Spheroid formation of human keratinocyte: Balancing between cell-substrate and cell-cell interaction

2020 ◽  
Vol 76 (2) ◽  
pp. 329-340
Author(s):  
Yan Nie ◽  
Xun Xu ◽  
Weiwei Wang ◽  
Nan Ma ◽  
Andreas Lendlein
Keyword(s):  
Hacat Cell ◽  
Cell Interaction ◽  
Adhesive Force ◽  
Design Criterion ◽  
Spheroid Formation ◽  
Cell Functions ◽  
Substrate Adhesion ◽  
Cell Substrate ◽  
Coated Surfaces ◽  
Cell Cell

BACKGROUND: The formation of spheroids is tightly regulated by intrinsic cell-cell and cell-substrate interactions. OBJECTIVE: The chitosan (CS)-coating was applied to investigate the driven force directed the spheroid formation. METHODS: The effects of CS on cell functions were studied. Atomic force microscopy was employed to measure the cell- biomaterial interplay at single cell level. RESULTS: HaCaT cells shifted from their flattened sheet to a compact 3D spheroidal morphology when increasing CS-coating concentration. The proliferative capacity of HaCaT was preserved in the spheroid. The expression and activation of integrin β1 (ITGB1) were enhanced on CS modified surfaces, while the active to total ratio of ITGB1 was decreased. The adhesive force of a single HaCaT cell to the tissue culture plate (TCP) was 4.84±0.72 nN. It decreased on CS-coated surfaces as CS concentration increased, from 2.16±0.26 nN to 0.96±0.17 nN. The adhesive force between the single HaCaT cell to its neighbor cell increased as CS concentration increased, from 1.15±0.09 nN to 2.60±0.51 nN. CONCLUSIONS: Conclusively, the decreased cell- substrate adhesion was the main driven force in the spheroid formation. This finding might serve as a design criterion for biomaterials facilitating the formation of epithelial spheroids.

scholarly journals Minireview: The Neuroendocrine Regulation of Puberty: Is the Time Ripe for a Systems Biology Approach?

Endocrinology ◽  
2006 ◽  
Vol 147 (3) ◽  
pp. 1166-1174 ◽  
Author(s):  
Sergio R. Ojeda ◽  
Alejandro Lomniczi ◽  
Claudio Mastronardi ◽  
Sabine Heger ◽  
Christian Roth ◽  
...  
Keyword(s):  
Global Analysis ◽  
Single Gene ◽  
Functional Integration ◽  
Cell Communication ◽  
Cell Interaction ◽  
Specific Cell ◽  
Gnrh Secretion ◽  
Cell Functions ◽  
Hierarchical Arrangement ◽  
Cell Cell

The initiation of mammalian puberty requires an increase in pulsatile release of GnRH from the hypothalamus. This increase is brought about by coordinated changes in transsynaptic and glial-neuronal communication. As the neuronal and glial excitatory inputs to the GnRH neuronal network increase, the transsynaptic inhibitory tone decreases, leading to the pubertal activation of GnRH secretion. The excitatory neuronal systems most prevalently involved in this process use glutamate and the peptide kisspeptin for neurotransmission/neuromodulation, whereas the most important inhibitory inputs are provided by γ-aminobutyric acid (GABA)ergic and opiatergic neurons. Glial cells, on the other hand, facilitate GnRH secretion via growth factor-dependent cell-cell signaling. Coordination of this regulatory neuronal-glial network may require a hierarchical arrangement. One level of coordination appears to be provided by a host of unrelated genes encoding proteins required for cell-cell communication. A second, but overlapping, level might be provided by a second tier of genes engaged in specific cell functions required for productive cell-cell interaction. A third and higher level of control involves the transcriptional regulation of these subordinate genes by a handful of upper echelon genes that, operating within the different neuronal and glial subsets required for the initiation of the pubertal process, sustain the functional integration of the network. The existence of functionally connected genes controlling the pubertal process is consistent with the concept that puberty is under genetic control and that the genetic underpinnings of both normal and deranged puberty are polygenic rather than specified by a single gene. The availability of improved high-throughput techniques and computational methods for global analysis of mRNAs and proteins will allow us to not only initiate the systematic identification of the different components of this neuroendocrine network but also to define their functional interactions.

scholarly journals The interplay of cell–cell and cell–substrate adhesion in collective cell migration

2014 ◽  
Vol 11 (100) ◽  
pp. 20140684 ◽  
Author(s):  
Chenlu Wang ◽  
Sagar Chowdhury ◽  
Meghan Driscoll ◽  
Carole A. Parent ◽  
S. K. Gupta ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cell Surface ◽  
Actin Polymerization ◽  
Collective Cell Migration ◽  
Cell Contacts ◽  
Substrate Adhesion ◽  
Cell Substrate ◽  
Cell Shapes ◽  
Cell Substrate Adhesion ◽  
Cell Cell

Collective cell migration often involves notable cell–cell and cell–substrate adhesions and highly coordinated motion of touching cells. We focus on the interplay between cell–substrate adhesion and cell–cell adhesion. We show that the loss of cell-surface contact does not significantly alter the dynamic pattern of protrusions and retractions of fast migrating amoeboid cells ( Dictyostelium discoideum ), but significantly changes their ability to adhere to other cells. Analysis of the dynamics of cell shapes reveals that cells that are adherent to a surface may coordinate their motion with neighbouring cells through protrusion waves that travel across cell–cell contacts. However, while shape waves exist if cells are detached from surfaces, they do not couple cell to cell. In addition, our investigation of actin polymerization indicates that loss of cell-surface adhesion changes actin polymerization at cell–cell contacts. To further investigate cell–cell/cell–substrate interactions, we used optical micromanipulation to form cell–substrate contact at controlled locations. We find that both cell-shape dynamics and cytoskeletal activity respond rapidly to the formation of cell–substrate contact.

