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1
Kawao, Naoyuki, and Hiroshi Kaji. "Interactions Between Muscle Tissues and Bone Metabolism." Journal of Cellular Biochemistry 116, no. 5 (March 9, 2015): 687–95. http://dx.doi.org/10.1002/jcb.25040.
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Tomas, Eva, Meghan Kelly, Xiaoqin Xiang, Tsu-Shuen Tsao, Charlotte Keller, Pernille Keller, Zhijun Luo, et al. "Metabolic and hormonal interactions between muscle and adipose tissue." Proceedings of the Nutrition Society 63, no. 2 (May 2004): 381–85. http://dx.doi.org/10.1079/pns2004356.
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From the perspective of a muscle physiologist, adipose tissue has long been perceived predominantly as a fuel reservoir that provides muscle and other tissues with NEFA when exogenous nutrients are insufficient for their energy needs. Recently, studies have established that adipose tissue is also an endocrine organ. Among the hormones it releases are adiponectin and leptin, both of which can activate AMP-activated protein kinase and increase fatty acid oxidation in skeletal muscle and probably other tissues. Deficiencies of leptin or leptin receptor, adiponectin and IL-6 are associated with obesity, insulin resistance and a propensity to type 2 diabetes. In addition, a lack of adiponectin has been linked to atherosclerosis. Whether this pathology reflects a deficient activation of AMP-activated protein kinase in peripheral tissues remains to be determined. Finally, recent studies have suggested that skeletal muscle may also function as an endocrine organ when it releases the cytokine IL-6 into the circulation during sustained exercise. Interestingly, one of the apparent effects of IL-6 is to stimulate lipolysis, causing the release of NEFA from the adipocyte. Thus, hormonal communications exist between the adipocyte and muscle that could enable them to talk to each other. The physiological relevance of this cross talk clearly warrants further study.
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Tsang, Anthony H., Johanna L. Barclay, and Henrik Oster. "Interactions between endocrine and circadian systems." Journal of Molecular Endocrinology 52, no. 1 (August 30, 2013): R1—R16. http://dx.doi.org/10.1530/jme-13-0118.
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In most species, endogenous circadian clocks regulate 24-h rhythms of behavior and physiology. Clock disruption has been associated with decreased cognitive performance and increased propensity to develop obesity, diabetes, and cancer. Many hormonal factors show robust diurnal secretion rhythms, some of which are involved in mediating clock output from the brain to peripheral tissues. In this review, we describe the mechanisms of clock–hormone interaction in mammals, the contribution of different tissue oscillators to hormonal regulation, and how changes in circadian timing impinge on endocrine signalling and downstream processes. We further summarize recent findings suggesting that hormonal signals may feed back on circadian regulation and how this crosstalk interferes with physiological and metabolic homeostasis.
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Nammour, S., H. S. Loh, R. De Moor, and C. P. Eduardo. "Interactions between Oral Tissues and External Light and Matters." International Journal of Dentistry 2012 (2012): 1. http://dx.doi.org/10.1155/2012/726259.
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Nagase, T., T. Ito, M. Yanai, J. G. Martin, and M. S. Ludwig. "Responsiveness of and interactions between airways and tissue in guinea pigs during induced constriction." Journal of Applied Physiology 74, no. 6 (June 1, 1993): 2848–54. http://dx.doi.org/10.1152/jappl.1993.74.6.2848.
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Mechanical interdependence between airways and tissues can modify the magnitude of induced bronchoconstriction. We questioned whether the guinea pig, an animal with abundant airway smooth muscle, would differ from other species in the relative responsiveness of and interactions between airways and tissues. Therefore we induced constriction with aerosolized methacholine (MCh) and partitioned responses into airway and tissue components. We measured tracheal and alveolar pressures using alveolar capsules in open-chest guinea pigs (n = 9) during mechanical ventilation [frequency = 1 Hz, tidal volume = 6 ml/kg, positive end-expiratory pressure (PEEP) = 5 cmH2O] and calculated the resistance of lung (RL), tissue (Rti), and airway (Raw) before and after administration of aerosols of MCh in progressively doubling concentrations (0.063–16 mg/ml). In separate animals (n = 10), measurements were made at 3–13 cmH2O PEEP. After aerosols of saline and MCh (0.125-32 mg/ml), measurements were repeated at 3, 7, and 11 cmH2O PEEP. At submaximal levels of constriction, the airways and lung tissues demonstrated similar responsiveness. Increasing PEEP increased RL and Rti and decreased Raw under baseline conditions. At low concentrations of MCh, increasing PEEP increased RL but decreased RL at the highest concentration. Increases in PEEP significantly increased Rti at all concentrations of MCh but decreased Raw only at 8 mg/ml of MCh. These observations demonstrate that, in guinea pigs, during submaximal constriction, airways and tissues behave similarly; moreover, airway-parenchymal interdependence is important in determining the level of bronchoconstriction.
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Wang, Congcong, Zihan Yi, Ye Jiao, Zhong Shen, Fei Yang, and Shankuan Zhu. "Gut Microbiota and Adipose Tissue Microenvironment Interactions in Obesity." Metabolites 13, no. 7 (July 5, 2023): 821. http://dx.doi.org/10.3390/metabo13070821.
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Obesity is an increasingly serious global health problem. Some studies have revealed that the gut microbiota and its metabolites make important contributions to the onset of obesity. The gut microbiota is a dynamic ecosystem composed of diverse microbial communities with key regulatory functions in host metabolism and energy balance. Disruption of the gut microbiota can result in obesity, a chronic metabolic condition characterized by the excessive accumulation of adipose tissue. Host tissues (e.g., adipose, intestinal epithelial, and muscle tissues) can modulate the gut microbiota via microenvironmental interactions that involve hormone and cytokine secretion, changes in nutrient availability, and modifications of the gut environment. The interactions between host tissues and the gut microbiota are complex and bidirectional, with important effects on host health and obesity. This review provides a comprehensive summary of gut microbiota changes associated with obesity, the functional roles of gut microbiota-derived metabolites, and the importance of the complex interactions between the gut microbiota and target tissues in the pathogenesis of obesity. It places particular emphasis on the roles of adipose tissue microenvironment interactions in the onset of obesity.
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Rainbow, Roshni, Weiping Ren, and Li Zeng. "Inflammation and Joint Tissue Interactions in OA: Implications for Potential Therapeutic Approaches." Arthritis 2012 (June 18, 2012): 1–8. http://dx.doi.org/10.1155/2012/741582.
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It is increasingly recognized that the pathogenesis of cartilage degradation in osteoarthritis (OA) is multifactorial and involves the interactions between cartilage and its surrounding tissues. These interactions regulate proinflammatory cytokine-mediated cartilage destruction, contributing to OA progression as well as cartilage repair. This review explores the pathogenesis of OA in the context of the multiple tissue types in the joint and discusses the implications of such complex tissue interaction in the development of anti-inflammatory therapeutics for the treatment of OA.
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Amponsah, N. T., E. E. Jones, H. J. Ridgway, and M. V. Jaspers. "Microscopy of some interactions between Botryosphaeriaceae species and grapevine tissues." Australasian Plant Pathology 41, no. 6 (August 5, 2012): 665–73. http://dx.doi.org/10.1007/s13313-012-0159-x.
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Herrmann, Marietta, Klaus Engelke, Regina Ebert, Sigrid Müller-Deubert, Maximilian Rudert, Fani Ziouti, Franziska Jundt, Dieter Felsenberg, and Franz Jakob. "Interactions between Muscle and Bone—Where Physics Meets Biology." Biomolecules 10, no. 3 (March 10, 2020): 432. http://dx.doi.org/10.3390/biom10030432.
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Muscle and bone interact via physical forces and secreted osteokines and myokines. Physical forces are generated through gravity, locomotion, exercise, and external devices. Cells sense mechanical strain via adhesion molecules and translate it into biochemical responses, modulating the basic mechanisms of cellular biology such as lineage commitment, tissue formation, and maturation. This may result in the initiation of bone formation, muscle hypertrophy, and the enhanced production of extracellular matrix constituents, adhesion molecules, and cytoskeletal elements. Bone and muscle mass, resistance to strain, and the stiffness of matrix, cells, and tissues are enhanced, influencing fracture resistance and muscle power. This propagates a dynamic and continuous reciprocity of physicochemical interaction. Secreted growth and differentiation factors are important effectors of mutual interaction. The acute effects of exercise induce the secretion of exosomes with cargo molecules that are capable of mediating the endocrine effects between muscle, bone, and the organism. Long-term changes induce adaptations of the respective tissue secretome that maintain adequate homeostatic conditions. Lessons from unloading, microgravity, and disuse teach us that gratuitous tissue is removed or reorganized while immobility and inflammation trigger muscle and bone marrow fatty infiltration and propagate degenerative diseases such as sarcopenia and osteoporosis. Ongoing research will certainly find new therapeutic targets for prevention and treatment.
