Loss of myeloid cell-derived vascular endothelial growth factor accelerates fibrosis

Loss of myeloid cell-derived vascular endothelial growth factor accelerates fibrosis

Christian Stockmann, Yann Kerdiles, Marc Nomaksteinsky, Alexander Weidemann, Norihiko Takeda, Andrew Doedens, Antonio X. Torres-Collado, Luisa Iruela-Arispe, Victor Nizet, and Randall S. Johnson

PNAS, Published online before print February 8, 2010, doi: 10.1073/pnas.0912766107

beta-catenin-mediated signaling and cell adhesion in postgastrulation mouse embryos.

beta-catenin-mediated signaling and cell adhesion in postgastrulation mouse embryos.

Hierholzer A, Kemler R

Dev Dyn. 2009 Aug 24;

Non-redundant roles for Profilin2 and Profilin1 during vertebrate gastrulation

Non-redundant roles for Profilin2 and Profilin1 during vertebrate gastrulation

Deepak K. Khadka, Wei Liu and Raymond Habas

Developmental Biology Article in Press, Corrected Proof doi:10.1016/j.ydbio.2009.06.008

Dysregulation of the Wnt pathway inhibits timely myelination and remyelination in the mammalian CNS

Dysregulation of the Wnt pathway inhibits timely myelination and remyelination in the mammalian CNS

Stephen P.J. Fancy, Sergio E. Baranzini, Chao Zhao, Dong-In Yuk, Karen-Amanda Irvine, Sovann Kaing, Nader Sanai, Robin J.M. Franklin and David H. Rowitch

Published in Advance June 10, 2009, doi:10.1101/gad.1806309

A systems biology approach to Down syndrome: Identification of Notch/Wnt dysregulation in a model of stem cells aging

A systems biology approach to Down syndrome: Identification of Notch/Wnt dysregulation in a model of stem cells aging.

Cairney CJ, Sanguinetti G, Ranghini E, Chantry AD, Nostro MC, Bhattacharyya A, Svendsen CN, Keith WN, Bellantuono I.

Biochim Biophys Acta. 2009 Apr;1792(4):353-63 doi:10.1016/j.bbadis.2009.01.015

Contact inhibition of locomotion in vivo controls neural crest directional migration

Contact inhibition of locomotion in vivo controls neural crest directional migration

Carlos Carmona-Fontaine, Helen K. Matthews, Sei Kuriyama, Mauricio Moreno, Graham A. Dunn, Maddy Parsons, Claudio D. Stern & Roberto Mayor

Nature | doi:10.1038/nature07441 Published online 10 December 2008

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Voir aussi (just for the fun), FAQ5 :

La première cause « d’inhibition de contact », c’est la simple présence d’une cellule voisine, avant de parler de ce qu’elles s’échangent chimiquement.

et comparer avec les résultats de l’expérimentation montrés à la figure 2 du papier, montrant une inhibition de contact lors ce que deux populations de cellules de CN se rencontrent versus l’envahissement d’une population de cellules mésothéliales par les cellules de CN en l’absence d’inhibition de contact. Les cellules de CN ne surfent pas le Net pour savoir comment il faudrait qu’elles fassent. Pas très platonicien comme attitude 😀
« l’expérience est nécessaire« 

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Wnt Signaling Mediates Self-Organization and Axis Formation in Embryoid Bodies

Wnt Signaling Mediates Self-Organization and Axis Formation in Embryoid Bodies

Derk ten Berge, Wouter Koole, Christophe Fuerer, Matt Fish, Elif Eroglu and Roel Nusse

Cell Stem Cell, Volume 3, Issue 5, 6 November 2008, Pages 508-518 doi:10.1016/j.stem.2008.09.013

A Cryptic Frizzled Module in Cell Surface Collagen 18 Inhibits Wnt/β−Catenin Signaling

A Cryptic Frizzled Module in Cell Surface Collagen 18 Inhibits Wnt/β−Catenin Signaling: « 

by Delphine Quélard, Elise Lavergne, Ismaïl Hendaoui, Harri Elamaa, Ulla Tiirola, Ritva Heljasvaara, Taina Pihlajaniemi, Bruno Clément, Orlando Musso

Collagens contain cryptic polypeptide modules that regulate major cell functions, such as cell proliferation or death. Collagen XVIII (C18) exists as three amino terminal end variants with specific amino terminal polypeptide modules. We investigated the function of the variant 3 of C18 (V3C18) containing a frizzled module (FZC18), which carries structural identity with the extracellular cysteine-rich domain of the frizzled receptors. We show that V3C18 is a cell surface heparan sulfate proteoglycan, its topology being mediated by the FZC18 module. V3C18 mRNA was expressed at low levels in 21 normal adult human tissues. Its expression was up-regulated in fibrogenesis and in small well-differentiated liver tumors, but decreased in advanced human liver cancers. Low FZC18 immunostaining in liver cancer nodules correlated with markers of high Wnt/β−catenin activity. V3C18 (M_r = 170 kD) was proteolytically processed into a cell surface FZC18-containing 50 kD glycoprotein precursor that bound Wnt3a in vitro through FZC18 and suppressed Wnt3a-induced stabilization of β−catenin. Ectopic expression of either FZC18 (35 kD) or its 50 kD precursor inhibited Wnt/β−catenin signaling in colorectal and liver cancer cell lines, thus downregulating major cell cycle checkpoint gatekeepers cyclin D1 and c-myc and reducing tumor cell growth. By contrast, full-length V3C18 was unable to inhibit Wnt signaling. In summary, we identified a cell-surface signaling pathway whereby FZC18 inhibits Wnt/β−catenin signaling. The signal, encrypted within cell-surface C18, is released by enzymatic processing as an active frizzled cysteine-rich domain (CRD) that reduces cancer cell growth. Thus, extracellular matrix controls Wnt signaling through a collagen-embedded CRD behaving as a cell-surface sensor of proteolysis, conveying feedback cues to control cancer cell fate.