The molecular basis of induction and formation of tunneling nanotubes

Kimura, Shunsuke; Hase, Koji; Ohno, Hiroshi

doi:10.1007/s00441-012-1518-1

Cited by 65 publications

(59 citation statements)

References 67 publications

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“…It is interesting that tunneling nanotubes are now recognized as structures for intercellular communication and organelle transfer (49)(50)(51). There are at least two types of nanotubes: thin nanotubes contain actin, while nanotubes with diameters of at least 0.7 m contain both actin and microtubules (49)(50)(51).…”

Section: Discussionmentioning

confidence: 99%

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Serogroup-Specific Interaction of Neisseria meningitidis Capsular Polysaccharide with Host Cell Microtubules and Effects on Tubulin Polymerization

et al. 2014

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We have previously shown that during late stages of the infectious process, serogroup B meningococci (MenB) are able to escape the phagosome of in vitro-infected human epithelial cells. They then multiply in the cytosolic environment and spread intracellularly and to surrounding cells by exploiting the microtubule cytoskeleton, as suggested by results of infections in the presence of microtubule inhibitors and evidence of nanotubes connecting neighboring cells. In this study, by using microtubule binding assays with purified microtubule asters and bundles and microtubule bundles synthesized in vitro, we demonstrate that the MenB capsule directly mediates the interaction between bacteria and microtubules. The direct interaction between the microtubules and the MenB capsular polysaccharide was confirmed by coimmunoprecipitation experiments. Unexpectedly, serogroup C meningococci (MenC), which have a capsular polysaccharide that differs from that of MenB only by its anomeric linkage, ␣(2¡9) instead of ␣(2¡8), were not able to interact with the microtubules, and the lack of interaction was not due to capsular polysaccharide O-acetylation that takes place in most MenC strains but not in MenB strains. Moreover, we demonstrate that the MenB capsular polysaccharide inhibits tubulin polymerization in vitro. Thus, at variance with MenC, MenB may interfere with microtubule dynamics during cell infection.

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Section: Discussionmentioning

confidence: 99%

“…These nanotubes are also exploited by pathogens to spread among cells. Indeed, bacterial, viral, and prion infective agents spread intracellularly and extracellularly using these structures (50). Therefore, it is tempting to speculate that MenB induces the formation of nanotubes by acting on microtubule and actin cytoskeleton.…”

Section: Discussionmentioning

confidence: 99%

Serogroup-Specific Interaction of Neisseria meningitidis Capsular Polysaccharide with Host Cell Microtubules and Effects on Tubulin Polymerization

et al. 2014

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“…Thus far, M-Sec that shares homology with a component of the exocyst complex Sec6 (32,33) and Myo10 that is an unconventional actin-based motor protein have been identified as key regulators of TNT formation (34), although the precise mechanisms by which they induce TNT formation remain unclear. In this study, we focused on M-Sec, a 73-kDa cytosolic protein, because Myo10 is undetectable in the leukocyte fraction containing monocytes/macrophages (35).…”

Section: M-sec Is Expressed In Mdms and Exhibits An Altered Intracellmentioning

confidence: 99%

Potential Role of the Formation of Tunneling Nanotubes in HIV-1 Spread in Macrophages

Hashimoto

Bhuyan

Hiyoshi

et al. 2016

The Journal of Immunology

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146

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Tunneling nanotubes (TNTs), the long membrane extensions connecting distant cells, have emerged as a novel form of cell-to-cell communication. However, it is not fully understood how and to what extent TNTs contribute to intercellular spread of pathogens including HIV-1. In this study, we show that HIV-1 promotes TNT formation per se via its protein Nef and a cellular protein M-Sec, which appears to mediate approximately half of viral spread among monocyte-derived macrophages (MDMs). A small compound that inhibits M-Sec–induced TNT formation reduced HIV-1 production by almost half in MDMs. Such inhibition was not observed with Nef-deficient mutant HIV-1 that fails to promote TNT formation and replicates less efficiently than the wild-type HIV-1 in MDMs. The TNT inhibitor–sensitive/Nef-promoting viral production was also observed in a T cell line ectopically expressing M-Sec, but not in another M-Sec− T cell line. Our results suggest the importance of TNTs in HIV-1 spread among MDMs and might answer the long-standing question how Nef promotes HIV-1 production in a cell type–specific manner.

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“…Formation of TNTs could be triggered by inflammation or cellular stress such as oxidative stress. 175 Recently, cell adhesion molecules and receptor-ligand interactions have been shown to be essential for the initiation of TNT formation. 175,176 M-Sec, a mammalian protein formerly known as tumor necrosis factor-α-induced protein 2, is reported to trigger de novo membrane protrusions, which could tether to neighboring cells and form TNTs.…”

Section: Tunneling Nanotubesmentioning

confidence: 99%

Matrix as an Interstitial Transport System

Fan

Creemers²,

Kassiri³

2014

Circulation Research

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T he extracellular space, or the interstitium, can be broadly divided into a fluid phase (water, electrolytes, nutrients, and some plasma proteins) and the extracellular matrix (ECM). In the heart, the ECM comprises structural proteins (primarily collagen types I and III) that form the fibrillar structure of the matrix; the basement membrane that forms an interface between the cardiomyocytes and the interstitial space as well as the molecules that mediate the cell-ECM connection; and the nonstructural proteins such as proteoglycans. Molecules traveling in the extracellular space come in contact with different ECM components, and these interactions determine the direction, speed, and distance of their transport, whereas the ECM can also provide a reservoir for several growth factors and cytokines. Moreover, the cell-ECM connection allows for transmission of signals across the cell membrane. Therefore, in addition to the classical role of ECM in providing structural support, it contributes to a multitude of intra-and extracellular events. Several thorough reviews have been published recently on the structural properties of the ECM and its remodeling in heart disease. [1][2][3] In this review, we will discuss less explored aspects of ECM function, such as its conductivity in extracellular transportation, its role in cell-cell interactions, and different modes of cell-cell communication through the extracellular space.

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The molecular basis of induction and formation of tunneling nanotubes

Cited by 65 publications

References 67 publications

Serogroup-Specific Interaction of Neisseria meningitidis Capsular Polysaccharide with Host Cell Microtubules and Effects on Tubulin Polymerization

Serogroup-Specific Interaction of Neisseria meningitidis Capsular Polysaccharide with Host Cell Microtubules and Effects on Tubulin Polymerization

Potential Role of the Formation of Tunneling Nanotubes in HIV-1 Spread in Macrophages

Matrix as an Interstitial Transport System

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