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Elofsson, Hampus, Doroteya Raykova, and Agata Zieba Wicher. "Abstract 6772: Powerful background reduction in fluorescent tissue stains with an improved proximity-based technology for detection of protein-protein interactions." Cancer Research 83, no. 7_Supplement (April 4, 2023): 6772. http://dx.doi.org/10.1158/1538-7445.am2023-6772.
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Abstract Immunofluorescent staining of tissues via in situ proximity ligation assay (isPLA) is now a well-established tool for highly sensitive detection of protein-protein interactions and their localization. It finds versatile applications in basic research, understanding of cellular processes, visualization of tissue architecture, and identification of biomarkers, among others. However, standard IF and isPLA techniques alike may suffer from high background. Tissues are particularly affected by background problems caused by autofluorescence and tissue infiltration of various cell types (e.g., immune, endothelial) where the fluorescently labelled oligos used for detection in isPLA may bind unspecifically. To address this, we developed a next generation isPLA-based technology for fluorescent detection of protein interactions in FFPE and fresh frozen human and mouse tissues, called NaveniFlex Tissue. In contrast to previously available protocols, it can visualize signal that would otherwise be obscured by background, thereby increasing sensitivity. Here, we compare the ability of NaveniFlex Tissue and similar commercial kits to detect the interaction between low abundance proteins Podocalyxin and Ezrin in the glomeruli of healthy kidney and in breast cancer, where co-expression is a prognostic marker for increased metastatic potential. While other kits generate high background which masks isPLA signal entirely, NaveniFlex Tissue dramatically reduces cell-based background and visualizes the interaction in its specific localization. Furthermore, in a TMA staining for the Mucin 16/Mesothelin interaction, our method successfully demonstrates strong and clear signal in stage III ovarian cancer. Moreover, it sensitively detects even low abundance interaction in a stage Ia tumor. In contrast, a different commercial kit detects significantly less interactions in the stage III tumor, while in the lower grade tumor it does not generate signals above background level. Therefore, NaveniFlex Tissue improves detection in tissues with varying disease progression, thus adding information and prognostic value to the staining. Taken together, our data illustrate that NaveniFlex Tissue outperforms current isPLA-based techniques by efficiently reducing background, which improves visualization of signal and signal-to-noise ratios in various healthy and diseased tissues. Citation Format: Hampus Elofsson, Doroteya Raykova, Agata Zieba Wicher. Powerful background reduction in fluorescent tissue stains with an improved proximity-based technology for detection of protein-protein interactions. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 6772.
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Borrmann, Helene, and Filipa Rijo-Ferreira. "Crosstalk between circadian clocks and pathogen niche." PLOS Pathogens 20, no. 5 (May 9, 2024): e1012157. http://dx.doi.org/10.1371/journal.ppat.1012157.
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Circadian rhythms are intrinsic 24-hour oscillations found in nearly all life forms. They orchestrate key physiological and behavioral processes, allowing anticipation and response to daily environmental changes. These rhythms manifest across entire organisms, in various organs, and through intricate molecular feedback loops that govern cellular oscillations. Recent studies describe circadian regulation of pathogens, including parasites, bacteria, viruses, and fungi, some of which have their own circadian rhythms while others are influenced by the rhythmic environment of hosts. Pathogens target specific tissues and organs within the host to optimize their replication. Diverse cellular compositions and the interplay among various cell types create unique microenvironments in different tissues, and distinctive organs have unique circadian biology. Hence, residing pathogens are exposed to cyclic conditions, which can profoundly impact host–pathogen interactions. This review explores the influence of circadian rhythms and mammalian tissue-specific interactions on the dynamics of pathogen–host relationships. Overall, this demonstrates the intricate interplay between the body’s internal timekeeping system and its susceptibility to pathogens, which has implications for the future of infectious disease research and treatment.
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Davey, Marie L., and Randolph S. Currah. "Interactions between mosses (Bryophyta) and fungi." Canadian Journal of Botany 84, no. 10 (October 2006): 1509–19. http://dx.doi.org/10.1139/b06-120.
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A taxonomically diverse suite of fungi interacts with bryophytes as pathogens, parasites, saprobes, and commensals. Necrotrophic pathogens such as Tephrocybe palustris (Peck) Donk and Nectria mnii Döbbeler form patches of moribund gametophytes in otherwise healthy mats of mosses. These pathogens exhibit different methods of host cell disruption; N. mnii appears to displace the host cell protoplast with intracellular hyphae, while T. palustris causes host protoplast degeneration. Host responses to infection by bryopathogens are also variable. Host–pathogen relationships can be highly evolved, as in Bryophytomyces sphagni (Navashin) Cif., in which fungal propagules replace the bryophyte spores, and exploit the explosive dispersal mechanisms of the Sphagnum host. Bryophilous parasites tend to exhibit high tissue or cellular specificity with varying host specificity. For example, Octospora similis (Kirchstein) Benkert infects the rhizoids of species of Bryum, and Discinella schimperi (Navashin) Redhead specifically colonizes the mucilage producing cells of stems of Sphagnum squarrosum Crome. Eocronartium muscicola (Pers.) Fitzp. demonstrates a highly evolved host–parasite relationship in which the basidiocarp displaces the sporophyte and is fed directly by the gametophyte through specialized transfer tissues. Fungi such as Oidiodendron maius Barron are capable of decomposing moss cell walls that are generally resistant to decomposition because of their polyphenolic component. Mycorrhizal fungi, including Glomus, Suillus, and Endogone, have not been observed to form functional, nutrient-exchanging mycorrhizal interfaces with bryophytes, rather, they function as saprobes on moribund and senescent gametophytes. Finally, endophytic fungi may provide bryophyte hosts with greater tolerance to extreme pH or promote vegetative growth. In vivo observation of bryophyte–fungus interactions has provided insight into the types of interactions that occur; however to further understand the physiology, anatomy, and etiology of these interactions, it is necessary to culture bryophilous fungi in vitro and create artificial axenic systems for study.
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Mahmood, R., K. C. Flanders, and G. M. Morriss-Kay. "Interactions between retinoids and TGF beta s in mouse morphogenesis." Development 115, no. 1 (May 1, 1992): 67–74. http://dx.doi.org/10.1242/dev.115.1.67.
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Using immunocytochemical methods we describe the distribution of different TGF beta isoforms and the effects of excess retinoic acid on their expression during early mouse embryogenesis (8 1/2 - 10 1/2 days of development). In normal embryos at 9 days, intracellular TGF beta 1 is expressed most intensely in neuroepithelium and cardiac myocardium whereas extracellular TGF beta 1 is expressed in mesenchymal cells and in the endocardium of the heart. At later stages, intracellular TGF beta 1 becomes very restricted to the myocardium and to a limited number of head mesenchymal cells; extracellular TGF beta 1 continues to be expressed widely in cells of mesenchymal origin, particularly in head and trunk mesenchyme, and also in endocardium. TGF beta 2 is widely expressed at all stages investigated while TGF beta 3 is not expressed strongly in any tissue at the stages examined. Exposure of early neural plate stage embryos to retinoic acid caused reduced expression of TGF beta 1 and TGF beta 2 proteins but had no effect on TGF beta 3. Intracellular TGF beta 1 expression was reduced in all tissues except in the myocardium, while extracellular TGF beta 1 was specifically reduced in neuroepithelium and cranial neural crest cells at early stages. TGF beta 2 was reduced in all embryonic tissues. The down-regulation of intracellular TGF beta 1 was observed up to 48 hours after initial exposure to retinoic acid while some down-regulation of TGF beta 2 was still seen up to 60 hours after initial exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
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Kim-Hellmuth, Sarah, François Aguet, Meritxell Oliva, Manuel Muñoz-Aguirre, Silva Kasela, Valentin Wucher, Stephane E. Castel, et al. "Cell type–specific genetic regulation of gene expression across human tissues." Science 369, no. 6509 (September 10, 2020): eaaz8528. http://dx.doi.org/10.1126/science.aaz8528.
