addition to those effects, 4-PBA enhanced paracellular hyperpermeability in inflamed bovine pulmonary endothelial cells, and did not affect cell viability in moderate concentrations. Our observations suggest that UPR suppression due to 4-PBA augments LPS-induced endothelial injury, as well as the corresponding barrier disruption.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2232245"},"PeriodicalIF":3.1,"publicationDate":"2024-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11042058/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9767577","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}
Tissue BarriersPub Date : 2024-04-02Epub Date: 2023-06-21DOI: 10.1080/21688370.2023.2222632
Alicia M Barnett, Jane A Mullaney, Warren C McNabb, Nicole C Roy
{"title":"Culture media and format alter cellular composition and barrier integrity of porcine colonoid-derived monolayers.","authors":"Alicia M Barnett, Jane A Mullaney, Warren C McNabb, Nicole C Roy","doi":"10.1080/21688370.2023.2222632","DOIUrl":"10.1080/21688370.2023.2222632","url":null,"abstract":"<p><p>Intestinal organoid technology has revolutionized our approach to <i>in vitro</i> cell culture due in part to their three-dimensional structures being more like the native tissue from which they were derived with respect to cellular composition and architecture. For this reason, organoids are becoming the new gold standard for undertaking intestinal epithelial cell research. Unfortunately, their otherwise advantageous three-dimensional geometry prevents easy access to the apical epithelium, which is a major limitation when studying interactions between dietary or microbial components and host tissues. To overcome this problem, we developed porcine colonoid-derived monolayers cultured on both permeable Transwell inserts and tissue culture treated polystyrene plates. We found that seeding density and culture format altered the expression of genes encoding markers of specific cell types (stem cells, colonocytes, goblets, and enteroendocrine cells), and barrier maturation (tight junctions). Additionally, we found that changes to the formulation of the culture medium altered the cellular composition of colonoids and of monolayers derived from them, resulting in cultures with an increasingly differentiated phenotype that was similar to that of their tissue of origin.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2222632"},"PeriodicalIF":3.1,"publicationDate":"2024-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11042055/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9669957","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}
Tissue BarriersPub Date : 2024-04-02Epub Date: 2023-05-31DOI: 10.1080/21688370.2023.2219605
Brooke E Chambers, Nicole E Weaver, Caroline M Lara, Thanh Khoa Nguyen, Rebecca A Wingert
{"title":"(Zebra)fishing for nephrogenesis genes.","authors":"Brooke E Chambers, Nicole E Weaver, Caroline M Lara, Thanh Khoa Nguyen, Rebecca A Wingert","doi":"10.1080/21688370.2023.2219605","DOIUrl":"10.1080/21688370.2023.2219605","url":null,"abstract":"<p><p>Kidney disease is a devastating condition affecting millions of people worldwide, where over 100,000 patients in the United States alone remain waiting for a lifesaving organ transplant. Concomitant with a surge in personalized medicine, single-gene mutations, and polygenic risk alleles have been brought to the forefront as core causes of a spectrum of renal disorders. With the increasing prevalence of kidney disease, it is imperative to make substantial strides in the field of kidney genetics. Nephrons, the core functional units of the kidney, are epithelial tubules that act as gatekeepers of body homeostasis by absorbing and secreting ions, water, and small molecules to filter the blood. Each nephron contains a series of proximal and distal segments with explicit metabolic functions. The embryonic zebrafish provides an ideal platform to systematically dissect the genetic cues governing kidney development. Here, we review the use of zebrafish to discover nephrogenesis genes.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2219605"},"PeriodicalIF":3.6,"publicationDate":"2024-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11042071/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9540652","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}
Tissue BarriersPub Date : 2024-04-02Epub Date: 2023-07-13DOI: 10.1080/21688370.2023.2232248
Swati Singh, Deepraj Paul, Virendra Nath, Rohini A
