scholarly journals Exit from quiescence couples epithelial stress amplification to fluidization

2021 ◽  
Author(s):  
Emma Lang ◽  
Christian Pedersen ◽  
Anna Lang ◽  
Pernille Blicher ◽  
Arne Klungland ◽  
...  
Keyword(s):  
Tissue Repair ◽  
Cell Sheet ◽  
Viscoelastic Flow ◽  
Cell Monolayers ◽  
Stem Cell Maintenance ◽  
Cycle Arrest ◽  
Human Keratinocyte ◽  
Cellular Quiescence ◽  
Stress Amplification ◽  
Rapid Amplification

Cellular quiescence is a state of reversible cell cycle arrest that is associated with tissue dormancy. Timely regulated entry into and exit from quiescence is important for processes such as tissue homeostasis, tissue repair, stem cell maintenance, developmental processes and immunity. Here we show that quiescent human keratinocyte monolayers contain an actinomyosin-based system that facilitates global viscoelastic flow upon serum-stimulated exit from quiescence. Mechanistically, serum exposure causes rapid amplification of pre-existing contractile sites leading to a burst in monolayer stress that subsequently drives monolayer fluidization. The stress magnitude after quiescence exit correlates with quiescence depth, and a critical stress level must be reached to overcome the cell sheet displacement barrier. The study shows that static quiescent cell monolayers are mechanically poised for motility and identifies global stress amplification as a mechanism for tissue fluidization.

Cell behaviour in a polygonal cell sheet*

Development ◽  
1984 ◽  
Vol 83 (Supplement) ◽  
pp. 313-327
Author(s):  
H. Honda ◽  
R. Kodama ◽  
T. Takeuchi ◽  
H. Yamanaka ◽  
K. Watanabe ◽  
...  
Keyword(s):  
Cell Sheet ◽  
Cell Monolayer ◽  
Time Lapse ◽  
Geometrical Method ◽  
Cell Behaviour ◽  
Cell Monolayers ◽  
Polygonal Cell ◽  
Computer Based ◽  
Insight Into

Cell monolayers on culture dishes were divided into two groups: tensile monolayers and non-tensile ones. In the development of an epithelium, a non-tensile cell monolayer turns into a tightly bound tensile one. Detection of these states was carried out by using the boundary shortening procedure, a computer-based geometrical method to show how much the polygonal cell boundary contracts. Non-tensile monolayers were divided further into two groups according to their motility: a fluctuating monolayer in which cells move laterally, and a stable monolayer in which cells are immobilized. Quantitative determination of cell motility was performed by analysing time-lapse cellular patterns. These computer-based geometrical analyses enabled us to divide monolayers into three groups: tensile stable monolayers, non-tensile stable monolayers and fluctuating monolayers, and this study therefore gives an insight into the way in which changing conformations of cells may be assayed.

scholarly journals Stem cell-derived cell sheet transplantation for heart tissue repair in myocardial infarction

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Rui Guo ◽  
Masatoshi Morimatsu ◽  
Tian Feng ◽  
Feng Lan ◽  
Dehua Chang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Stem Cell ◽  
Tissue Repair ◽  
Cardiac Tissue ◽  
Cell Sheet ◽  
Clinical Manifestations ◽  
Induced Pluripotent Stem Cell ◽  
Heart Tissue ◽  
Therapeutic Effects ◽  
Cell Sheets

AbstractStem cell-derived sheet engineering has been developed as the next-generation treatment for myocardial infarction (MI) and offers attractive advantages in comparison with direct stem cell transplantation and scaffold tissue engineering. Furthermore, induced pluripotent stem cell-derived cell sheets have been indicated to possess higher potential for MI therapy than other stem cell-derived sheets because of their capacity to form vascularized networks for fabricating thickened human cardiac tissue and their long-term therapeutic effects after transplantation in MI. To date, stem cell sheet transplantation has exhibited a dramatic role in attenuating cardiac dysfunction and improving clinical manifestations of heart failure in MI. In this review, we retrospectively summarized the current applications and strategy of stem cell-derived cell sheet technology for heart tissue repair in MI.

scholarly journals Temperature-responsive intelligent interfaces for biomolecular separation and cell sheet engineering