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The Genotype-Tissue Expression (GTEx) project has identified expression and splicing quantitative trait loci in cis (QTLs) for the majority of genes across a wide range of human tissues. However, the functional characterization of these QTLs has been limited by the heterogeneous cellular composition of GTEx tissue samples. We mapped interactions between computational estimates of cell type abundance and genotype to identify cell type–interaction QTLs for seven cell types and show that cell type–interaction expression QTLs (eQTLs) provide finer resolution to tissue specificity than bulk tissue cis-eQTLs. Analyses of genetic associations with 87 complex traits show a contribution from cell type–interaction QTLs and enables the discovery of hundreds of previously unidentified colocalized loci that are masked in bulk tissue.
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Mijanović, Olja, Timofey Pylaev, Angelina Nikitkina, Margarita Artyukhova, Ana Branković, Maria Peshkova, Polina Bikmulina, et al. "Tissue Engineering Meets Nanotechnology: Molecular Mechanism Modulations in Cornea Regeneration." Micromachines 12, no. 11 (October 30, 2021): 1336. http://dx.doi.org/10.3390/mi12111336.
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Nowadays, tissue engineering is one of the most promising approaches for the regeneration of various tissues and organs, including the cornea. However, the inability of biomaterial scaffolds to successfully integrate into the environment of surrounding tissues is one of the main challenges that sufficiently limits the restoration of damaged corneal tissues. Thus, the modulation of molecular and cellular mechanisms is important and necessary for successful graft integration and long-term survival. The dynamics of molecular interactions affecting the site of injury will determine the corneal transplantation efficacy and the post-surgery clinical outcome. The interactions between biomaterial surfaces, cells and their microenvironment can regulate cell behavior and alter their physiology and signaling pathways. Nanotechnology is an advantageous tool for the current understanding, coordination, and directed regulation of molecular cell–transplant interactions on behalf of the healing of corneal wounds. Therefore, the use of various nanotechnological strategies will provide new solutions to the problem of corneal allograft rejection, by modulating and regulating host–graft interaction dynamics towards proper integration and long-term functionality of the transplant.
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Rey, P., N. Benhamou, E. Wulff, and Y. Tirilly. "Interactions between tomato (Lycopersicon esculentum) root tissues and the mycoparasitePythium oligandrum." Physiological and Molecular Plant Pathology 53, no. 2 (August 1998): 105–22. http://dx.doi.org/10.1006/pmpp.1998.0159.
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Tsuneda, Akihiko, and Greg Thorn. "Interactions between Lentinula edodes and pseudomonads." Canadian Journal of Microbiology 40, no. 11 (November 1, 1994): 937–43. http://dx.doi.org/10.1139/m94-150.
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Interactions between four dikaryotic strains of Lentinula edodes and seven strains of Pseudomonas species were investigated in vitro. Two strains of Pseudomonas tolaasii were strongly pathogenic to fruiting bodies of L. edodes, causing browning and lysis of the inoculated tissues. The mode and outcome of interactions on agar varied with the combination between strains of L. edodes and bacteria. Pseudomonas cepacia and two strains of Pseudomonas tolaasii inhibited hyphal growth of L. edodes strains, whereas Pseudomonas fluorescens and one strain of Pseudomonas tolaasii were generally susceptible to bacteriolysis by L. edodes. Strains of L. edodes differed markedly in their ability to attack and lyse bacteria. In general, hyphal tips were the most potent in bacteriolysis. Ultrastructural variations were recognized in the process of bacterial wall degradation by L. edodes hyphae, but walls were eventually disintegrated to minute granules that ranged in diameter from 0.05 μm to smaller than measurable by scanning electron microscopy.Key words: bacteriolysis, cell wall, Pseudomonas, Lentinula, SEM.
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Edén, Desirée, Jonas Vennberg, Tanja Büsgen, Doroteya Raykova, and Agata Zieba-Wicher. "Abstract 72: A spatial interactomics approach reveals interplay between the tumor microenvironment and T cell activation." Cancer Research 84, no. 6_Supplement (March 22, 2024): 72. http://dx.doi.org/10.1158/1538-7445.am2024-72.
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Abstract Background: T cells play a fundamental role in immune response to tumors. However, the tumor microenvironment (TME) - a complex network of cells, signaling molecules, and extracellular matrix components - employs various strategies to evade immune surveillance and suppress T cell activity. Among the many molecular interactions taking place in the TME, the role of CD8/MHC I, LAG3/MHC II and PD1/PDL1 is pivotal in modulating anti-cancer response and the escape routes that cancer in turn uses to withstand immune defense. LAG3/MHC II and PD1/PDL1 interactions are inhibitory, causing T cell dysfunction and exhaustion, while the CD8/MHC I interaction is essential for initiating an effective anti-tumor response. Here, we used a cutting-edge in situ proximity ligation strategy combined with immunofluorescence (IF) to reveal these key interactions and TME biomarkers in hepatocellular carcinoma and Hodgkin lymphoma. Since the method does not compromise the structural integrity of tissues, communication between proteins can be studied in their native milieu. Method: Protein-protein interactions (PPIs) were detected with the NaveniFlex Tissue Atto647N kit in human FFPE tissues according to the manufacturer’s protocol. This technique can detect proteins located within interaction range (<40 nm) via oligonucleotide-antibody conjugates that create amplified fluorescent signal. Parallel IF co-staining for α-fetoprotein, Ki67, CD30 and CD3 was performed during the Naveni® detection step. Slides were mounted and imaged on the Olympus V200 automated scanner. Results: Tumor cells were identified by α-fetoprotein/Ki67 (hepatocellular carcinoma) or CD30 (Reed-Sternberg in Hodgkin lymphoma) IF staining, and tumor-infiltrating lymphocytes were visualized by CD3 staining. With the help of the Naveni® assay, we observed abundant interaction between CD8/MHC I in hepatocellular carcinoma and Hodgkin lymphoma. Suppressive immune checkpoint interactions such as LAG3/MHC II and PD1/PDL1 were also detected. In the case of Hodgkin lymphoma, the CD8/MHC I, LAG3/MHC II and PD1/PDL1 interactions were largely seen in the same areas, and specifically between T cells and Reed-Sternberg cells, indicating a crosstalk between the TME and the immune landscape in the cancer tissues. Conclusion: The interactomics approach, employing in situ proximity ligation for observing protein function as opposed to mere expression, allows the detection of key PPIs in the TME. Understanding the intricate crosstalk between them is crucial in developing effective immunotherapies. Targeting these pathways simultaneously or in combination, such as using immune checkpoint inhibitors against PD1/PDL1 while exploring strategies to modulate LAG3/MHC II and CD8/MHC I interactions, holds promise in reinvigorating T cell responses against cancer and improving the efficacy of immunotherapies within the complex landscape of the TME. Citation Format: Desirée Edén, Jonas Vennberg, Tanja Büsgen, Doroteya Raykova, Agata Zieba-Wicher. A spatial interactomics approach reveals interplay between the tumor microenvironment and T cell activation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 72.
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Pond, C. M. "Adipose tissue, the immune system and exercise fatigue: how activated lymphocytes compete for lipids." Biochemical Society Transactions 30, no. 2 (April 1, 2002): 270–75. http://dx.doi.org/10.1042/bst0300270.
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Adipose depots that contain lymph nodes, and probably intermuscular fat in skeletal and cardiac muscle, are specialized to provision adjacent tissue in a paracrine mode. Perinodal adipocytes respond selectively to various cytokines and incorporate proportionately more polyunsaturated fatty acids. Lipolysis in the adipocytes of node-containing depots can be stimulated via inflammation of the enclosed lymph nodes. Repeated immune stimulation elicits properties characteristic of perinodal adipocytes in those elsewhere in the same depot, and hours later in other node-containing depots, but not in nodeless depots. Such site-specific properties of adipose tissue enable partitioning of dietary and metabolic supplies of fatty acids between competing tissues. Local interactions emancipate the peripheral immune system from competing with other tissues for lipids during immune responses, and may be especially important during periods of high demand, such as strenuous exercise. Biopsies of subcutaneous adipose tissue from sites remote from lymph nodes do not adequately represent the composition of fatty acids available to the immune system in situ, and perhaps that supplied to other tissues. Intermuscular fat in skeletal and cardiac muscle may also indicate paracrine relationships between adipocytes and ‘end-user’ tissues. The concept of paracrine interactions between certain adipocytes and ‘user’ tissue may account for the widespread contiguity between these tissues in vivo.
