Epithelial Morphogenesis Driven by Cell-Matrix vs. Cell-Cell Adhesion

2020 ◽  
Author(s):  
Shaohe Wang ◽  
Kazue Matsumoto ◽  
Kenneth M. Yamada
Keyword(s):  
Cell Adhesion ◽  
Epithelial Morphogenesis ◽  
Cell Matrix ◽  
Cell Cell

scholarly journals Epithelial Morphogenesis Driven by Cell-Matrix vs. Cell-Cell Adhesion

2020 ◽  
Author(s):  
Shaohe Wang ◽  
Kazue Matsumoto ◽  
Kenneth M. Yamada
Keyword(s):  
Cell Adhesion ◽  
Single Cell ◽  
Cell Sheet ◽  
Branching Morphogenesis ◽  
Epithelial Morphogenesis ◽  
Epithelial Surface ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion ◽  
Cell Cell

SUMMARYMany embryonic organs undergo epithelial morphogenesis to form tree-like hierarchical structures. However, it remains unclear what drives the budding and branching of stratified epithelia, such as in embryonic salivary gland and pancreas. Here, we performed live-organ imaging of mouse embryonic salivary glands at single-cell resolution to reveal that budding morphogenesis is driven by expansion and folding of a distinct epithelial surface cell sheet characterized by strong cell-matrix adhesions and weak cell-cell adhesions. Profiling of single-cell transcriptomes of this epithelium revealed spatial patterns of transcription underlying these cell adhesion differences. We then synthetically reconstituted budding morphogenesis by experimentally suppressing E-cadherin expression and inducing basement membrane formation in 3D spheroid cultures of engineered cells, which required β1 integrin-mediated cell-matrix adhesion for successful budding. Thus, stratified epithelial budding, the key first step of branching morphogenesis, is driven by an overall combination of strong cell-matrix adhesion and weak cell-cell adhesion by peripheral epithelial cells.

scholarly journals Budding epithelial morphogenesis driven by cell-matrix versus cell-cell adhesion

Cell ◽  
2021 ◽  
Author(s):  
Shaohe Wang ◽  
Kazue Matsumoto ◽  
Samantha R. Lish ◽  
Alexander X. Cartagena-Rivera ◽  
Kenneth M. Yamada
Keyword(s):  
Cell Adhesion ◽  
Epithelial Morphogenesis ◽  
Matrix Versus ◽  
Cell Matrix ◽  
Cell Cell

scholarly journals Myosin VI plays a role in cell–cell adhesion during epithelial morphogenesis

2004 ◽  
Vol 121 (11) ◽  
pp. 1335-1351 ◽  
Author(s):  
Hadas Millo ◽  
Kevin Leaper ◽  
Vasiliki Lazou ◽  
Mary Bownes
Keyword(s):  
Cell Adhesion ◽  
Epithelial Morphogenesis ◽  
Myosin Vi ◽  
Cell Cell

scholarly journals Tetraspanin CD151 maintains vascular stability by balancing the forces of cell adhesion and cytoskeletal tension

Blood ◽  
2011 ◽  
Vol 118 (15) ◽  
pp. 4274-4284 ◽  
Author(s):  
Feng Zhang ◽  
Jarett E. Michaelson ◽  
Simon Moshiach ◽  
Norman Sachs ◽  
Wenyuan Zhao ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Endothelial Cell ◽  
Cell Matrix ◽  
Vascular Morphogenesis ◽  
Vascular Stability ◽  
Optimal Functions ◽  
Cytoskeletal Tension ◽  
Cell Cell

Abstract Tetraspanin CD151 is highly expressed in endothelial cells and regulates pathologic angiogenesis. However, the mechanism by which CD151 promotes vascular morphogenesis and whether CD151 engages other vascular functions are unclear. Here we report that CD151 is required for maintaining endothelial capillary-like structures formed in vitro and the integrity of endothelial cell-cell and cell-matrix contacts in vivo. In addition, vascular permeability is markedly enhanced in the absence of CD151. As a global regulator of endothelial cell-cell and cell-matrix adhesions, CD151 is needed for the optimal functions of various cell adhesion proteins. The loss of CD151 elevates actin cytoskeletal traction by up-regulating RhoA signaling and diminishes actin cortical meshwork by down-regulating Rac1 activity. The inhibition of RhoA or activation of cAMP signaling stabilizes CD151-silenced or -null endothelial structure in vascular morphogenesis. Together, our data demonstrate that CD151 maintains vascular stability by promoting endothelial cell adhesions, especially cell-cell adhesion, and confining cytoskeletal tension.

