The world of epithelial sheets

Honda, Hiroaki

doi:10.1111/dgd.12350

Cited by 28 publications

(27 citation statements)

References 39 publications

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“…The results reported in the present study indicate that β‐cells plated after trypsin dissociation under conditions that abolish or reduce cell–cell and cell–substrate interactions form intracellular compartments, which share morphological, biochemical and physiological properties with elsewhere described vacuoles developing in different epithelial cell types [Vega‐Salas et al., 1987; Gilbert and Rodriguez‐Boulan 1991; Honda 2017]. We showed that aggregated β‐cells or cells attached to laminin‐coated Petri dish have a reduced tendency to develop vacuoles when compared to isolated β‐cells and cultured in suspension.…”

Section: Discussionsupporting

confidence: 83%

“…When removed from their original environment, cells encounter different changes, including loss of cell–cell and cell–substrate contacts as well as interaction with their extracellular matrix. In most cases, these changes lead to rearrangement of cytoplasmic and membrane components that impairs intracellular trafficking and disturbs cell polarity and identity [Honda 2017; Vaidziulyte et al., 2019]. One of the common traits seen in dissociated epithelial cells with loss of cell–cell and cell–substrate contacts is intracellular vacuolation.…”

Section: Introductionmentioning

confidence: 99%

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Loss of cell–cell and cell–substrate contacts in single pancreatic β‐cells divert insulin release to intracellular vesicular compartments

Ljubicic

Cottet‐Dumoulin

Bosco

2020

Biology of the Cell

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Background information. Cell-cell or cell-substrate interactions are lost when cells are dissociated in culture, or during pathophysiological breakdowns, therefore impairing their structure and polarity, and affecting their function. We show that single rat β-cells, cultured under non-adhesive conditions, form intracytoplasmic vacuoles increasing in number and size over time. We characterized these structures and their implication in β-cell function. Results. Ultrastructurally, the vacuoles resemble vesicular apical compartments and are delimited by a membrane, containing microvilli and expressing markers of the plasma membrane, including glucose transporter 2 and actin. When insulin secretion is stimulated, insulin accumulates in the lumen of the vacuoles. By contrast, when the cells are incubated under low calcium levels, the hormone is undetectable in vesicular compartments. Insulin release studies from single cells revealed that vacuole-containing cells release less insulin as compared to control cells. When added to the medium, a non-permeant fluid phase marker becomes trapped within vacuoles. Inhibition of vesicular trafficking and exocytosis as well as dynamin-dependent endocytosis changed the percentage of vacuolecontaining cells, suggesting that both endocytic and exocytic track contribute to their formation. Conclusions. These results suggest that loss of cell-cell and cell-substrate contacts in isolated β-cells affect normal vesicular trafficking and redirects insulin secretion to intracellular vesicular compartments. Significance. Our study reveals for the first time that single β-cells develop vacuolar compartments when cultured in suspension and redirect their insulin secretion to these vacuoles. This may underlie a compensatory process for cultured cells who lost their interactions with adhesive substrates or neighbouring cells.

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Section: Discussionsupporting

confidence: 83%

Section: Introductionmentioning

confidence: 99%

Loss of cell–cell and cell–substrate contacts in single pancreatic β‐cells divert insulin release to intracellular vesicular compartments

Ljubicic

Cottet‐Dumoulin

Bosco

2020

Biology of the Cell

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“…E PITHELIA are abundant tissue types in metazoan organisms whose structure is established early in embryonic development (Honda 2017). Two defining properties of epithelia are that their constituent cells are (1) physically linked through adhesions to form a sheet, or layer of cells, with important barrier and compartmentalization functions; and (2) polarized across the sheet such that the protein composition on the outer/lumenal side (i.e., apical) of the sheet differs from that on the inner side (i.e., basal).…”

mentioning

confidence: 99%

The Physical Mechanisms ofDrosophilaGastrulation: Mesoderm and Endoderm Invagination