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Noden, Drew M. "Interactions and fates of avian craniofacial mesenchyme." Development 103, Supplement (September 1, 1988): 121–40. http://dx.doi.org/10.1242/dev.103.supplement.121.
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Craniofacial mesenchyme is composed of three mesodermal populations – prechordal plate, lateral mesoderm and paraxial mesoderm, which includes the segmented occipital somites and the incompletely segmented somitomeres – and the neural crest. This paper outlines the fates of each of these, as determined using quail–chick chimaeras, and presents similarities and differences between these cephalic populations and their counterparts in the trunk. Prechordal and paraxial mesodermal populations are the sources of all voluntary muscles of the head. The latter also provides most of the connective precursors of the calvaria, occipital, otic–parietal and basisphenoid tissues. Lateral mesoderm is the source of peripharyngeal connective tissues; the most rostral skeletal tissues it forms are the laryngeal and tracheal cartilages. When migrating neural crest cells encounter segmented paraxial mesoderm (occipital and trunk somites), most move into the region between the dermamyotome and sclerotome in the cranial half of each somite. In contrast, most cephalic crest cells migrate superficial to somitomeres. There is, however, a small subpopulation of the head crest that invades somitomeric mesoderm. These cells subsequently segregate presumptive myogenic precursors of visceral arch voluntary muscles from underlying mesenchyme. In the neurula-stage avian embryo, all paraxial and lateral mesodermal populations contain precursors of vascular endothelial cells, which can be detected in chimaeric embryos using anti-quail endothelial antibodies. Some of these angioblasts differentiate in situ, contributing directly to pre-existing vessels or forming isolated, nonpatent, cords that subsequently vesiculate and fuse with nearby vessels. Many angioblasts migrate in all directions, invading embryonic mesenchymal and epithelial tissues and participating in new blood vessel formation in distant sites. The interactions leading to proper spatial patterning of craniofacial skeletal, muscular, vascular and peripheral neural tissues has been studied by performing heterotopic transplants of each of these mesodermal and neural crest populations. The results consistently indicate that connective tissue precursors, regardless of their origin, contain spatial information used by the precursors of muscles and blood vessels and by outgrowing peripheral nerves. Some of these connective tissue precursors (e.g. the neural crest, paraxial mesoderm) acquire their spatial programming while in association with the central nervous system or developing sensory epithelia (e.g. otic, optic, nasal epithelia).
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ten Cate, J. M., and J. D. B. Featherstone. "Mechanistic Aspects of the Interactions Between Fluoride and Dental Enamel." Critical Reviews in Oral Biology & Medicine 2, no. 3 (July 1991): 283–96. http://dx.doi.org/10.1177/10454411910020030101.
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For many years after the discovery of its caries preventive effect, fluoride was thought to be primarily active by lowering the solubility of the apatitic mineral phase of the dental hard tissues. Recent findings have shed new light on the mechanisms by which fluoride inhibits or delays dental caries. Fluoride present in the oral fluids alters the rate of the naturally occurring dissolution and reprecipitation processes at the tooth-oral fluid interface. Demineralization of enamel is inhibited by concentrations of fluoride in the sub-ppm range. Likewise, remineralization of incipient caries lesions (the earliest stage of enamel caries) is accelerated by trace amounts of fluoride. As these two processes comprise dental caries the physiological balance between hard tissue breakdown and repair is favorably shifted by fluoride. The driving force for both phenomena is thermodynamic, that is, fluorapatite or a fluoridated hydroxyapatite may form when fluoride is supplied at low concentrations. This article critically reviews the current information about tooth-fluoride interactions, both from laboratory and clinical studies.
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Barz, Cristian, Marek Petters, Adam Dorsz, and Przemysław Syrek. "Possible Interactions Between Stent and Electromagnetic Field." Science, Technology and Innovation 3, no. 2 (December 23, 2018): 48–51. http://dx.doi.org/10.5604/01.3001.0012.8156.
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Over the past years, an increase in the amount of the electromagnetic sources could be observed. Model presented in this article is limited to the impact of low frequency fields generated by the e.g. electrical power lines or magnetic coils in a bone fractures therapy. Particularly, the effect of the magnetic component of the electromagnetic field on stents will be evaluated. The conductivity of human tissues will be investigated. Yielded results will be used to simplify complicated, three-dimensional problem of the current distribution in stent branches, to one-dimensional one. The merits of the paper is proposing, implementing and using for analysis a numerical model of the stent in magnetic field. The impact of frequency and positioning of stent in the magnetic field will be investigated and current distributions found.
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Sorrell, J. Michael, and Arnold I. Caplan. "Heparan Sulfate: A Regulator of White Adipocyte Differentiation and of Vascular/Adipocyte Interactions." Biomedicines 10, no. 9 (August 29, 2022): 2115. http://dx.doi.org/10.3390/biomedicines10092115.
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White adipose tissues are major endocrine organs that release factors, termed adipokines, which affect other major organ systems. The development and functions of adipose tissues depend largely upon the glycosaminoglycan heparan sulfate. Heparan sulfate proteoglycans (HSPGs) surround both adipocytes and vascular structures and facilitate the communication between these two components. This communication mediates the continued export of adipokines from adipose tissues. Heparan sulfates regulate cellular physiology and communication through a sulfation code that ionically interacts with heparan-binding regions on a select set of proteins. Many of these proteins are growth factors and chemokines that regulate tissue function and inflammation. Cells regulate heparan sulfate sulfation through the release of heparanases and sulfatases. It is now possible to tissue engineer vascularized adipose tissues that express heparan sulfate proteoglycans. This makes it possible to use these tissue constructs to study the role of heparan sulfates in the regulation of adipokine production and release. It is possible to regulate the production of heparanases and sulfatases in order to fine-tune experimental studies.
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Bonnet, Muriel, Nicolas Kaspric, Kimberly Vonnahme, Didier Viala, Christophe Chambon, and Brigitte Picard. "Prediction of the Secretome and the Surfaceome: A Strategy to Decipher the Crosstalk between Adipose Tissue and Muscle during Fetal Growth." International Journal of Molecular Sciences 21, no. 12 (June 19, 2020): 4375. http://dx.doi.org/10.3390/ijms21124375.
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Crosstalk between adipose and muscular tissues is hypothesized to regulate the number of muscular and adipose cells during fetal growth, with post-natal consequences on lean and fat masses. Such crosstalk largely remains, however, to be described. We hypothesized that a characterization of the proteomes of adipose and muscular tissues from bovine fetuses may enhance the understanding of the crosstalk between these tissues through the prediction of their secretomes and surfaceomes. Proteomic experiments have identified 751 and 514 proteins in fetal adipose tissue and muscle. These are mainly involved in the regulation of cell proliferation or differentiation, but also in pathways such as apoptosis, Wnt signalling, or cytokine-mediated signalling. Of the identified proteins, 51 adipokines, 11 myokines, and 37 adipomyokines were predicted, together with 26 adipose and 13 muscular cell surface proteins. Analysis of protein–protein interactions suggested 13 links between secreted and cell surface proteins that may contribute to the adipose–muscular crosstalk. Of these, an interaction between the adipokine plasminogen and the muscular cell surface alpha-enolase may regulate the fetal myogenesis. The in silico secretome and surfaceome analyzed herein exemplify a powerful strategy to enhance the elucidation of the crosstalk between cell types or tissues.
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Eun, C. S., E. H. Oh, A. R. Lee, C. H. Park, and D. S. Han. "P913 Interactions between Intestinal Microbiota and micro-RNAs in Inflammatory Bowel Disease." Journal of Crohn's and Colitis 17, Supplement_1 (January 30, 2023): i1025. http://dx.doi.org/10.1093/ecco-jcc/jjac190.1043.
