Actin stress fibres

Pellegrin, Stéphanie; Mellor, Harry

doi:10.1242/jcs.018473

Cited by 643 publications

(601 citation statements)

References 118 publications

(111 reference statements)

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“…C3 decreased RhoA-GTP levels in C2C12 cells by >70% (Fig. S4), and C3-treated cells on Ncad-Fc substrate displayed a virtually complete loss of stress fibers, production of which is known to require RhoA activity (28) (Fig. 3C).…”

Section: Resultsmentioning

confidence: 97%

N-cadherin ligation, but not Sonic hedgehog binding, initiates Cdo-dependent p38α/β MAPK signaling in skeletal myoblasts

Lü

Krauss

2010

Proc. Natl. Acad. Sci. U.S.A.

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The p38α/β mitogen-activated protein kinase (MAPK) pathway promotes muscle-specific gene expression and myoblast differentiation but how pathway activity is initiated during these processes is poorly understood. During myoblast differentiation, the intracellular region of the promyogenic cell surface protein Cdo (also known as Cdon) binds to Bnip-2 and JLP, scaffold proteins for Cdc42 and p38α/β MAPK, respectively. The Bnip-2/Cdc42 and JLP/p38α/β complexes associate in a Cdo-dependent manner, resulting in Bnip-2/Cdc42-dependent p38α/β activation and stimulation of cell differentiation. Although the Cdo ectodomain binds to several different proteins, it is unclear how Cdo-dependent p38α/β activation is initiated. In myoblasts, Cdo interacts with the cell–cell adhesion molecule N-cadherin. Cdo also binds directly to the secreted morphogen Sonic hedgehog (Shh) to promote Shh pathway signaling. We report here that N-cadherin ligation activates p38α/β in myoblasts in a Cdo-, Bnip-2-, and JLP-dependent manner. Furthermore, these proteins and activated Cdc42 cluster at sites of N-cadherin ligation. In contrast, neither JLP nor Bnip-2 is associated with Cdo bound to Shh, and Shh does not activate p38α/β in myoblasts. Taken together, these results link cadherin-based cell–cell adhesion to a defined signaling pathway (Cdo → p38α/β) that directly regulates a cell-type-specific differentiation program. Furthermore, they are consistent with a model whereby Cdo serves as a multifunctional coreceptor with mechanistically distinct roles in multiple signaling pathways.

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Section: Resultsmentioning

confidence: 97%

N-cadherin ligation, but not Sonic hedgehog binding, initiates Cdo-dependent p38α/β MAPK signaling in skeletal myoblasts

Lü

Krauss

2010

Proc. Natl. Acad. Sci. U.S.A.

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“…Rho controls cell motility through the formation of stress fiber and focal adhesion. Cell motility is generally described as a cyclical process divided into alternating phases of protrusion and contraction (Pellegrin and Mellor, 2007). Based on the contractile nature of stress fibers, they are thought to provide a contractile force for cell migration (Kreis and Birchmeier, 1980).…”

Section: Discussionmentioning

confidence: 99%

Lipocalin-2 Is an Autocrine Mediator of Reactive Astrocytosis

Lee¹,

Park²,

Lee³

et al. 2009

J. Neurosci.

238

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Astrocytes, the most abundant glial cell type in the brain, provide metabolic and trophic support to neurons and modulate synaptic activity. In response to a brain injury, astrocytes proliferate and become hypertrophic with an increased expression of intermediate filament proteins. This process is collectively referred to as reactive astrocytosis. Lipocalin 2 (lcn2) is a member of the lipocalin family that binds to small hydrophobic molecules. We propose that lcn2 is an autocrine mediator of reactive astrocytosis based on the multiple roles of lcn2 in the regulation of cell death, morphology, and migration of astrocytes. lcn2 expression and secretion increased after inflammatory stimulation in cultured astrocytes. Forced expression of lcn2 or treatment with LCN2 protein increased the sensitivity of astrocytes to cytotoxic stimuli. Iron and BIM (Bcl-2-interacting mediator of cell death) proteins were involved in the cytotoxic sensitization process. LCN2 protein induced upregulation of glial fibrillary acidic protein (GFAP), cell migration, and morphological changes similar to characteristic phenotypic changes termed reactive astrocytosis. The lcn2-induced phenotypic changes of astrocytes occurred through a Rho-ROCK (Rho kinase)-GFAP pathway, which was positively regulated by nitric oxide and cGMP. In zebrafishes, forced expression of rat lcn2 gene increased the number and thickness of cellular processes in GFAP-expressing radial glia cells, suggesting that lcn2 expression in glia cells plays an important role in vivo. Our results suggest that lcn2 acts in an autocrine manner to induce cell death sensitization and morphological changes in astrocytes under inflammatory conditions and that these phenotypic changes may be the basis of reactive astrocytosis in vivo.

