Relevant bibliographies by topics / Tissue folding

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  1. Journal articles

Academic literature on the topic 'Tissue folding'

Author: Grafiati
Published: 25 May 2024

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Journal articles on the topic "Tissue folding"

1

Zečić, Aleksandra, and Chadanat Noonin. "Whole-mount in situ hybridization: minimizing the folding problem of thin-sheet tissue-like crayfish haematopoietic tissue." Crustaceana 91, no. 1 (2018): 1–15. http://dx.doi.org/10.1163/15685403-00003745.

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Crayfish haematopoietic tissue (HPT) has a thin-sheet-like structure with a thickness of 100-160 μm and a width of approximately 1-2 cm. This structure makes HPT extremely easy to fold after removal from the animal. Therefore, it is difficult to handle the tissue without folding when processing for sectioning and histological study. The degree of tissue folding reflects the size of the tissue sections obtained, how complicated it is to interpret the location of each tissue section, and the accuracy of the interpretation of the location of a specific transcript. To facilitate the interpretation of a specific transcript location in the HPT, we optimized a whole-mount in situ hybridization technique to minimize tissue folding. This optimized protocol effectively reduced the tissue folding. Therefore, the location of a specific transcript in the HPT was easily and accurately defined. This protocol will be useful for whole-mount staining of other tissues with similar structure.
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2

Inoue, Yasuhiro, Itsuki Tateo, and Taiji Adachi. "Epithelial tissue folding pattern in confined geometry." Biomechanics and Modeling in Mechanobiology 19, no. 3 (2019): 815–22. http://dx.doi.org/10.1007/s10237-019-01249-8.

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AbstractThe primordium of the exoskeleton of an insect is epithelial tissue with characteristic patterns of folds. As the insect develops from larva to pupa, the spreading of these folds produces the three-dimensional shape of the exoskeleton of the insect. It is known that the three-dimensional exoskeleton shape has already been encoded in characteristic patterns of folds in the primordium; however, a description of how the epithelial tissue forms with the characteristic patterns of folds remains elusive. The present paper suggests a possible mechanism for the formation of the folding pattern. During the primordium development, because of the epithelial tissue is surrounded by other tissues, cell proliferation proceeds within a confined geometry. To elucidate the mechanics of the folding of the epithelial tissue in the confined geometry, we employ a three-dimensional vertex model that expresses tissue deformations based on cell mechanical behaviors and apply the model to examine the effects of cell divisions and the confined geometry on epithelial folding. Our simulation results suggest that the orientation of the axis of cell division is sufficient to cause different folding patterns in silico and that the restraint of out-of-plane deformation due to the confined geometry determines the interspacing of the folds.
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3

Hookway, Tracy A. "Engineering Biology by Controlling Tissue Folding." Trends in Biotechnology 36, no. 4 (2018): 341–43. http://dx.doi.org/10.1016/j.tibtech.2018.02.003.

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4

Allen, Simon, Hassan Y. Naim, and Neil J. Bulleid. "Intracellular Folding of Tissue-type Plasminogen Activator." Journal of Biological Chemistry 270, no. 9 (1995): 4797–804. http://dx.doi.org/10.1074/jbc.270.9.4797.

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5

Zartman, Jeremiah J., and Stanislav Y. Shvartsman. "Unit Operations of Tissue Development: Epithelial Folding." Annual Review of Chemical and Biomolecular Engineering 1, no. 1 (2010): 231–46. http://dx.doi.org/10.1146/annurev-chembioeng-073009-100919.

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6

Hiraiwa, Tetsuya, Fu-Lai Wen, Tatsuo Shibata, and Erina Kuranaga. "Mathematical Modeling of Tissue Folding and Asymmetric Tissue Flow during Epithelial Morphogenesis." Symmetry 11, no. 1 (2019): 113. http://dx.doi.org/10.3390/sym11010113.

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Recent studies have revealed that intrinsic, individual cell behavior can provide the driving force for deforming a two-dimensional cell sheet to a three-dimensional tissue without the need for external regulatory elements. However, whether intrinsic, individual cell behavior could actually generate the force to induce tissue deformation was unclear, because there was no experimental method with which to verify it in vivo. In such cases, mathematical modeling can be effective for verifying whether a locally generated force can propagate through an entire tissue and induce deformation. Moreover, the mathematical model sometimes provides potential mechanistic insight beyond the information obtained from biological experimental results. Here, we present two examples of modeling tissue morphogenesis driven by cell deformation or cell interaction. In the first example, a mathematical study on tissue-autonomous folding based on a two-dimensional vertex model revealed that active modulations of cell mechanics along the basal–lateral surface, in addition to the apical side, can induce tissue-fold formation. In the second example, by applying a two-dimensional vertex model in an apical plane, a novel mechanism of tissue flow caused by asymmetric cell interactions was discovered, which explained the mechanics behind the collective cellular movement observed during epithelial morphogenesis.
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7

Chan, Hon Fai, Ruike Zhao, German A. Parada, et al. "Folding artificial mucosa with cell-laden hydrogels guided by mechanics models." Proceedings of the National Academy of Sciences 115, no. 29 (2018): 7503–8. http://dx.doi.org/10.1073/pnas.1802361115.