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Abstract Background Both gut microbiota and micro-RNAs (miRNAs) have been implicated in the pathogenesis of inflammatory bowel disease (IBD). We aimed to investigate the interactions between gut microbiota and miRNAs which are altered in murine colitis models and patients with IBD using multi-omics analysis. Methods Gut microbiota and miRNAs were analyzed in a mouse experiment (7 dextran sodium sulfate [DSS]-treated mice, 7 azoxymethane [AOM] and DSS-treated mice, and 6 controls) and a human experiment (10 patients with active Crohn’s disease, 10 patients with active ulcerative colitis [UC], and 8 healthy controls). DNA was extracted from mouse feces and human colonic tissues, and 16S rRNA gene sequencing was performed to evaluate changes in gut microbiota. miRNA expression levels were measured by microarray analysis from mouse and human colonic tissues. mRNA expression levels were examined by microarray analysis from colonic tissues of UC patients. Correlation and network analyses were performed to evaluate the interactions among gut microbiota, miRNAs and mRNAs. Results Principal coordinate analysis showed distinct gut microbiota composition and miRNA expressions among the groups in the mouse and human experiments. Also, comparative analysis showed many miRNAs differentially expressed and many bacterial amplicon sequence variants (ASVs) differentially identified among the groups. Spearman correlation rank test and network analysis revealed multiple correlations and interactions among specific miRNAs and bacterial ASVs. In UC patients, genes associated with functional categories in biological process, such as positive regulation of cytokine production, cytokine-mediated signaling pathway, cell adhesion, positive regulation of response to external stimulus, and leukocyte migration were upregulated than healthy controls. mRNAs in UC patients also showed multiple correlations and interactions with specific miRNAs and bacterial ASVs. Conclusion Gut microbiota composition and miRNA expressions were distinctly altered in patients with IBD and murine colitis models. Specific miRNAs were associated with specific bacterial ASVs and mRNAs, suggesting the interactions among miRNAs, gut microbiota and mRNAs in the pathogenesis of IBD. Our data imply that global complicated interactions between gut microbiota and miRNAs, rather than specific individual microbiota-miRNA interaction, might play more important role in IBD.
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Rhodes, Judith C. "Aspergillusproteinases and their interactions with host tissues." Canadian Journal of Botany 73, S1 (December 31, 1995): 1126–31. http://dx.doi.org/10.1139/b95-368.
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Invasive aspergillosis is a life-threatening infection that is caused primarily by the species Aspergillus fumigatus and A. flavus, both of which are highly angioinvasive. From this observation, interest has focused on proteinases produced by these organisms and their possible roles in the pathogenesis of infection. Both species produce alkaline serine proteinases (ALP) and metalloproteinases during the course of infection based on immunohistochemistry of experimental lesions and serologic response of patients. These enzymes can be shown to degrade numerous biologically relevant targets, including elastin, collagen, laminin, fibrinogen, and iC3b. Physicochemical properties, immunoreactivities, and amino acid sequences of the ALP of A. fumigatus and A. flavus show that these two enzymes are closely related. The metalloproteinases, however, appear to represent members of a small family of similar enzymes. Finally, although studies using conventionally produced mutants support roles for these hydrolases as virulence factors in aspergillosis, similar studies using strains of A. fumigatus in which the enzymatic activity has been ablated through gene disruption do not reveal differences in virulence between the wild-type strains and the mutants. Key words: aspergillosis, proteinase, pathogenesis.
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Bose, Subhaya, Kinjal Dasbiswas, and Arvind Gopinath. "Matrix Stiffness Modulates Mechanical Interactions and Promotes Contact between Motile Cells." Biomedicines 9, no. 4 (April 15, 2021): 428. http://dx.doi.org/10.3390/biomedicines9040428.
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The mechanical micro-environment of cells and tissues influences key aspects of cell structure and function, including cell motility. For proper tissue development, cells need to migrate, interact, and form contacts. Cells are known to exert contractile forces on underlying soft substrates and sense deformations in them. Here, we propose and analyze a minimal biophysical model for cell migration and long-range cell–cell interactions through mutual mechanical deformations of the substrate. We compute key metrics of cell motile behavior, such as the number of cell-cell contacts over a given time, the dispersion of cell trajectories, and the probability of permanent cell contact, and analyze how these depend on a cell motility parameter and substrate stiffness. Our results elucidate how cells may sense each other mechanically and generate coordinated movements and provide an extensible framework to further address both mechanical and short-range biophysical interactions.
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Onita (Mladin), Bianca, Paul Albu, Hildegard Herman, Cornel Balta, Vasile Lazar, Andras Fulop, Edina Baranyai, et al. "Correlation between Heavy Metal-Induced Histopathological Changes and Trophic Interactions between Different Fish Species." Applied Sciences 11, no. 9 (April 21, 2021): 3760. http://dx.doi.org/10.3390/app11093760.
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This study assessed the distribution of heavy metals in the gills, kidney, and liver, correlated with the severity of histopathological changes, of three fish species with different feeding habitats (Barbus barbus, Squalius cephalus, and Chondrostoma nasus) from the Crișul Negru river, Romania. The levels of copper (Cu), chromium (Cr), cadmium (Cd), lead (Pb), and zinc (Zn) in fish tissues were measured by atomic absorption spectrophotometry. Histopathology and the expressions of TNF-α and proliferation cell nuclear antigen (PCNA) were investigated by immunohistochemistry and Western blot. Our data suggest a significant correlation between the bioconcentration level of metals and structural changes. The carnivorous species was the most affected compared to the omnivorous and herbivorous ones, and the most affected organ was the kidney. Moreover, the correlation of tissue damage with the PCNA and TNF-α expression levels revealed that the herbivorous species presented less extended lesions, likely due to higher activated repair mechanisms and lower levels of inflammation. In conclusion, our data and the subsequent statistical analysis suggest that feeding behavior could be correlated with the histopathological alterations and might be used for a more profound evaluation of aquatic environment safety and analysis of aquatic ecosystems.
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Feng, Tzu-Yu, Francesca N. Azar, Mitchell T. McGinty, and Melanie R. Rutkowski. "Reciprocal interactions between the gut microbiome and mammary tissue microenvironment promote distant regulation of breast tumor metastasis." Journal of Immunology 206, no. 1_Supplement (May 1, 2021): 56.12. http://dx.doi.org/10.4049/jimmunol.206.supp.56.12.
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Abstract Establishing commensal dysbiosis, defined as an inflammatory gut microbiome with low biodiversity, prior to breast tumor initiation enhances early dissemination of hormone-receptor positive (HR+) mammary tumor cells into the circulation, distal lymph nodes, and lungs. Here, we sought to define mammary tissue mediators of dysbiosis-induced tumor dissemination. Commensal dysbiosis increased mast cell numbers in the pre-malignant mammary tissue, with numbers remaining elevated in the presence of a tumor. During early tumor progression, increased mast cell numbers correlated with increased numbers of activated fibroblasts and collagen I protein levels in mammary tissues. Fibroblast activation and tissue remodeling are associated with enhanced breast tumor metastasis. Although mast cell degranulation is known to trigger fibrosis in other disease models, it is unknown whether mammary tissue mast cells influence dissemination of tumor cells. To investigate the role of mast cells during tumor dissemination, mice were treated with mast cell stabilizers ketotifen or cromolyn. Notably, inhibition of mast cell degranulation significantly reduced fibroblast activation and dissemination of tumor cells into the blood of dysbiotic animals. Collagen levels in mammary tissues from women diagnosed with HR+ breast cancer also correlated with mast cell abundance, suggesting mast cell-mediated fibroblast activation is relevant to human disease. Together, these data demonstrate that mast cells recruited into the pre-malignant mammary tissue in response to commensal dysbiosis orchestrate early dissemination of HR+ breast tumors through activation of tissue fibroblasts.
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Muzzopappa, Mariana, Lada Murcia, and Marco Milán. "Feedback amplification loop drives malignant growth in epithelial tissues." Proceedings of the National Academy of Sciences 114, no. 35 (August 14, 2017): E7291—E7300. http://dx.doi.org/10.1073/pnas.1701791114.
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Interactions between cells bearing oncogenic mutations and the surrounding microenvironment, and cooperation between clonally distinct cell populations, can contribute to the growth and malignancy of epithelial tumors. The genetic techniques available in Drosophila have contributed to identify important roles of the TNF-α ligand Eiger and mitogenic molecules in mediating these interactions during the early steps of tumor formation. Here we unravel the existence of a tumor-intrinsic—and microenvironment-independent—self-reinforcement mechanism that drives tumor initiation and growth in an Eiger-independent manner. This mechanism relies on cell interactions between two functionally distinct cell populations, and we present evidence that these cell populations are not necessarily genetically different. Tumor-specific and cell-autonomous activation of the tumorigenic JNK stress-activated pathway drives the expression of secreted signaling molecules and growth factors to delaminating cells, which nonautonomously promote proliferative growth of the partially transformed epithelial tissue. We present evidence that cross-feeding interactions between delaminating and nondelaminating cells increase each other’s sizes and that these interactions can explain the unlimited growth potential of these tumors. Our results will open avenues toward our molecular understanding of those social cell interactions with a relevant function in tumor initiation in humans.
