Role for differential cell proliferation in perforation and rupture of chick pharyngeal closing plates

1993 ◽  
Vol 237 (3) ◽  
pp. 408-414 ◽  
Author(s):  
Sue Ann Miller ◽  
Alicia M. Favale ◽  
Stephen J. Knohl
Keyword(s):  
Cell Proliferation ◽  
Differential Cell

A Wearable Photobiomodulation Patch Using a Flexible Red-Wavelength OLED and Its In Vitro Differential Cell Proliferation Effects

2018 ◽  
Vol 3 (5) ◽  
pp. 1700391 ◽  
Author(s):  
Yongmin Jeon ◽  
Hye-Ryung Choi ◽  
Myungsub Lim ◽  
Seungyeop Choi ◽  
Hyuncheol Kim ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Differential Cell

scholarly journals Molar Bud-to-Cap Transition Is Proliferation Independent

2019 ◽  
Vol 98 (11) ◽  
pp. 1253-1261 ◽  
Author(s):  
S. Yamada ◽  
R. Lav ◽  
J. Li ◽  
A.S. Tucker ◽  
J.B.A. Green
Keyword(s):  
Cell Proliferation ◽  
Cell Shape ◽  
Tooth Germ ◽  
Odontogenic Epithelium ◽  
Differential Cell ◽  
Cell Shapes ◽  
Genetic Mechanisms ◽  
Cell Trajectory ◽  
Tooth Germs ◽  
Different Parts

Tooth germs undergo a series of dynamic morphologic changes through bud, cap, and bell stages, in which odontogenic epithelium continuously extends into the underlying mesenchyme. During the transition from the bud stage to the cap stage, the base of the bud flattens and then bends into a cap shape whose edges are referred to as “cervical loops.” Although genetic mechanisms for cap formation have been well described, little is understood about the morphogenetic mechanisms. Computer modeling and cell trajectory tracking have suggested that the epithelial bending is driven purely by differential cell proliferation and adhesion in different parts of the tooth germ. Here, we show that, unexpectedly, inhibition of cell proliferation did not prevent bud-to-cap morphogenesis. We quantified cell shapes and actin and myosin distributions in different parts of the tooth epithelium at the critical stages and found that these are consistent with basal relaxation in the forming cervical loops and basal constriction around enamel knot at the center of the cap. Inhibition of focal adhesion kinase, which is required for basal constriction in other systems, arrested the molar explant morphogenesis at the bud stage. Together, these results show that the bud-to-cap transition is largely proliferation independent, and we propose that it is driven by classic actomyosin-driven cell shape–dependent mechanisms. We discuss how these results can be reconciled with the previous models and data.

Amphiregulin in lung branching morphogenesis: interaction with heparan sulfate proteoglycan modulates cell proliferation

Development ◽  
1996 ◽  
Vol 122 (6) ◽  
pp. 1759-1767 ◽  
Author(s):  
L. Schuger ◽  
G.R. Johnson ◽  
K. Gilbride ◽  
G.D. Plowman ◽  
R. Mandel
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cells ◽  
Heparan Sulfate ◽  
Branching Morphogenesis ◽  
Mesenchymal Cells ◽  
Heparan Sulfate Proteoglycan ◽  
Sulfate Proteoglycan ◽  
Epithelial Proliferation ◽  
Differential Cell ◽  
Embryonic Lungs

Epithelial and mesenchymal cells isolated from mouse embryonic lungs synthesized and responded to amphiregulin (AR) in a different fashion. Mesenchymal cells produced and deposited 3- to 4-fold more AR than epithelial cells, proliferated in the presence of exogenous AR, and their spontaneous growth was blocked by up to 85% by anti-AR antibodies. In contrast, epithelial cells exhibited a broad response to this growth regulator factor depending on whether they were supplemented with extracellular matrix (ECM) and whether this ECM was of epithelial or mesenchymal origin. AR-treated epithelial cells proliferated by up to 3-fold in the presence of mesenchymal-deposited ECM, remained unchanged in the presence of epithelial-deposited ECM, and decreased in their proliferation rate below controls in the absence of ECM supplementation. This effect was abolished by treatment with the glycosaminoglycan-degrading enzymes heparinase and heparitinase suggesting the specific involvement of heparan sulfate proteoglycan (HSPG) in AR-mediated cell proliferation. In whole lung explants, branching morphogenesis was inhibited by antibodies against the AR heparan sulfate binding site and stimulated by exogenous AR. Since during development, epithelial cells are in contact with mesenchymal ECM at the tips of the growing buds and alongside the basement membrane, focal variations in the proportion of epithelial and mesenchymal HSPG will focally affect epithelial proliferation rates. Therefore, AR-HSPG interaction may underlie the process of branching morphogenesis by inducing differential cell proliferation.

scholarly journals Role of differential cell proliferation in the tail bud in aberrant mouse neurulation

1998 ◽  
Vol 211 (4) ◽  
pp. 382-389 ◽  
Author(s):  
Marian C.E. Peeters ◽  
Bert Schutte ◽  
Marie-Hélène J.N. Lenders ◽  
Johan W.M. Hekking ◽  
Jan Drukker ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Tail Bud ◽  
Differential Cell

Differential cell proliferation in the cortex of the appsweps1de9 alzheimer's disease mouse model

Glia ◽  
2012 ◽  
Vol 60 (4) ◽  
pp. 615-629 ◽  
Author(s):  
Willem Kamphuis ◽  
Marie Orre ◽  
Lieneke Kooijman ◽  
Maurice Dahmen ◽  
Elly M. Hol
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Proliferation ◽  
Mouse Model ◽  
Differential Cell

Domains of differential cell proliferation suggest hinged folding in avian gut endoderm

1999 ◽  
Vol 216 (4/5) ◽  
pp. 398-410 ◽  
Author(s):  
Sue Ann Miller ◽  
Michael Adornato ◽  
Ailish Briglin ◽  
Megan Cavanaugh ◽  
Todd Christian ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Differential Cell ◽  
Gut Endoderm
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