Cell-cell and cell-substrate adhesion molecules

Pathology ◽  
1992 ◽  
Vol 24 ◽  
pp. 26
Author(s):  
M.A. Vadas ◽  
J.R. Gamble ◽  
Y. Khew-Goodall ◽  
P. Kaur
Keyword(s):  
Adhesion Molecules ◽  
Substrate Adhesion ◽  
Cell Substrate ◽  
Cell Substrate Adhesion ◽  
Cell Cell

Modulation of epidermal differentiation by epiligrin and integrin alpha 3 beta 1

1995 ◽  
Vol 108 (2) ◽  
pp. 831-838 ◽  
Author(s):  
B.E. Symington ◽  
W.G. Carter
Keyword(s):  
Cell Adhesion ◽  
Close Contact ◽  
Intercellular Adhesion ◽  
Epidermal Differentiation ◽  
Basal Cells ◽  
Substrate Adhesion ◽  
Cell Substrate ◽  
High Calcium ◽  
Cell Substrate Adhesion ◽  
Cell Cell

We previously reported that integrin alpha 3 beta 1 mediates epidermal intercellular adhesion as well as cell-substrate adhesion. P1B5, an anti-alpha 3 beta 1 specific monoclonal antibody, is a potent in vitro trigger of epidermal cell-cell adhesion and an inhibitor of cell-substrate adhesion. We now show that P1B5 specifically induces the intercellular localization of integrins alpha 2 beta 1 and alpha 3 beta 1, consistent with its role in inducing intercellular adhesion via these two integrins. P1F2, another anti-alpha 3 beta 1 antibody, does not induce either intercellular adhesion or intercellular accumulation of alpha 3 beta 1 and alpha 2 beta 1. Growth of epidermal cells in high calcium, known to induce epidermal differentiation, also induces intercellular accumulation of alpha 3 beta 1 and alpha 2 beta 1 and increased cell-cell adhesion. We therefore asked whether P1B5 treatment induces epidermal differentiation. P1B5 treatment induces changes consistent with epidermal differentiation, including increased involucrin expression, stratification, and production of squames. P1F2 treatment has none of these effects. In vivo, epidermal basal cells are in close contact with the epithelial basement membrane component epiligrin. Growth of keratinocytes on purified epiligrin but not other matrix components specifically reduces involucrin expression by P1B5-treated keratinocytes. These results suggest that integrin alpha 3 beta 1 has a unique role in epidermal differentiation, that the epitope recognized by P1B5 is involved in triggering this differentiation, and that keratinocyte adhesion to epiligrin inhibits alpha 3 beta 1-mediated differentiation.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals NGF IMPROVES NEURITE FASCICULATION OF EMBRYONIC RAT CEREBRAL CORTICAL NEURAL STEM CELLS ON EVAL SUBSTRATES UNDER SERUM FREE CONDITIONS

2006 ◽  
Vol 18 (04) ◽  
pp. 207-213
Author(s):  
CHIH-HUANG HUNG ◽  
TAI-HORNG YOUNG
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Cell Interaction ◽  
Developmental Potential ◽  
Growth And Survival ◽  
Serum Free ◽  
Cell Substrate ◽  
Nerve Growth Factors ◽  
Serum Free Conditions ◽  
Cell Cell

The behaviors of multipotential neural stem cells are regulated by several factors, including culture substrates, soluble factors, and cell-cell interactions. The purpose of this study was to explore the effects of cell-cell and cell-substrate interactions on developmental potential of neural stem cells from embryonic rat cerebral cortex at neurosphere level in the presence of nerve growth factors (NGF). The results suggested that, in combination with NGF, EVAL substrates could induce neurite fasciculation of differentiated forming-neurosphere cells under serum free conditions. Quantitative analysis of process growth reveals that, under serum free conditions, when NGF was present the process breadth was significantly larger than that of neurospheres cultured without NGF. In contrast, when serum were added in the medium, regardless of the addition of NGF or not, the neurospheres were induced into typically an extensive cellular substratum of protoplasmic cells upon which process-bearing cells spread. It indicated that, when serum was present, the differentiated GFAP-positive astrocytes layer could serve as a supported architectural for growth and survival of process-bearing cells. At this time, neurites were failed to fasciculate. Here, we proposed that the mediation of cell-biomaterial interaction by cell-cell interaction should be taken into account for regulation of neurites fasciculation. Moreover, the pattern of neural stem cell growth on EVAL subtrates with or without NGF in the absence or presence of serum in this studies suggested that neurons are more adherent to glail cells than to other neurons but are more adherent to other neurons than to EVAL substrates.

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