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The surfaces of many hollow or tubular tissues/organs in our respiratory, gastrointestinal, and urogenital tracts are covered by mucosa with folded patterns. The patterns are induced by mechanical instability of the mucosa under compression due to constrained growth. Recapitulating this folding process in vitro will facilitate the understanding and engineering of mucosa in various tissues/organs. However, scant attention has been paid to address the challenge of reproducing mucosal folding. Here we mimic the mucosal folding process using a cell-laden hydrogel film attached to a prestretched tough-hydrogel substrate. The cell-laden hydrogel constitutes a human epithelial cell lining on stromal component to recapitulate the physiological feature of a mucosa. Relaxation of the prestretched tough-hydrogel substrate applies compressive strains on the cell-laden hydrogel film, which undergoes mechanical instability and evolves into morphological patterns. We predict the conditions for mucosal folding as well as the morphology of and strain in the folded artificial mucosa using a combination of theory and simulation. The work not only provides a simple method to fold artificial mucosa but also demonstrates a paradigm in tissue engineering via harnessing mechanical instabilities guided by quantitative mechanics models.
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8

Ko, Clint S., Vardges Tserunyan, and Adam C. Martin. "Microtubules promote intercellular contractile force transmission during tissue folding." Journal of Cell Biology 218, no. 8 (2019): 2726–42. http://dx.doi.org/10.1083/jcb.201902011.

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During development, forces transmitted between cells are critical for sculpting epithelial tissues. Actomyosin contractility in the middle of the cell apex (medioapical) can change cell shape (e.g., apical constriction) but can also result in force transmission between cells via attachments to adherens junctions. How actomyosin networks maintain attachments to adherens junctions under tension is poorly understood. Here, we discovered that microtubules promote actomyosin intercellular attachments in epithelia during Drosophila melanogaster mesoderm invagination. First, we used live imaging to show a novel arrangement of the microtubule cytoskeleton during apical constriction: medioapical Patronin (CAMSAP) foci formed by actomyosin contraction organized an apical noncentrosomal microtubule network. Microtubules were required for mesoderm invagination but were not necessary for initiating apical contractility or adherens junction assembly. Instead, microtubules promoted connections between medioapical actomyosin and adherens junctions. These results delineate a role for coordination between actin and microtubule cytoskeletal systems in intercellular force transmission during tissue morphogenesis.
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9

Codd, S. L., R. K. Lambert, M. R. Alley, and R. J. Pack. "Tensile stiffness of ovine tracheal wall." Journal of Applied Physiology 76, no. 6 (1994): 2627–35. http://dx.doi.org/10.1152/jappl.1994.76.6.2627.

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The epithelial folding that occurs during bronchoconstriction requires that the pressure on the muscle side of the folding membrane be greater than that on the lumen side. The pressure required for a given level of folding depends on the elastic properties of the tissue and on the geometry of the folding. To quantify the elastic properties, uniaxial tensile stiffness of the tracheal inner wall of nine sheep was measured in two directions: parallel to the tracheal axis and circumferentially. The tissue showed anisotropic behavior, being approximately three times stiffer longitudinally than circumferentially. Histological examination showed that collagen in the lamina propria was randomly arranged, whereas there were straight elastin fibers aligned with the tracheal axis. This observation could explain the observed elastic anisotropy. Mechanical removal of the epithelium had no effect on tensile stiffness. It was also found that the tissue was under tension in situ. When a strip was excised, its length decreased by > or = 30%. After allowing for the systematic errors inherent in this experiment, the in situ circumferential tensile stiffness is estimated to be > or = 20 kPa. If the equivalent tissue in the bronchioles has the same tensile stiffness as that in the trachea, the forces required to fold the membrane are significant at small transbronchial pressure differences and increase in the presence of membrane thickening such as that seen in asthma.
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10

Tozluoǧlu, Melda, and Yanlan Mao. "On folding morphogenesis, a mechanical problem." Philosophical Transactions of the Royal Society B: Biological Sciences 375, no. 1809 (2020): 20190564. http://dx.doi.org/10.1098/rstb.2019.0564.

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Tissue folding is a fundamental process that sculpts a simple flat epithelium into a complex three-dimensional organ structure. Whether it is the folding of the brain, or the looping of the gut, it has become clear that to generate an invagination or a fold of any form, mechanical asymmetries must exist in the epithelium. These mechanical asymmetries can be generated locally, involving just the invaginating cells and their immediate neighbours, or on a more global tissue-wide scale. Here, we review the different mechanical mechanisms that epithelia have adopted to generate folds, and how the use of precisely defined mathematical models has helped decipher which mechanisms are the key driving forces in different epithelia. This article is part of a discussion meeting issue ‘Contemporary morphogenesis'.
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