{"title":"Exosomes: current knowledge and future perspectives.","authors":"Swati Singh, Deepraj Paul, Virendra Nath, Rohini A","doi":"10.1080/21688370.2023.2232248","DOIUrl":"10.1080/21688370.2023.2232248","url":null,"abstract":"<p><p>Exosomes are membrane-bound micro-vesicles that possess endless therapeutic potential for treatment of numerous pathologies including autoimmune, cardiovascular, ocular, and nervous disorders. Despite considerable knowledge about exosome biogenesis and secretion, still, there is a lack of information regarding exosome uptake by cell types and internal signaling pathways through which these exosomes process cellular response. Exosomes are key components of cell signaling and intercellular communication. In central nervous system (CNS), exosomes can penetrate BBB and maintain homeostasis by myelin sheath regulation and the waste products elimination. Therefore, the current review summarizes role of exosomes and their use as biomarkers in cardiovascular, nervous and ocular disorders. This aspect of exosomes provides positive hope to monitor disease development and enable early diagnosis and treatment optimization. In this review, we have summarized recent findings on physiological and therapeutic effects of exosomes and also attempt to provide insights about stress-preconditioned exosomes and stem cell-derived exosomes.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2232248"},"PeriodicalIF":3.6,"publicationDate":"2024-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11042064/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9776715","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}
{"title":"Fibroblasts/three-dimensional scaffolds complexes promote wound healing in rats with skin defects.","authors":"Ting Jiang, Qiang Liu, Er-Chang Xu, Si-Yu He, Hong-Yan Liu, Chao Tian, Lan-Fang Zhang, Ze-Long Yang","doi":"10.1080/21688370.2024.2334544","DOIUrl":"https://doi.org/10.1080/21688370.2024.2334544","url":null,"abstract":"<p><p>We aim to construct a three-dimensional nano-skin scaffold material in vitro and study its promoting effect on wound healing in vivo. In this study, hybrid constructs of three-dimensional (3D) scaffolds were successfully fabricated by combination of type I collagen (COL-1) and polylactic-glycolic acid (PLGA). Fibroblasts and human umbilical cord mesenchymal stem cells (hUCMSCs) were used to implanted into 3D scaffolds and constructed into SD skin scaffolds in vitro. Finally, the fibroblasts/scaffolds complexes were inoculated on the surface of rat wound skin to study the promoting effect of the complex on wound healing. In our study, we successfully built a 3D scaffold, which had a certain porosity. Meanwhile, the content of COL-1 in the cell supernatant of fibroblast/scaffold complexes was increased. Furthermore, the expression of F-actin, CD105, integrin β, VEGF, and COL-1 was up-regulated in hUCMSC/scaffold complexes compared with the control group. In vivo, fibroblast/scaffold complexes promoted wound healing in rats. Our data suggested that the collagen Ⅳ and vimentin were elevated and collagen fibers were neatly arranged in the fibroblast/scaffold complex group was significantly higher than that in the scaffold group. Taken together, fibroblast/scaffold complexes were expected to be novel materials for treating skin defects.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2334544"},"PeriodicalIF":3.1,"publicationDate":"2024-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140307054","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}
Tissue BarriersPub Date : 2024-03-17DOI: 10.1080/21688370.2024.2330773
Wanapas Wachiradejkul, Pawin Pongkorpsakol
{"title":"Inter-claudin antagonism of paracellular pore function: mechanism and beyond.","authors":"Wanapas Wachiradejkul, Pawin Pongkorpsakol","doi":"10.1080/21688370.2024.2330773","DOIUrl":"https://doi.org/10.1080/21688370.2024.2330773","url":null,"abstract":"<p><p>Claudin-2-dependent pore function mediates paracellular cation permeability and can result in pathogenesis of many diseases. Although existing various types of claudins, including barrier-forming and pore-forming claudins, their heterodimeric interaction affecting barrier and pore functions has never been fully elucidated yet. Recently, Shashikanth and colleagues demonstrated that expression of claudin-4 was able to antagonize paracellular pore activity of claudin-2. This commentary will emphasize the mechanism underlying claudin-4-mediated claudin-2-dependent pore inhibition and discuss its potential therapeutic and prognostic applications.</p>","PeriodicalId":23469,"journal":{"name":"Tissue Barriers","volume":" ","pages":"2330773"},"PeriodicalIF":3.1,"publicationDate":"2024-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140144150","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}