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“…Stress fibers are composed of actin bundle held together by α-actinin, fascin, espin, filamin, and myosin II bundle (Pellegrin & Mellor 2007). They generate contractile force and play a central role in adhesion, motility, morphogenesis, and cell-to-cell interaction of many specialized eukaryotic cells (Tojkander et al 2012).…”

Section: Discussionmentioning

confidence: 99%

“…Myofibroblast stress fibers are mechanically associated to the ECM through their large focal adhesions and the contractile forces generated through this linking lead to the arrangement of collagen fiber, one of fibrous components of the ECM, in the wound area (Leask et al 2008). Indeed, myofibroblast in nonwound tissues are found in sites that require significant matrix reconstitution (Pellegrin & Mellor 2007). Moreover, the fibroblasts in the connective tissues are embedded in the ECM (Pellegrin & Mellor 2007).…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, myofibroblast in nonwound tissues are found in sites that require significant matrix reconstitution (Pellegrin & Mellor 2007). Moreover, the fibroblasts in the connective tissues are embedded in the ECM (Pellegrin & Mellor 2007). FRC ensheaths the reticular fiber, fibrous components of the ECM, to make the stromal reticulum at T zone in LN (Katakai et al 2004b).…”

Section: Discussionmentioning

confidence: 99%

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Involvement of RhoA/ROCK signaling for alteration of stress fiber via lymphotoxin β receptor stimulation in fibroblastic reticular cell isolated from lymph node

Lee

Kim

Lee

2013

Animal Cells and Systems

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The heterotrimeric transmembrane lymphotoxin α1β2 (LTα1β2), member of the tumor necrosis factor family cytokines including soluble homotrimeric lymphotoxin α (LTα), plays an important role in lymphoid tissue architecture and organogenesis. We found that lymphotoxin β receptor (LTβR) stimulation using agonistic anti-LTβR antibody induced the changes in actin stress fiber and morphology of cells. To address the possibility that LTβR stimulation is involved in RhoA/ Rho-associated protein kinase (ROCK) signaling, we checked the level of Rho-guanosine diphosphate (GDP)/guanosine triphosphate (GTP) exchange activity with fibroblastic reticular cell (FRC) lysate. When LTβR was stimulated with agonistic anti-LTβR antibody, the Rho-GDP/GTP exchange activity was markedly reduced. Inhibition of ROCK activity induced changes in actin cytoskeleton organization and cell morphology in FRC. We showed that the phosphorylation of myosin light chains (MLCs) was reduced by LTβR stimulation in FRC. DNA gene chip demonstrated that agonistic anti-LTβR antibody in FRC affected the downregulation of actin filament and myosin component transcripts. The results provided here indicated that RhoA/ROCK was responsible for the observed phosphorylation of MLC. Collectively, these results suggest that LTβR stimulation is involved in change of stress fiber via RhoA/ROCK signaling in FRC.

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Actin stress fibres

Cited by 643 publications

References 118 publications

N-cadherin ligation, but not Sonic hedgehog binding, initiates Cdo-dependent p38α/β MAPK signaling in skeletal myoblasts

N-cadherin ligation, but not Sonic hedgehog binding, initiates Cdo-dependent p38α/β MAPK signaling in skeletal myoblasts

Lipocalin-2 Is an Autocrine Mediator of Reactive Astrocytosis

Involvement of RhoA/ROCK signaling for alteration of stress fiber via lymphotoxin β receptor stimulation in fibroblastic reticular cell isolated from lymph node

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