Basic mechanism of three-dimensional collagen fibre transport by fibroblasts

Meshel, Adam S.; Wei, Qize; Adelstein, Robert S.; Sheetz, Michael P.

doi:10.1038/ncb1216

Cited by 263 publications

(220 citation statements)

References 30 publications

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“…This process was dependent on integrin ␣-2/␤-1-mediated adhesion and on the contractile activity of the actomyosin cytoskeleton. 20 However, in our case, the adhesion receptor responsible for the binding of collagen I in the pillar remains unknown. We could not detect integrin ␣-1 or ␣-11 expression levels, and integrin ␣-2 was present only occasionally at a low density, which did not correlate with the number of adhesion spots containing vinculin within the pillar.…”

Section: Discussionmentioning

confidence: 71%

A New Mechanism for Pillar Formation during Tumor-Induced Intussusceptive Angiogenesis: Inverse Sprouting

Paku

Dezső

Bugyik

et al. 2011

The American Journal of Pathology

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One of the hallmarks of intussusceptive angiogenesis is the development of intraluminal connective tissue pillars. The exact mechanism of pillar formation has not yet been elucidated. By using electron and confocal microscopy, we observed intraluminal nascent pillars that contain a collagen bundle covered by endothelial cells (ECs) in the vasculature of experimental tumors. We proposed a new mechanism for the development of these pillars. First, intraluminal endothelial bridges are formed. Second, localized dissolution of the basement membrane occurs and a bridging EC attaches to a collagen bundle in the underlying connective tissue. A pulling force is then exerted by the actin cytoskeleton of the ECs via specific attachment points, which contain vinculin, to the collagen bundle, resulting in suction and subsequent transport of the collagen bundle into and through the vessel lumen. Third, the pillar matures through the immigration of connective tissue cells and the deposition of new collagenous connective tissue. The proposed simple mechanism generates a connection between the processes of endothelial bridging and intussusceptive angiogenesis and identifies the source of the force behind pillar formation. Moreover, it ensures the rapid formation of pillars from pre-existing building blocks and the maintenance of EC polarity. To describe it, we coined the term inverse sprouting.

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Section: Discussionmentioning

confidence: 71%

A New Mechanism for Pillar Formation during Tumor-Induced Intussusceptive Angiogenesis: Inverse Sprouting

Paku

Dezső

Bugyik

et al. 2011

The American Journal of Pathology

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“…The tips of such pseudopodia might be too small to enable cell motility in a particular direction. Alternatively, the tip structures of pseudopodia might produce a locomotive force in 3D collagen gels in a manner similar to that in which lamellipodial protrusions attach to collagen fibers and retract them into fibroblasts (Meshel et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Involvement of Rac and Rho signaling in cancer cell motility in 3D substrates

2009

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The motility of cancer cells in 3D matrices is of two types: mesenchymal motility, in which the cells are elongated and amoeboid motility, in which the cells are round. Amoeboid motility is driven by an actomyosin-based contractile force, which is regulated by the Rho/ROCK pathway. However, the molecular mechanisms underlying the motility of elongated cells remain unknown. Here, we show that the motility of elongated cells is regulated by Rac signaling through the WAVE2/Arp2/3-dependent formation of elongated pseudopodia and cell-substrate adhesion in 3D substrates. The involvement of Rac signaling in cell motility was different in cell lines that displayed an elongated morphology in 3D substrates. In U87MG glioblastoma cells, most of which exhibit mesenchymal motility, inhibition of Rac signaling blocked the invasion of these cells in 3D substrates. In HT1080 fibrosarcoma cells, which display mixed cell motility involving both elongated and rounded cells, inhibition of Rac1 signaling not only blocked mesenchymal motility but also caused a mesenchymalamoeboid transition. Additionally, Rac1 and RhoA signaling regulated the mesenchymal and amoeboid motility in these cells, respectively, and the inhibition of both pathways dramatically decreased cell invasion. Hence, we could conclude that Rac1 and RhoA signaling simultaneously regulate cell invasion in 3D matrices.

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“…The latter aspects are now being investigated in the looping heart. NMHC-IIB is reported to be in cell processes within lamellipodia/filopodia, and it is associated also with fibroblast collagen fiber transport and deposition during remodeling of the ECM (Meshel et al, 2005). Either tension fiber formation or matrix deposition could explain the seemingly extracellular and/or subepithelial localization initially reported for flectin-F22 protein (Lash et al, 1992).…”

Section: Nonmuscle Myosin II Proteins and Heart Loopingmentioning

confidence: 96%

Cellular nonmuscle myosins NMHC‐IIA and NMHC‐IIB and vertebrate heart looping

Lu¹,

Seeholzer²,

Han³

et al. 2008

Developmental Dynamics

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Flectin, a protein previously described to be expressed in a left-dominant manner in the embryonic chick heart during looping, is a member of the nonmuscle myosin II (NMHC-II) protein class. During looping, both NMHC-IIA and NMHC-IIB are expressed in the mouse heart on embryonic day 9.5. The patterns of localization of NMHC-IIB, rather than NMHC-IIA in the mouse looping heart and in neural crest cells, are equivalent to what we reported previously for flectin. Expression of full-length human NMHC-IIA and -IIB in 10 T1/2 cells demonstrated that flectin antibody recognizes both isoforms. Electron microscopy revealed that flectin antibody localizes in short cardiomyocyte cell processes extending from the basal layer of the cardiomyocytes into the cardiac jelly. Flectin antibody also recognizes stress fibrils in the cardiac jelly in the mouse and chick heart; while NMHC-IIB antibody does not. Abnormally looping hearts of the Nodal ⌬ 600 homozygous mouse embryos show decreased NMHC-IIB expression on both the mRNA and protein levels. These results document the characterization of flectin and extend the importance of NMHC-II and the cytoskeletal actomyosin complex to the mammalian heart and cardiac looping. Developmental Dynamics 237:3577-3590, 2008.

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Basic mechanism of three-dimensional collagen fibre transport by fibroblasts

Cited by 263 publications

References 30 publications

A New Mechanism for Pillar Formation during Tumor-Induced Intussusceptive Angiogenesis: Inverse Sprouting

A New Mechanism for Pillar Formation during Tumor-Induced Intussusceptive Angiogenesis: Inverse Sprouting

Involvement of Rac and Rho signaling in cancer cell motility in 3D substrates

Cellular nonmuscle myosins NMHC‐IIA and NMHC‐IIB and vertebrate heart looping

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