scholarly journals Cell-matrix adhesion and cell-cell adhesion differentially control basal myosin oscillation and Drosophila egg chamber elongation

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Xiang Qin ◽  
Byung Ouk Park ◽  
Jiaying Liu ◽  
Bing Chen ◽  
Valerie Choesmel-Cadamuro ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Egg Chamber ◽  
Cell Matrix Adhesion ◽  
Cell Cell

Regulation of cell???matrix adhesion and potentially also cell???cell adhesion by MIA

2006 ◽  
Vol 16 (Supplement 1) ◽  
pp. S18-S19
Author(s):  
A. Winklmeier ◽  
R. Bauer ◽  
S. Arndt ◽  
A. Bosserhoff
Keyword(s):  
Cell Adhesion ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion ◽  
Cell Cell

Characterization of integrins in cultured human renal cortical tubule epithelial cells

1994 ◽  
Vol 267 (4) ◽  
pp. F612-F623
Author(s):  
E. E. Simon ◽  
C. H. Liu ◽  
M. Das ◽  
S. Nigam ◽  
T. J. Broekelmann ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Cell Adhesion ◽  
Epithelial Cells ◽  
Initial Attachment ◽  
Cell Contacts ◽  
Cell Matrix ◽  
Beta 1 Integrin ◽  
Tubule Cells ◽  
Alpha V Beta 3 ◽  
Cell Cell

We have characterized the integrins present on cultured tubule epithelial cells from human renal cortexes, enriched for proximal cells, using fluorescence microscopy, immunoprecipitation, and cell adhesion assays. By immunofluorescence, the alpha 3-integrin subunit stained most intensely and was present on all cells predominantly at cell-cell contacts. The alpha 6-subunit was present on all cells in a pattern consistent with extracellular matrix contacts. The alpha 5-subunit was present on most cells in a cell-matrix contact pattern; alpha V-subunit was weakly positive and occasionally seen in cell-matrix contacts. The alpha 2-subunit was present on clusters of distal tubule cells, predominantly at cell-cell contacts. Immunoprecipitation revealed the predominant integrin to be alpha 3 beta 1 with some alpha 2 beta 1, presumably contributed by distal cells. The alpha 5 beta 1-, alpha 6 beta 1-, alpha 6 beta 4-, and alpha V beta 3-integrins, as well as trace amounts of alpha 1 beta 1-integrins, were also present. The alpha 4 beta 1-integrin was not detected. Initial attachment to fibronectin was mediated by alpha V beta 3- and alpha 5 beta 1-integrins; initial attachment to laminin was mediated by the alpha 6 beta 1- and alpha 3 beta 1- integrins and, in some preparations, by an unidentified integrin; and initial attachment to collagen type IV was mediated by alpha V beta 3-integrin and an unidentified beta 1-integrin. After extensively immunodepleting membrane extracts with anti-alpha 1, -alpha 2, -alpha 3, -alpha 4, -alpha 5, -alpha 6, and -alpha V antibodies, an anti-beta 1 antibody still precipitated an integrin. Its electrophoretic mobility differs from the laminin-binding alpha 7 beta 1-integrin. Thus we have identified many of the integrins on cortical tubule cells and their role in mediating initial attachment to extracellular matrix. However, the cell adhesion assays and immunoprecipitations suggest the presence of an unidentified beta 1-integrin that may mediate renal tubule cell attachment to laminin and collagen.

scholarly journals DISC1 regulates cell–cell adhesion, cell–matrix adhesion and neurite outgrowth

2010 ◽  
Vol 15 (8) ◽  
pp. 798-809 ◽  
Author(s):  
T Hattori ◽  
S Shimizu ◽  
Y Koyama ◽  
K Yamada ◽  
R Kuwahara ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Neurite Outgrowth ◽  
Matrix Adhesion ◽  
Cell Matrix ◽  
Cell Matrix Adhesion ◽  
Cell Cell
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