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Zhang, Chen-xing, Hui-yu Wang, and Tong-xin Chen. "Interactions between Intestinal Microflora/Probiotics and the Immune System." BioMed Research International 2019 (November 20, 2019): 1–8. http://dx.doi.org/10.1155/2019/6764919.
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The digestive tract is home to millions of microorganisms and is the main and most important part of bacterial colonization. On one hand, the abundant bacterial community in intestinal tissues may pose potential health challenges such as inflammation and sepsis in cases of opportunistic invasion. Thus, the immune system has evolved and adapted to maintain the symbiotic relationship between host and microbiota. On the other hand, the intestinal microflora also exerts an immunoregulatory function to maintain host immune homeostasis, which cannot be neglected. In addition, the interaction of either microbiota or probiotics with immune system in regard to therapeutic applications is an area of great interest, and novel therapeutic strategies remain to be investigated. The review will elucidate interactions between intestinal microflora/probiotics and the immune system as well as novel therapeutic strategies.
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Vanpouille, Christophe, Angélique Biancotto, Andrea Lisco, and Beda Brichacek. "Interactions between Human Immunodeficiency Virus Type 1 and Vaccinia Virus in Human Lymphoid Tissue Ex Vivo." Journal of Virology 81, no. 22 (September 5, 2007): 12458–64. http://dx.doi.org/10.1128/jvi.00326-07.
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ABSTRACT Vaccinia virus (VACV) has been attracting attention recently not only as a vector for various vaccines but also as an immunization tool against smallpox because of its potential use as a bioterrorism agent. It has become evident that in spite of a long history of studies of VACV, its tissue pathogenesis remains to be fully understood. Here, we investigated the pathogenesis of VACV and its interactions with human immunodeficiency virus type 1 (HIV-1) in the context of human lymphoid tissues. We found that ex vivo-cultured tonsillar tissue supports productive infection by the New York City Board of Health strain, the VACV strain of the Dryvax vaccine. VACV readily infected both T and non-T (B) lymphocytes and depleted cells of both of these subsets equally over a 12-day period postinfection. Among T lymphocytes, CD8+ cells are preferentially depleted in accordance with their preferential infection: the probability that a CD8+ T cell will be productively infected is almost six times higher than for a CD4+ T cell. T cells expressing CCR5 and the activation markers CD25, CD38, and HLA-DR are other major targets for infection by VACV in lymphoid tissue. As a consequence, VACV predominantly inhibits the replication of the R5SF162 phenotype of HIV-1 in coinfected tissues, as R5-tropic HIV-1 requires activated CCR5+ CD4+ cells for productive infection. Human lymphoid tissue infected ex vivo by VACV can be used to investigate interactions of VACV with other viruses, in particular HIV-1, and to evaluate various VACV vectors for the purpose of recombinant vaccine development.
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Eisenberg, S. R., and A. J. Grodzinsky. "The Kinetics of Chemically Induced Nonequilibrium Swelling of Articular Cartilage and Corneal Stroma." Journal of Biomechanical Engineering 109, no. 1 (February 1, 1987): 79–89. http://dx.doi.org/10.1115/1.3138647.
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An electromechanical model for charged, hydrated tissues is developed to predict the kinetics of changes in swelling and isometric compressive stress induced by changes in bath salt concentration. The model focuses on ionic transport as the rate limiting step in chemically modulating electrical interactions between the charged macromolecules of the extracellular matrix. The swelling response to such changes in local interaction forces is determined by the relative rates of chemical diffusion and fluid redistribution in the tissue sample. We have tested the model by comparing the experimentally observed salt-induced stress relaxation response in bovine articular cartilage and corneal stroma to the response predicted by the model using constitutive relations for the concentration dependent material properties of the tissues reported in a related study. The qualitatively good agreement between our experimental measurements and the predictions of the model supports the physical basis of the model and demonstrates the model’s ability to discriminate between the two soft connective tissues that were examined.
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Havran, Wendy L., Julie M. Jameson, and Deborah A. Witherden. "Epithelial Cells and Their Neighbors. III. Interactions between intraepithelial lymphocytes and neighboring epithelial cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 289, no. 4 (October 2005): G627—G630. http://dx.doi.org/10.1152/ajpgi.00224.2005.
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Intraepithelial γδ-T cells are present in all epithelial tissues, where they reside in close contact with neighboring epithelial cells. Our data support the idea that the role of these cells is to monitor neighboring cells for signs of damage or disease. Once a problem is detected, the intraepithelial γδ-T cells can lyse damaged or malignant epithelial cells, directly participate in tissue repair through production of epithelial growth factors, and play a unique role in the recruitment of inflammatory cells to the site of damage. Intraepithelial γδ-T cells play unique roles in homeostasis and disease.
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Van Ryk, Donald, Sinmanus Vimonpatranon, Joe Hiatt, Sundar Ganesan, Nathalie Chen, Jordan McMurry, Saadiq Garba, et al. "The V2 domain of HIV gp120 mimics an interaction between CD4 and integrin ⍺4β7." PLOS Pathogens 19, no. 12 (December 8, 2023): e1011860. http://dx.doi.org/10.1371/journal.ppat.1011860.
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The CD4 receptor, by stabilizing TCR-MHC II interactions, plays a central role in adaptive immunity. It also serves as the HIV docking receptor. The HIV gp120 envelope protein binds directly to CD4. This interaction is a prerequisite for viral entry. gp120 also binds to ⍺4β7, an integrin that is expressed on a subset of memory CD4+ T cells. HIV tropisms for CD4+ T cells and gut tissues are central features of HIV pathogenesis. We report that CD4 binds directly to ⍺4β7 in a dynamic way, consistent with a cis regulatory interaction. The molecular details of this interaction are related to the way in which gp120 interacts with both receptors. Like MAdCAM-1 and VCAM-1, two recognized ligands of ⍺4β7, the binding interface on CD4 includes 2 sites (1° and accessory), distributed across its two N-terminal IgSF domains (D1 and D2). The 1° site includes a sequence in the G β-strand of CD4 D2, KIDIV, that binds directly to ⍺4β7. This pentapeptide sequence occurs infrequently in eukaryotic proteins. However, a closely related and conserved sequence, KLDIV, appears in the V2 domain of gp120. KLDIV mediates gp120-⍺4β7 binding. The accessory ⍺4β7 binding site on CD4 includes Phe43. The Phe43 aromatic ring protrudes outward from one edge of a loop connecting the C’C” strands of CD4 D1. Phe43 is a principal contact for HIV gp120. It interacts with conserved residues in the recessed CD4 binding pocket. Substitution of Phe43 abrogates CD4 binding to both gp120 and ⍺4β7. As such, the interactions of gp120 with both CD4 and ⍺4β7 reflect elements of their interactions with each other. These findings indicate that gp120 specificities for CD4 and ⍺4β7 are interrelated and suggest that selective pressures which produced a CD4 tropic virus that replicates in gut tissues are linked to a dynamic interaction between these two receptors.
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Goto, Shunsuke, Hisashi Anbutsu, and Takema Fukatsu. "Asymmetrical Interactions between Wolbachia and Spiroplasma Endosymbionts Coexisting in the Same Insect Host." Applied and Environmental Microbiology 72, no. 7 (July 2006): 4805–10. http://dx.doi.org/10.1128/aem.00416-06.
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ABSTRACT We investigated the interactions between the endosymbionts Wolbachia pipientis strain wMel and Spiroplasma sp. strain NSRO coinfecting the host insect Drosophila melanogaster. By making use of antibiotic therapy, temperature stress, and hemolymph microinjection, we established the following strains in the same host genetic background: the SW strain, infected with both Spiroplasma and Wolbachia; the S strain, infected with Spiroplasma only; and the W strain, infected with Wolbachia only. The infection dynamics of the symbionts in these strains were monitored by quantitative PCR during host development. The infection densities of Spiroplasma exhibited no significant differences between the SW and S strains throughout the developmental course. In contrast, the infection densities of Wolbachia were significantly lower in the SW strain than in the W strain at the pupal and young adult stages. These results indicated that the interactions between the coinfecting symbionts were asymmetrical, i.e., Spiroplasma organisms negatively affected the population of Wolbachia organisms, while Wolbachia organisms did not influence the population of Spiroplasma organisms. In the host body, the symbionts exhibited their own tissue tropisms: among the tissues examined, Spiroplasma was the most abundant in the ovaries, while Wolbachia showed the highest density in Malpighian tubules. Strikingly, basically no Wolbachia organisms were detected in hemolymph, the principal location of Spiroplasma. These results suggest that different host tissues act as distinct microhabitats for the symbionts and that the lytic process in host metamorphosis might be involved in the asymmetrical interactions between the coinfecting symbionts.