2009 ◽  
Vol 6 (suppl_3) ◽  
Author(s):  
Kenichi Nagase ◽  
Jun Kobayashi ◽  
Teruo Okano
Keyword(s):  
Cell Sheet ◽  
Copolymer Composition ◽  
Cell Sheets ◽  
Chromatographic Separations ◽  
Cell Sheet Engineering ◽  
External Temperature ◽  
Cell Monolayers ◽  
Temperature Responsive ◽  
Confluent Cell ◽  
Dependent Cell

Temperature-responsive intelligent surfaces, prepared by the modification of an interface with poly( N -isopropylacrylamide) and its derivatives, have been used for biomedical applications. Such surfaces exhibit temperature-responsive hydrophilic/hydrophobic alterations with external temperature changes, which, in turn, result in thermally modulated interactions with biomolecules and cells. In this review, we focus on the application of these intelligent surfaces to chromatographic separation and cell cultures. Chromatographic separations using several types of intelligent surfaces are mentioned briefly, and various effects related to the separation of bioactive compounds are discussed, including wettability, copolymer composition and graft polymer architecture. Similarly, we also summarize temperature-responsive cell culture substrates that allow the recovery of confluent cell monolayers as contiguous living cell sheets for tissue-engineering applications. The key factors in temperature-dependent cell adhesion/detachment control are discussed from the viewpoint of grafting temperature-responsive polymers, and new methodologies for effective cell sheet culturing and the construction of thick tissues are summarized.

scholarly journals Scaffold-Free 3-D Cell Sheet Technique Bridges the Gap between 2-D Cell Culture and Animal Models

2019 ◽  
Vol 20 (19) ◽  
pp. 4926 ◽  
Author(s):  
Ayidah Alghuwainem ◽  
Alaa T. Alshareeda ◽  
Batla Alsowayan
Keyword(s):  
Tissue Engineering ◽  
Cell Culture ◽  
Animal Models ◽  
Tissue Repair ◽  
Cell Sheet ◽  
Cell Sheets ◽  
Systemic Injection ◽  
In Vivo Testing ◽  
D Cell

Various tissue engineering techniques have been created in research spanning two centuries, resulting in new opportunities for growing cells in culture and the creation of 3-D tissue-like constructs. These techniques are classified as scaffold-based and scaffold-free techniques. Cell sheet, as a scaffold-free technique, has attracted research interest in the context of drug discovery and tissue repair, because it provides more predictive data for in vivo testing. It is one of the most promising techniques and has the potential to treat degenerative tissues such as heart, kidneys, and liver. In this paper, we argue the advantages of cell sheets as a scaffold-free approach, compared to other techniques, including scaffold-based and scaffold-free techniques such as the classic systemic injection of cell suspension.

scholarly journals Modelling mammalian cellular quiescence

2014 ◽  
Vol 4 (3) ◽  
pp. 20130074 ◽  
Author(s):  
Guang Yao
Keyword(s):  
Dynamic Control ◽  
Control Mechanisms ◽  
Bistable Switch ◽  
Environmental Signals ◽  
Tissue Repair And Regeneration ◽  
Cycle Arrest ◽  
Permanent Cell ◽  
Cellular Quiescence ◽  
Novel Therapeutic Strategies ◽  
Multicellular Organisms

Cellular quiescence is a reversible non-proliferating state. The reactivation of ‘sleep-like’ quiescent cells (e.g. fibroblasts, lymphocytes and stem cells) into proliferation is crucial for tissue repair and regeneration and a key to the growth, development and health of higher multicellular organisms, such as mammals. Quiescence has been a primarily phenotypic description (i.e. non-permanent cell cycle arrest) and poorly studied. However, contrary to the earlier thinking that quiescence is simply a passive and dormant state lacking proliferating activities, recent studies have revealed that cellular quiescence is actively maintained in the cell and that it corresponds to a collection of heterogeneous states. Recent modelling and experimental work have suggested that an Rb-E2F bistable switch plays a pivotal role in controlling the quiescence–proliferation balance and the heterogeneous quiescent states. Other quiescence regulatory activities may crosstalk with and impinge upon the Rb-E2F bistable switch, forming a gene network that controls the cells’ quiescent states and their dynamic transitions to proliferation in response to noisy environmental signals. Elucidating the dynamic control mechanisms underlying quiescence may lead to novel therapeutic strategies that re-establish normal quiescent states, in a variety of hyper- and hypo-proliferative diseases, including cancer and ageing.

