Cell‐cell signaling by direct contact increases cell proliferation via a PI3K‐dependent signal

Nelson, Celeste M.; Chen, Christopher

doi:10.1016/s0014-5793(02)02370-0

Cited by 241 publications

(212 citation statements)

References 27 publications

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“…This increase in P-Akt in HME was only partially blocked by LY, although the levels of P-Akt in HME appeared to be decreased more than in HMC also regulates cadherin-mediated adhesions, which might be modulated by shuttling of p85. Nelson and Chen reported that Pi3K activity is required for cellcell contact induced proliferation, which is in line with our results [17].…”

Section: Discussionsupporting

confidence: 93%

Cadherins are regulated by Ep-CAM via phosphaditylinositol-3 kinase

et al. 2007

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Section: Discussionsupporting

confidence: 93%

Cadherins are regulated by Ep-CAM via phosphaditylinositol-3 kinase

et al. 2007

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“…This result is in agreement with a recent report showing that cell-cell contact increases cell proliferation through a PI 3-K dependent signal. 41 Thus, R-Ras activates PI 3-K, and this activity induces cell cycle progression, which favors the increased growth of tumors in nude mice.…”

Section: Discussionmentioning

confidence: 99%

R‐Ras promotes tumor growth of cervical epithelial cells

Rincón-Arano

Rosales

Mora

et al. 2003

Cancer

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Objectives To investigate whether prenatal screening is effective in the detection of total anomalous pulmonary venous connection (TAPVC) and to identify common prenatal features. Methods This was a retrospective collaborative study involving 19 pediatric cardiac centers in the UK, Ireland and Sweden. Cases with TAPVC born between January 1, 1998 and December 31, 2004, and prenatally diagnosed cases whose estimated dates of delivery were within this time frame, were identified. Cases with functionally univentricular circulation or atrial isomerism were excluded. All available data and stored images were reviewed. Results Four‐hundred and twenty‐four cases with TAPVC were identified prenatally or postnatally, of whom eight (1.9%) had a prenatal diagnosis of TAPVC. Median gestational age at fetal diagnosis was 26 + 6 (range, 22 + 4 to 32 + 0) weeks. Six further fetuses with TAPVC had an abnormality diagnosed on prenatal ultrasound, but not the TAPVC. This included other congenital heart defects (four cases) and isolated pleural effusion (two cases). Seventeen (4.0%) of the 422 liveborn infants had a first‐degree relative with congenital heart disease; and six of 17 had a sibling with TAPVC. Two died in utero. Of the liveborn infants diagnosed prenatally with TAPVC, none required urgent intervention for pulmonary venous obstruction and all were alive and well at a median of 2.3 (range, 1.0–7.0) years after surgical repair. Conclusion Prenatal diagnosis of TAPVC is infrequent using current screening methods. Where there is a family history of TAPVC, specialized fetal echocardiography at 20 and 28 weeks' gestation may be indicated. Copyright © 2012 ISUOG. Published by John Wiley & Sons, Ltd.

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“…Substrates composed of bowtie-shaped microwells of agarose on glass (750 m 2 /half bowtie) were fabricated as described previously (Nelson and Chen, 2002). Briefly, masters of patterned SU-8 photoresist (MicroChem, Newton, MA) were prepared by conventional photolithography.…”

Section: Fabrication Of Substrates With Microwellsmentioning

confidence: 99%

Vascular Endothelial-Cadherin Regulates Cytoskeletal Tension, Cell Spreading, and Focal Adhesions by Stimulating RhoA

Nelson

Pirone

Tan

et al. 2004

MBoC

165

137

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Changes in vascular endothelial (VE)-cadherin-mediated cell-cell adhesion and integrin-mediated cell-matrix adhesion coordinate to affect the physical and mechanical rearrangements of the endothelium, although the mechanisms for such cross talk remain undefined. Herein, we describe the regulation of focal adhesion formation and cytoskeletal tension by intercellular VE-cadherin engagement, and the molecular mechanism by which this occurs. Increasing the density of endothelial cells to increase cell-cell contact decreased focal adhesions by decreasing cell spreading. This contact inhibition of cell spreading was blocked by disrupting VE-cadherin engagement with an adenovirus encoding dominant negative VE-cadherin. When changes in cell spreading were prevented by culturing cells on a micropatterned substrate, VE-cadherin-mediated cell-cell contact paradoxically increased focal adhesion formation. We show that VE-cadherin engagement mediates each of these effects by inducing both a transient and sustained activation of RhoA. Both the increase and decrease in cell-matrix adhesion were blocked by disrupting intracellular tension and signaling through the Rho-ROCK pathway. In all, these findings demonstrate that VE-cadherin signals through RhoA and the actin cytoskeleton to cross talk with cell-matrix adhesion and thereby define a novel pathway by which cell-cell contact alters the global mechanical and functional state of cells. INTRODUCTIONCoordinated changes between cell adhesion to the extracellular matrix (ECM) and to neighboring cells are crucial for the many physical transformations that cells must undergo during development, tissue homeostasis, and wound healing. In the endothelium, where a single layer of cells separates tissues from their blood supply, the concerted regulation of cell-cell and cell-ECM adhesion drives rapid changes in cell shape and vascular architecture essential to vascular remodeling in both normal and disease processes (Vestweber, 2000;Dudek and Garcia, 2001). Dynamic changes in cell-cell and cell-matrix adhesion and mechanical forces are responsible for regulating vascular permeability, and agents that alter permeability invariably affect both types of adhesion complexes (Dudek and Garcia, 2001). During blood vessel sprouting and migration in angiogenesis, endothelial cells must disassemble and reform their cell-cell and cell-ECM contacts in synchrony to generate appropriate structures. These two adhesion systems each regulate their functional effects through both biochemical and mechanical signals.Changes in integrin binding to ECM not only alter signals that regulate cell proliferation, migration, and survival (Assoian and Schwartz, 2001;Hood and Cheresh, 2002;Stupack and Cheresh, 2002) but also modulate cell mechanics by affecting focal adhesion (FA) maturation, adhesion strength, cytoskeletal contractility, and cell shape (Geiger and Bershadsky, 2002;Juliano, 2002). Likewise, changes in the engagement of vascular endothelial (VE)-cadherin, the principal junctional molecule in endothe...

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Cell‐cell signaling by direct contact increases cell proliferation via a PI3K‐dependent signal

Cited by 241 publications

References 27 publications

Cadherins are regulated by Ep-CAM via phosphaditylinositol-3 kinase

Cadherins are regulated by Ep-CAM via phosphaditylinositol-3 kinase

R‐Ras promotes tumor growth of cervical epithelial cells

Vascular Endothelial-Cadherin Regulates Cytoskeletal Tension, Cell Spreading, and Focal Adhesions by Stimulating RhoA

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