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Zhou, Jiong, Takashi Suzuki, Agnes Kovacic, Ryoko Saito, Yasuhiro Miki, Takanori Ishida, Takuya Moriya, Evan R. Simpson, Hironobu Sasano, and Colin D. Clyne. "Interactions between Prostaglandin E2, Liver Receptor Homologue-1, and Aromatase in Breast Cancer." Cancer Research 65, no. 2 (January 15, 2005): 657–63. http://dx.doi.org/10.1158/0008-5472.657.65.2.
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Abstract Local synthesis of estrogens within breast adipose tissue by cytochrome P450 aromatase contributes to the growth of postmenopausal breast cancers. One of the major stimulators of aromatase expression in breast is prostaglandin E2 (PGE2) derived from tumorous epithelium and/or infiltrating macrophages. Recently, the orphan nuclear receptor, liver receptor homologue-1 (LRH-1), has also been shown to regulate aromatase expression in breast adipose tissue. We therefore examined the expression of, and correlations between, aromatase and LRH-1 mRNA in a panel of breast carcinoma tissues and adjacent adipose tissue. LRH-1 mRNA expression was low in normal breast tissue but markedly elevated in both breast carcinoma tissue and adipose tissue surrounding the tumor invasion (thereby paralleling aromatase expression). Laser capture microdissection localized the site of LRH-1 expression to tumor epithelial cells but not to intratumoral stromal cells. A strong correlation between LRH-1 and aromatase mRNA levels was observed in tumor-containing adipose tissue but not in tumor tissue. Ectopic expression of LRH-1 in primary human adipose stromal cells strongly activated endogenous aromatase mRNA expression and enzyme activity. Finally, treatment of adipose stromal cells with PGE2 induced expression of both LRH-1 and aromatase. We suggest that PGE2 derived from breast tumor tissue may increase aromatase expression in the surrounding adipose stroma in part by inducing LRH-1 in these cells. The roles of LRH-1 in breast cancer proliferation merit further study.
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Veenstra, R. D., and R. L. DeHaan. "Electrotonic interactions between aggregates of chick embryo cardiac pacemaker cells." American Journal of Physiology-Heart and Circulatory Physiology 250, no. 3 (March 1, 1986): H453—H463. http://dx.doi.org/10.1152/ajpheart.1986.250.3.h453.
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Synchronization of spontaneously active heart cell aggregates occurs shortly after they are brought into contact. The synchronous rate is determined by pacemaker phase resetting and passive subthreshold electrotonic interactions. To further study the effects of passive electrical interactions, we have used 150-microns diameter aggregates prepared from cells of 4d (4-day ventricle + 1 day in vitro), 7d, and 14d embryonic chick ventricle as models of primary, latent, and nonpacemaker tissues, respectively. Coupling of 4d and 7d aggregates (4d/7d pairs) leads to intermediate synchronous rates. We show here that elevating external K+ from 1.3 to 2.8 mM, which has no effect on 4d/4d pairs but selectively reduces the beat rate of 7d/7d pairs by 42%, slows the synchronous beat rate of 4d/7d pairs by 23%. Increases in electrical coupling in newly joined 4d/14d pairs cause the 4d rate to slow to a minimum value (16 +/- 13 beats/min, n = 16) just prior to the onset of synchronous activity. The rate slowly recovers to a final value of 40 +/- 12 beat/min. We conclude that the spontaneous beat rate of a primary pacemaker is modulated by both active and passive interactions with latent or nonpacemaker tissues.
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Stern, Claudio D., Sanjay M. Sisodiya, and Roger J. Keynes. "Interactions between neurites and somite cells: inhibition and stimulation of nerve growth in the chick embryo." Development 91, no. 1 (February 1, 1986): 209–26. http://dx.doi.org/10.1242/dev.91.1.209.
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After neural processes emerge from the neural tube in the chick embryo, their growth is restricted to the cranial halves of the neighbouring somites. In this study we have developed an in vitro system to model the interactions between these tissue types. Pioneer neurites display a hierarchy of preferences in terms of the substrates they can grow on. As expected, tissue culture plastic does not support neural outgrowth, but this can be overcome by coating the plastic substrate with either collagen or poly-L-lysine. Neural crest, cranial half somite, and a number of other tissues support growth well, while caudal half somite and tail bud mesenchyme do so to a much smaller extent. The binding pattern of a variety of lectins was assessed in cryostat sections of embryos and in cultured cells of the above tissues. It was found that peanut agglutinin can discriminate between cranial and caudal sclerotome both in vitro and in the embryo, since it binds preferentially to caudal sclerotome in both cases. This difference is expressed as soon as the sclerotome forms. The significance of these findings is twofold: first, they show that the interactions that take place during peripheral neural segmentation can be modelled in vitro; second, they represent the first instance of a molecular difference between the cranial and caudal halves of the sclerotome, detectable both in culture and in the embryo.
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Clouthier, D. E., K. Hosoda, J. A. Richardson, S. C. Williams, H. Yanagisawa, T. Kuwaki, M. Kumada, R. E. Hammer, and M. Yanagisawa. "Cranial and cardiac neural crest defects in endothelin-A receptor-deficient mice." Development 125, no. 5 (March 1, 1998): 813–24. http://dx.doi.org/10.1242/dev.125.5.813.
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Neural crest cells arise in the dorsal aspect of the neural tube and migrate extensively to differentiate into a variety of neural and non-neural tissues. While interactions between neural crest cells and their local environments are required for the proper development of these tissues, little information is available about the molecular nature of the cell-cell interactions in cephalic neural crest development. Here we demonstrate that mice deficient for one type of endothelin receptor, ETA, mimic the human conditions collectively termed CATCH 22 or velocardiofacial syndrome, which include severe craniofacial deformities and defects in the cardiovascular outflow tract. We show that ETA receptor mRNA is expressed by the neural crest-derived ectomesenchymal cells of pharyngeal arches and cardiac outflow tissues, whereas ET-1 ligand mRNA is expressed by arch epithelium, paraxial mesoderm-derived arch core and the arch vessel endothelium. This suggests that paracrine interaction between neural crest-derived cells and both ectoderm and mesoderm is essential in forming the skeleton and connective tissue of the head. Further, we find that pharyngeal arch expression of goosecoid is absent in ETA receptor-deficient mice, placing the transcription factor as one of the possible downstream signals triggered by activation of the ETA receptor. These observations define a novel genetic pathway for inductive communication between cephalic neural crest cells and their environmental counterparts.
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Lampiasi, Nadia. "Interactions between Macrophages and Mast Cells in the Female Reproductive System." International Journal of Molecular Sciences 23, no. 10 (May 12, 2022): 5414. http://dx.doi.org/10.3390/ijms23105414.
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Mast cells (MCs) and macrophages (Mϕs) are innate immune cells that differentiate from early common myeloid precursors and reside in all body tissues. MCs have a unique capacity to neutralize/degrade toxic proteins, and they are hypothesized as being able to adopt two alternative polarization profiles, similar to Mϕs, with distinct or even opposite roles. Mϕs are very plastic phagocytic cells that are devoted to the elimination of senescent/anomalous endogenous entities (to maintain tissue homeostasis), and to the recognition and elimination of exogenous threats. They can adopt several functional phenotypes in response to microenvironmental cues, whose extreme profiles are the inflammatory/killing phenotype (M1) and the anti-inflammatory/healing phenotype (M2). The concomitant and abundant presence of these two cell types and the partial overlap of their defensive and homeostatic functions leads to the hypothesis that their crosstalk is necessary for the optimal coordination of their functions, both under physiological and pathological conditions. This review will examine the relationship between MCs and Mϕs in some situations of homeostatic regulation (menstrual cycle, embryo implantation), and in some inflammatory conditions in the same organs (endometriosis, preeclampsia), in order to appreciate the importance of their cross-regulation.
