Adhesion signaling – crosstalk between integrins, Src and Rho

Huveneers, Stephan; Danen, Erik H.J.

doi:10.1242/jcs.039446

Cited by 724 publications

(691 citation statements)

References 111 publications

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“…It is therefore likely that biochemical signals derived from endothelial adhesion to laminin 511 act downstream to regulate actin arrangements and thereby cortical stiffness and mechanotransduction processes (Hutcheson & Griffith, 1996; Tzima et al , 2001). Candidate downstream signalling molecules include RhoA, which has been implicated in force generation via β1‐integrins (Schiller et al , 2013) and shear responses (Jalali et al , 1998; Tzima et al , 2001), and Src kinase (Huveneers & Danen, 2009; Martinez‐Rico et al , 2010). …”

Section: Discussionmentioning

confidence: 99%

Endothelial basement membrane laminin 511 is essential for shear stress response

Russo¹,

Luik²,

Yousif³

et al. 2016

The EMBO Journal

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Shear detection and mechanotransduction by arterial endothelium requires junctional complexes containing PECAM‐1 and VE‐cadherin, as well as firm anchorage to the underlying basement membrane. While considerable information is available for junctional complexes in these processes, gained largely from in vitro studies, little is known about the contribution of the endothelial basement membrane. Using resistance artery explants, we show that the integral endothelial basement membrane component, laminin 511 (laminin α5), is central to shear detection and mechanotransduction and its elimination at this site results in ablation of dilation in response to increased shear stress. Loss of endothelial laminin 511 correlates with reduced cortical stiffness of arterial endothelium in vivo, smaller integrin β1‐positive/vinculin‐positive focal adhesions, and reduced junctional association of actin–myosin II. In vitro assays reveal that β1 integrin‐mediated interaction with laminin 511 results in high strengths of adhesion, which promotes p120 catenin association with VE‐cadherin, stabilizing it at cell junctions and increasing cell–cell adhesion strength. This highlights the importance of endothelial laminin 511 in shear response in the physiologically relevant context of resistance arteries.

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Section: Discussionmentioning

confidence: 99%

Endothelial basement membrane laminin 511 is essential for shear stress response

Russo¹,

Luik²,

Yousif³

et al. 2016

The EMBO Journal

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“…Cell adhesion and spreading is mediated by the recruitment of Src kinase to adhesion sites through the interaction of its SH2 domain with the autophosphorylation site of focal adhesion kinase (FAK), leading to the phosphorylation of focal adhesion proteins such as FAK itself, paxillin, and p130Cas 18, 19. These phosphorylated residues act as docking sites for proteins that regulate the activity of Rho family GTPases to advance cell protrusion and spreading.…”

Section: Introductionmentioning

confidence: 99%

CD151 mediates netrin‐1‐induced angiogenesis through the Src‐FAK‐Paxillin pathway

Yang

Zhong

et al. 2016

J Cellular Molecular Medi

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Crosstalk between the nervous and vascular systems is important during development and in response to injury, and the laminin‐like axonal guidance protein netrin‐1 has been studied for its involvement in angiogenesis and vascular remodelling. In this study, we examined the role of netrin‐1 in angiogenesis and explored the underlying mechanisms. The effect of netrin‐1 on brain tissues and endothelial cells was examined by immunohistochemistry and western blotting in a middle cerebral artery occlusion model and in human umbilical vein endothelial cells. Cell proliferation and cell cycle progression were assessed by the MTT assay and flow cytometry, and the Transwell and tube formation assays were used to examine endothelial cell motility and function. Netrin‐1 up‐regulated CD151 and VEGF concomitant with the activation of focal adhesion kinase (FAK), Src and Paxillin in vitro and in vivo and the induction of cell proliferation, migration and tube formation in vitro. Silencing of CD151 abolished the effects of netrin‐1 on promoting cell migration and tube formation mediated by the activation of FAK/Src signalling. Netrin‐1 promoted angiogenesis in vitro and in vivo by activating the FAK/Src/Paxillin signalling pathway through a mechanism dependent on the expression of the CD151 tetraspanin, suggesting the existence of a netrin‐1/FAK/Src/CD151 signalling axis involved in the modulation of angiogenesis.

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“…2). Activation of c-Src is induced by forming the complex with FAK or directly by engagement of integrin α IIb β 3 , α 4 β 1 , or α v β 3, which recognize RGD containing protein such as fibronectin and vitronectin [19]. Notably, the expression of MT1-MMP in prostate cancer LNCaP cells induces fibronectin expression in 3-D collagen [25], and intact type I collagen is a poor ligand for integrin α v β 3 , while degraded collagen exposes RGD epitopes [26].…”

Section: Discussionmentioning

confidence: 99%

MT1-MMP promotes cell growth and ERK activation through c-Src and paxillin in three-dimensional collagen matrix

Takino

Tsuge

Ozawa

et al. 2010

Biochemical and Biophysical Research Communications

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Adhesion signaling – crosstalk between integrins, Src and Rho

Cited by 724 publications

References 111 publications

Endothelial basement membrane laminin 511 is essential for shear stress response

Endothelial basement membrane laminin 511 is essential for shear stress response

CD151 mediates netrin‐1‐induced angiogenesis through the Src‐FAK‐Paxillin pathway

MT1-MMP promotes cell growth and ERK activation through c-Src and paxillin in three-dimensional collagen matrix

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