Cell sheet engineering for heart tissue repair

2008 ◽  
Vol 60 (2) ◽  
pp. 277-285 ◽  
Author(s):  
Shinako Masuda ◽  
Tatsuya Shimizu ◽  
Masayuki Yamato ◽  
Teruo Okano
Keyword(s):  
Tissue Repair ◽  
Cell Sheet ◽  
Heart Tissue ◽  
Cell Sheet Engineering

scholarly journals Yap1-driven intestinal repair is controlled by group 3 innate lymphoid cells

2019 ◽  
Author(s):  
Mónica Romera-Hernández ◽  
Patricia Aparicio-Domingo ◽  
Natalie Papazian ◽  
Julien J. Karrich ◽  
Ferry Cornelissen ◽  
...  
Keyword(s):  
Stem Cell ◽  
Tissue Regeneration ◽  
Tissue Repair ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Stem Cell Maintenance ◽  
Epithelial Regeneration ◽  
Group 3 ◽  
Intestinal Repair ◽  
Cell Maintenance

SUMMARYTissue repair requires temporal control of progenitor cell proliferation and differentiation to replenish damaged cells. In response to acute insult, group 3 innate lymphoid cells (ILC3) regulate intestinal stem cell maintenance and subsequent tissue repair. ILC3-derived IL-22 is important for stem cell protection, but the mechanisms of ILC3-driven tissue regeneration remain incompletely defined. Here we report that group 3 innate lymphoid cell (ILC3)-driven epithelial proliferation and tissue regeneration are independent of IL-22. In contrast, ILC3 amplify the magnitude of Hippo-Yap1 signaling in intestinal crypt cells, ensuring adequate initiation of tissue repair and preventing excessive pathology. Mechanistically, ILC3-driven tissue repair is Stat3-independent, but involves activation of Src family kinases. Our findings reveal that ILC3-driven intestinal repair entails distinct transcriptional networks to control stem cell maintenance and epithelial regeneration which implies that tissue repair and crypt proliferation can be influenced by targeting innate immune cells independent of the well-established effects of IL-22.

scholarly journals Is There a Histone Code for Cellular Quiescence?

2021 ◽  
Vol 9 ◽  
Author(s):  
Kenya Bonitto ◽  
Kirthana Sarathy ◽  
Kaiser Atai ◽  
Mithun Mitra ◽  
Hilary A. Coller
Keyword(s):  
Histone Code ◽  
Model Systems ◽  
Quiescent State ◽  
Histone Marks ◽  
Immunological Responses ◽  
Stem Cell Maintenance ◽  
Cellular Quiescence ◽  
Chromosomal Changes ◽  
And Function

Many of the cells in our bodies are quiescent, that is, temporarily not dividing. Under certain physiological conditions such as during tissue repair and maintenance, quiescent cells receive the appropriate stimulus and are induced to enter the cell cycle. The ability of cells to successfully transition into and out of a quiescent state is crucial for many biological processes including wound healing, stem cell maintenance, and immunological responses. Across species and tissues, transcriptional, epigenetic, and chromosomal changes associated with the transition between proliferation and quiescence have been analyzed, and some consistent changes associated with quiescence have been identified. Histone modifications have been shown to play a role in chromatin packing and accessibility, nucleosome mobility, gene expression, and chromosome arrangement. In this review, we critically evaluate the role of different histone marks in these processes during quiescence entry and exit. We consider different model systems for quiescence, each of the most frequently monitored candidate histone marks, and the role of their writers, erasers and readers. We highlight data that support these marks contributing to the changes observed with quiescence. We specifically ask whether there is a quiescence histone “code,” a mechanism whereby the language encoded by specific combinations of histone marks is read and relayed downstream to modulate cell state and function. We conclude by highlighting emerging technologies that can be applied to gain greater insight into the role of a histone code for quiescence.

Cell sheet transplantation for heart tissue repair

2013 ◽  
Vol 169 (3) ◽  
pp. 336-340 ◽  
Author(s):  
Katsuhisa Matsuura ◽  
Yuji Haraguchi ◽  
Tatsuya Shimizu ◽  
Teruo Okano
Keyword(s):  
Tissue Repair ◽  
Cell Sheet ◽  
Heart Tissue
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