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Wang, Maochun, Guihua Tan, Huiming Jiang, Anlong Liu, Rui Wu, Jiawei Li, Ziying Sun, Zhongyang Lv, Wei Sun, and Dongquan Shi. "Molecular crosstalk between articular cartilage, meniscus, synovium, and subchondral bone in osteoarthritis." Bone & Joint Research 11, no. 12 (December 1, 2022): 862–72. http://dx.doi.org/10.1302/2046-3758.1112.bjr-2022-0215.r1.
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Aims Osteoarthritis (OA) is a common degenerative joint disease worldwide, which is characterized by articular cartilage lesions. With more understanding of the disease, OA is considered to be a disorder of the whole joint. However, molecular communication within and between tissues during the disease process is still unclear. In this study, we used transcriptome data to reveal crosstalk between different tissues in OA. Methods We used four groups of transcription profiles acquired from the Gene Expression Omnibus database, including articular cartilage, meniscus, synovium, and subchondral bone, to screen differentially expressed genes during OA. Potential crosstalk between tissues was depicted by ligand-receptor pairs. Results During OA, there were 626, 97, 1,060, and 2,330 differentially expressed genes in articular cartilage, meniscus, synovium, and subchondral bone, respectively. Gene Ontology enrichment revealed that these genes were enriched in extracellular matrix and structure organization, ossification, neutrophil degranulation, and activation at different degrees. Through ligand-receptor pairing and proteome of OA synovial fluid, we predicted ligand-receptor interactions and constructed a crosstalk atlas of the whole joint. Several interactions were reproduced by transwell experiment in chondrocytes and synovial cells, including TNC- NT5E, TNC- SDC4, FN1- ITGA5, and FN1- NT5E. After lipopolysaccharide (LPS) or interleukin (IL)-1β stimulation, the ligand expression of chondrocytes and synovial cells was upregulated, and corresponding receptors of co-culture cells were also upregulated. Conclusion Each tissue displayed a different expression pattern in transcriptome, demonstrating their specific roles in OA. We highlighted tissue molecular crosstalk through ligand-receptor pairs in OA pathophysiology, and generated a crosstalk atlas. Strategies to interfere with these candidate ligands and receptors may help to discover molecular targets for future OA therapy. Cite this article: Bone Joint Res 2022;11(12):862–872.
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Fan, Xiang, Engda G. Hagos, Bo Xu, Christina Sias, Koichi Kawakami, Rebecca D. Burdine, and Scott T. Dougan. "Nodal signals mediate interactions between the extra-embryonic and embryonic tissues in zebrafish." Developmental Biology 310, no. 2 (October 2007): 363–78. http://dx.doi.org/10.1016/j.ydbio.2007.08.008.
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Kapfhammer, JP, and JA Raper. "Interactions between growth cones and neurites growing from different neural tissues in culture." Journal of Neuroscience 7, no. 5 (May 1, 1987): 1595–600. http://dx.doi.org/10.1523/jneurosci.07-05-01595.1987.
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Wagenknecht, Dawn R., AbdulRahman AbuBaker BalHaddad, and Richard L. Gregory. "Effects of Nicotine on Oral Microorganisms, Human Tissues, and the Interactions between Them." Current Oral Health Reports 5, no. 1 (February 24, 2018): 78–87. http://dx.doi.org/10.1007/s40496-018-0173-3.
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Retana-Lobo DDS, MSD, Cristina. "Dental Pulp Regeneration: Insights from Biological Processes." Odovtos - International Journal of Dental Sciences 20, no. 1 (November 16, 2017): 10–16. http://dx.doi.org/10.15517/ijds.v0i0.31269.
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One of the major approaches on dentistry research in this century is the development of biological strategies (tissue engineering) to regenerate/ biomineralize lost dental tissues. During dentin-pulp regeneration, the interaction between stem cells, signaling molecules, biomaterials and the microenvironment in the periapical area drives the process for dental pulp tissue engineering. Understanding the signaling mechanisms and interactions involved with the biological process for the formation of a new tissue, is essential. The knowledge of the micro-environment is the key for the application of tissue engineering. The present article is a short review of the current state of this topic, with the purpose of showing insights of pulp regeneration.
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Retana-Lobo DDS, MSD, Cristina. "Dental Pulp Regeneration: Insights from Biological Processes." Odovtos - International Journal of Dental Sciences 20, no. 1 (November 16, 2017): 10–16. http://dx.doi.org/10.15517/ijds.v20i1.31269.
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One of the major approaches on dentistry research in this century is the development of biological strategies (tissue engineering) to regenerate/ biomineralize lost dental tissues. During dentin-pulp regeneration, the interaction between stem cells, signaling molecules, biomaterials and the microenvironment in the periapical area drives the process for dental pulp tissue engineering. Understanding the signaling mechanisms and interactions involved with the biological process for the formation of a new tissue, is essential. The knowledge of the micro-environment is the key for the application of tissue engineering. The present article is a short review of the current state of this topic, with the purpose of showing insights of pulp regeneration.
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Vianello, Elena, Marta Kalousová, Elena Dozio, Lorenza Tacchini, Tomáš Zima, and Massimiliano Marco Corsi Romanelli. "Osteopontin: The Molecular Bridge between Fat and Cardiac–Renal Disorders." International Journal of Molecular Sciences 21, no. 15 (August 4, 2020): 5568. http://dx.doi.org/10.3390/ijms21155568.
Full textAbstract:
Osteopontin (OPN) is a multifaceted matricellular protein, with well-recognized roles in both the physiological and pathological processes in the body. OPN is expressed in the main organs and cell types, in which it induces different biological actions. During physiological conditioning, OPN acts as both an intracellular protein and soluble excreted cytokine, regulating tissue remodeling and immune-infiltrate in adipose tissue the heart and the kidney. In contrast, the increased expression of OPN has been correlated with the severity of the cardiovascular and renal outcomes associated with obesity. Indeed, OPN expression is at the “cross roads” of visceral fat extension, cardiovascular diseases (CVDs) and renal disorders, in which OPN orchestrates the molecular interactions, leading to chronic low-grade inflammation. The common factor associated with OPN overexpression in adipose, cardiac and renal tissues seems attributable to the concomitant increase in visceral fat size and the increase in infiltrated OPN+ macrophages. This review underlines the current knowledge on the molecular interactions between obesity and the cardiac–renal disorders ruled by OPN.
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Brisbin, Jennifer T., Joshua Gong, and Shayan Sharif. "Interactions between commensal bacteria and the gut-associated immune system of the chicken." Animal Health Research Reviews 9, no. 1 (June 2008): 101–10. http://dx.doi.org/10.1017/s146625230800145x.
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AbstractThe chicken gut-associated lymphoid tissue is made up of a number of tissues and cells that are responsible for generating mucosal immune responses and maintaining intestinal homeostasis. The normal chicken microbiota also contributes to this via the ability to activate both innate defense mechanisms and adaptive immune responses. If left uncontrolled, immune activation in response to the normal microbiota would pose a risk of excessive inflammation and intestinal damage. Therefore, it is important that immune responses to the normal microbiota be under strict regulatory control. Through studies of mammals, it has been established that the mucosal immune system has specialized regulatory and anti-inflammatory mechanisms for eliminating or tolerating the normal microbiota. The mechanisms that exist in the chicken to control host responses to the normal microbiota, although assumed to be similar to that of mammals, have not yet been fully described. This review summarizes what is currently known about the host response to the intestinal microbiota, particularly in the chicken.
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Brossaud, J., V. Pallet, and J.-B. Corcuff. "Vitamin A, endocrine tissues and hormones: interplay and interactions." Endocrine Connections 6, no. 7 (October 2017): R121—R130. http://dx.doi.org/10.1530/ec-17-0101.
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Vitamin A (retinol) is a micronutrient critical for cell proliferation and differentiation. In adults, vitamin A and metabolites such as retinoic acid (RA) play major roles in vision, immune and brain functions and tissue remodelling and metabolism. This review presents the physiological interactions of retinoids and endocrine tissues and hormonal systems. Two endocrine systems have been particularly studied. In the pituitary, retinoids target the corticotrophs with a possible therapeutic use in corticotropinomas. In the thyroid, retinoids interfere with iodine metabolism and vitamin A deficiency aggravates thyroid dysfunction caused by iodine-deficient diets. Retinoids use in thyroid cancer appears less promising than expected. Recent and still controversial studies investigated the relations between retinoids and metabolic syndrome. Indeed, retinoids contribute to pancreatic development and modify fat and glucose metabolism. However, more detailed studies are needed before planning any therapeutic use. Finally, retinoids probably play more minor roles in adrenal and gonads development and function apart from their major effects on spermatogenesis.