Tissue Barriers最新文献

The skin is the largest organ of the human body and is widely considered to be the first-line defense of the body, providing essential protection against mechanical, physical, and chemical damage. Keratinocytes are the primary cells of the outer layer of the epidermis, which acts as a mechanical and permeability barrier. The epidermis is a permanently renewed tissue where undifferentiated keratinocytes located at the basal layer proliferate and migrate to the overlying layers. Here we report that some components of keratinocytes affect the formation and differentiation of the stratum corneum, which is the most specialized layer of the epidermis.

The fungus Cryptococcus neoformans is pervasive in our environment and causes the infectious disease cryptococcosis in humans, most commonly in immunocompromised patients. In addition to corroborating the avian origins of a case of cryptococcosis in an immunocompromised patient in 2000, a fascinating recent report has now characterized the genetic and phenotypic changes that occur in this C. neoformans during passage in mammalian hosts. Interestingly, mouse-passaged isolates showed differences in virulence factors ranging from capsule size, melanization, nonlytic macrophage exocytosis, and amoeba predation resistance as compared to the patient strain. Taken together, these results provide new insights about the relationship between mutations acquired during an infection and changes in virulence.

Adenoid organoids, as the primary immune barrier of the airway, provide valuable models for studying lymphatic tissue function, but their histological processing remains challenging due to their fragile structure and lack of adhesion. Here, we introduce a novel approach that combines eosin pre-staining with agarose pre-embedding to enhance visibility and structural integrity during paraffin embedding. This method simplifies sectioning and improves the quality of hematoxylin and eosin (HE) and immunofluorescence (IF) staining, yielding clear and stable signals. By addressing key limitations in lymphatic organoid processing, this technique provides a reliable solution for histological and IF studies, facilitating future research on adenoid organoids.

VE-cadherin is a key transmembrane protein involved in endothelial cell-cell junctions, playing a crucial role in maintaining vascular integrity and regulating selective leukocyte extravasation into inflamed tissue. The extracellular domain of human VE-cadherin contains two arginine-glycine-aspartate (RGD) motifs, which are known integrin-binding sites within extracellular matrix proteins, particularly for integrins of the β1, β3, and β5 families. In this study, we examined the functional relevance of these RGD motifs by generating VE-cadherin variants in which the RGD sequences were mutated to nonfunctional RGE. Immunofluorescence analysis showed that the VE-cadherin [D238E], VE-cadherin [D301E], and double-mutant VE-cadherin [D238/301E] variants formed stable endothelial cell-cell junctions that were comparable to junctions based on wild-type VE-cadherin. Additionally, electric cell-substrate impedance sensing (ECIS) confirmed that endothelial cells expressing each VE-cadherin RGD>RGE variant maintained efficient barrier function capacity. Moreover, monocyte transmigration assays demonstrated that the RGD>RGE mutations did not affect monocyte-endothelial interactions during transmigration. In summary, our findings indicate that the VE-cadherin RGD motifs are not essential for endothelial junction formation or monocyte transmigration.

Statement of RetractionWe, the Editors and Publisher of the journal Tissue Barriers, have retracted the following article:Cao, Q., Zeng, W., Nie, J., Ye, Y., & Chen, Y. (2024). The protective effects of apelin-13 in HIV-1 tat- induced macrophage infiltration and BBB impairment. Tissue Barriers. https://doi.org/10.1080/21688370.2024.2392361After publication, the corresponding author requested the withdrawal of the article because none of the listed authors had agreed to the publication of the article. When contacted for further information, only the corresponding author has responded. The corresponding author has provided proof of their affiliation and details of their current email address, which differs from the email address associated with the submission and publication of the article.As determining authorship is core to the integrity of published work, we are therefore retracting the article. The corresponding author listed in this publication has been informed.We have been informed in our decision-making by our editorial policies and the COPE guidelines.The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as 'Retracted'.

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.

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.

The blood-brain barrier (BBB) regulates the exchange of metabolites and cells between the blood and brain, and maintains central nervous system homeostasis. Various factors affect BBB barrier functions, including reactive oxygen species (ROS). ROS can act as stressors, damaging biological molecules, but they also serve as secondary messengers in intracellular signaling cascades during redox signaling. The impact of ROS on the BBB has been observed in multiple sclerosis, stroke, trauma, and other neurological disorders, making blocking ROS generation a promising therapeutic strategy for BBB dysfunction. However, it is important to consider ROS generation during normal BBB functioning for signaling purposes. This review summarizes data on proteins expressed by BBB cells that can be targets of redox signaling or oxidative stress. It also provides examples of signaling molecules whose impact may cause ROS generation in the BBB, as well as discusses the most common diseases associated with BBB dysfunction and excessive ROS generation, open questions that arise in the study of this problem, and possible ways to overcome them.

The immunohistochemical expression of various members of the claudin family has already been studied in pathological affections of the vulva whether to differentiate precancerous lesions from vulvar squamous cell carcinoma or in inflammatory conditions such as lichen sclerosus. From an oncological perspective, however, immunohistochemical analysis of claudin 18.2 protein expression has become increasingly clinically relevant nowadays since the impressive therapeutic benefits of the claudin 18.2 antibody zolbetuximab have been widely recognized. Systematic studies evaluating its expression, including in vulvar cancer, are needed to understand whether such treatment strategies may eventually benefit patients with vulvar neoplasia.

In this review we discuss mucus, the viscoelastic secretion from goblet or mucous producing cells that covers and protects all non-keratinized wet epithelial surfaces. In addition to the surface of organs directly contacting with the external environment such as the eyes, this layer provides protection to the underlying gastrointestinal, respiratory and female reproductive tracts by trapping pathogens, irritants, environmental fine particles and potentially harmful foreign substances. Mucins, the primary structural components of mucus, form structurally different mucus layers at different sites in a process regulated by a variety of factors. Currently, more and more studies have shown that the mucus barrier is not only closely related to various intestinal mucus diseases, but also involved in the occurrence and development of various airway diseases and mucus-related diseases, thus it may become a new target for the treatment of various related diseases in the future. Since the dysfunction of the mucous layer is closely related to various pathological processes, in-depth understanding of its molecular mechanism and physiological role is of great theoretical and practical significance for disease prevention and treatment. Here, we discuss different aspects of the mucus layer by focusing on its chemical composition, synthetic pathways, and some of the characteristics of the mucus layer in physiological and pathological situations.