Martin

2020

Genetics

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A critical juncture in early development is the partitioning of cells that will adopt different fates into three germ layers: the ectoderm, the mesoderm, and the endoderm. This step is achieved through the internalization of specified cells from the outermost surface layer, through a process called gastrulation. In Drosophila, gastrulation is achieved through cell shape changes (i.e., apical constriction) that change tissue curvature and lead to the folding of a surface epithelium. Folding of embryonic tissue results in mesoderm and endoderm invagination, not as individual cells, but as collective tissue units. The tractability of Drosophila as a model system is best exemplified by how much we know about Drosophila gastrulation, from the signals that pattern the embryo to the molecular components that generate force, and how these components are organized to promote cell and tissue shape changes. For mesoderm invagination, graded signaling by the morphogen, Spätzle, sets up a gradient in transcriptional activity that leads to the expression of a secreted ligand (Folded gastrulation) and a transmembrane protein (T48). Together with the GPCR Mist, which is expressed in the mesoderm, and the GPCR Smog, which is expressed uniformly, these signals activate heterotrimeric G-protein and small Rho-family G-protein signaling to promote apical contractility and changes in cell and tissue shape. A notable feature of this signaling pathway is its intricate organization in both space and time. At the cellular level, signaling components and the cytoskeleton exhibit striking polarity, not only along the apical–basal cell axis, but also within the apical domain. Furthermore, gene expression controls a highly choreographed chain of events, the dynamics of which are critical for primordium invagination; it does not simply throw the cytoskeletal “on” switch. Finally, studies of Drosophila gastrulation have provided insight into how global tissue mechanics and movements are intertwined as multiple tissues simultaneously change shape. Overall, these studies have contributed to the view that cells respond to forces that propagate over great distances, demonstrating that cellular decisions, and, ultimately, tissue shape changes, proceed by integrating cues across an entire embryo.

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“…MUC4 and MUC1, two transmembrane mucins, have been involved in wide-ranging studies in relation to their pathological implication in malignancies and other disease processes due to their overor mis-expression [31,32]. The epithelium separates multicellular animals from the external environment by means of its identity of a transversely connected layer of cells with apical-basal polarity [33]. Mucins were secreted early in the evolution of metazoan as part of transmembrane structures functioning in the protection, repairing and survival of epithelia in vertebrates [34].…”

Section: Discussionmentioning

confidence: 99%

Mucin 4 Gene Silencing Reduces Oxidative Stress and Calcium Oxalate Crystal Formation in Renal Tubular Epithelial Cells Through the Extracellular Signal-Regulated Kinase Signaling Pathway in Nephrolithiasis Rat Model

Sun¹,

Zou²,

Wang³

et al. 2018

Kidney Blood Press Res

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Background/Aims: Nephrolithiasis plagues a great number of patients all over the world. Increasing evidence shows that the extracellular signal-regulated kinase (ERK) signaling pathway and renal tubular epithelial cell (RTEC) dysfunction and attrition are central to the pathogenesis of kidney diseases. Mucin 4 (MUC4) is reported as an activator of ERK signaling pathway in epithelial cells. In this study, using rat models of calcium oxalate (CaOx) nephrolithiasis, the present study aims to define the roles of MUC4 and ERK signaling pathway as contributors to oxidative stress and CaOx crystal formation in RTEC. Methods: Data sets of nephrolithiasis were searched using GEO database and a heat flow map was drawn. Then MUC4 function was predicted. Wistar rats were prepared for the purpose of model establishment of ethylene glycol and ammonium chloride induced CaOx nephrolithiasis. In order to assess the detailed regulatory mechanism of MUC4 silencing on the ERK signaling pathway and RTEC, we used recombinant plasmid to downregulate MUC4 expression in Wistar rat-based models. Samples from rat urine, serum and kidney tissues were reviewed to identify oxalic acid and calcium contents, BUN, Cr, Ca²⁺ and P³⁺ levels, calcium crystal formation in renal tubules and MUC4 positive expression rate. Finally, RT-qPCR, Western blot analysis, and ELISA were employed to access oxidative stress state and CaOx crystal formation in RTEC. Results: Initially, MUC4 was found to have an influence on the process of nephrolithiasis. MUC4 was upregulated in the CaOx nephrolithiasis model rats. We proved that the silencing of MUC4 triggered the inactivation of ERK signaling pathway. Following the silencing of MUC4 or the inhibition of ERK signaling pathway, the oxalic acid and calcium contents in rat urine, BUN, Cr, Ca²⁺ and P³⁺ levels in rat serum, p-ERK1/2, MCP-1 and OPN expressions in RTEC and H₂O₂ and MDA levels in the cultured supernatant were downregulated, but the GSH-Px, CAT and SOD levels in the cultured supernatant were increased. Moreover, MUC4 silencing or ERK signaling pathway inactivation may decrease the formation of CaOx crystals. Conclusion: Taken together, silencing of MUC4 can inactivate the ERK signaling pathway and further restrain oxidative stress and CaOx crystal formation in RTEC. Thus, MUC4 represents a potential investigative focus target in nephrolithiasis.

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The world of epithelial sheets

Cited by 28 publications

References 39 publications

Loss of cell–cell and cell–substrate contacts in single pancreatic β‐cells divert insulin release to intracellular vesicular compartments

Loss of cell–cell and cell–substrate contacts in single pancreatic β‐cells divert insulin release to intracellular vesicular compartments

The Physical Mechanisms ofDrosophilaGastrulation: Mesoderm and Endoderm Invagination

Mucin 4 Gene Silencing Reduces Oxidative Stress and Calcium Oxalate Crystal Formation in Renal Tubular Epithelial Cells Through the Extracellular Signal-Regulated Kinase Signaling Pathway in Nephrolithiasis Rat Model

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