Isolation of bone marrow mesenchymal stem cells by anti-nerve growth factor receptor antibodies

Quirici, N.; Soligo, Davide; Bossolasco, Patrizia; Servida, Federica; Lumini, Cristina; Deliliers, Giorgio Lambertenghi

doi:10.1016/s0301-472x(02)00812-3

Cited by 511 publications

(443 citation statements)

References 33 publications

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“…Further, macrophage infiltration of the infarcted area was substantially suppressed by injection of a neutralizing anti-HMGB1 antibody prior to myocardial infarction, indicating an HMGB1-dependent phenomenon like it has been observed in vitro as well. Interestingly, infiltrated CD271-positive cells indicative for MSC 39 in the infarcted areas were notably increased in anti-HMGB1-treated animals, which supports our in vitro observation of HMGB1 interfering with apoptosis-induced MSC recruitment. Thereby, therapeutically suppressing HMGB1 bioactivity with a specific inhibitor might increase recruitment of endogenous MSC into infarcted hearts but it might also substantially improve efficacy of transplantation of regenerative MSC.…”

Section: Migration Of Msc Towards Recombinant Hgf Was Inhibitedsupporting

confidence: 88%

“…Because these observations were very suggestive, we finally investigated in vivo the role of HMGB1 in recruitment of Mac-3-positive macrophages and cells expressing CD271, which may be considered as a marker for MSC. 39 In tissue remodeling or repair. 1 The type of cell death during tissue injury appears to have a key role in a differential initiation of these processes.…”

Section: Resultsmentioning

confidence: 99%

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Necrotic cell-derived high mobility group box 1 attracts antigen-presenting cells but inhibits hepatocyte growth factor-mediated tropism of mesenchymal stem cells for apoptotic cell death

et al. 2015

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Tissue damage due to apoptotic or necrotic cell death typically initiates distinct cellular responses, leading either directly to tissue repair and regeneration or to immunological processes first, to clear the site, for example, of potentially damage-inducing agents. Mesenchymal stem cells (MSC) as well as immature dendritic cells (iDC) and monocytes migrate to injured tissues. MSC have regenerative capacity, whereas monocytes and iDC have a critical role in inflammation and induction of immune responses, including autoimmunity after tissue damage. Here, we investigated the influence of apoptotic and necrotic cell death on recruitment of MSC, monocytes and iDC, and identified hepatocyte growth factor (HGF) and the alarmin high mobility group box 1 (HMGB1) as key factors differentially regulating these migratory responses. MSC, but not monocytes or iDC, were attracted by apoptotic cardiomyocytic and neuronal cells, whereas necrosis induced migration of monocytes and iDC, but not of MSC. Only apoptotic cell death resulted in HGF production and HGF-mediated migration of MSC towards the apoptotic targets. In contrast, HMGB1 was predominantly released by the necrotic cells and mediated recruitment of monocytes and iDC via the receptor of advanced glycation end products. Moreover, necrotic cardiomyocytic and neuronal cells caused an HMGB1/toll-like receptor-4-dependent inhibition of MSC migration towards apoptosis or HGF, while recruitment of monocytes and iDC by necrosis or HMGB1 was not affected by apoptotic cells or HGF. Thus, the type of cell death differentially regulates recruitment of either MSC or monocytes and iDC through HGF and HMGB1, respectively, with a dominant, HMGB1-mediated role of necrosis in determining tropism after tissue injury.

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Section: Migration Of Msc Towards Recombinant Hgf Was Inhibitedsupporting

confidence: 88%

Section: Resultsmentioning

confidence: 99%

Necrotic cell-derived high mobility group box 1 attracts antigen-presenting cells but inhibits hepatocyte growth factor-mediated tropism of mesenchymal stem cells for apoptotic cell death

et al. 2015

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“…Thus, it is reasonable to consider that a phenotypic marker of EFT was induced in UET-13 cells by EWS/ETS expression. On the other hand, CD54 and CD271 are positive in human primary MPCs (8,25,42), whereas these markers are negative in UET-13 cells. However, a previous report showed the disappearance of some positive markers, including CD271, from primary human MPCs during the process of ex vivo expansion (25), and it has been speculated that the expression of these molecules in MPCs is induced in vivo via interaction with the bone marrow microenvironment and that the necessary stimuli are absent from ex vivo culture conditions.…”

Section: Discussionmentioning

confidence: 92%

“…EWS/ETS expression altered the immunophenotype of UET-13 cells. Human MPCs reveal a characteristic expression of several surface antigens and can be identified on the basis of the reactivity with a set of monoclonal antibodies against CD antigens (25,42). On the other hand, some CD antigens are characteristically expressed on EFT cells (17,28,33).…”

Section: Vol 28 2008 Effects Of Ews/ets Expression In Human Mpcs 2129mentioning

confidence: 99%

Inducible Expression of Chimeric EWS/ETS Proteins Confers Ewing's Family Tumor-Like Phenotypes to Human Mesenchymal Progenitor Cells

Miyagawa

Okita

Nakaijima

et al. 2008

Molecular and Cellular Biology

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Ewing's family tumor (EFT) is a rare pediatric tumor of unclear origin that occurs in bone and soft tissue. Specific chromosomal translocations found in EFT cause EWS to fuse to a subset of ets transcription factor genes (ETS), generating chimeric EWS/ETS proteins. These proteins are believed to play a crucial role in the onset and progression of EFT. However, the mechanisms responsible for the EWS/ETS-mediated onset remain unclear. Here we report the establishment of a tetracycline-controlled EWS/ETS-inducible system in human bone marrow-derived mesenchymal progenitor cells (MPCs). Ectopic expression of both EWS/FLI1 and EWS/ERG proteins resulted in a dramatic change of morphology, i.e., from a mesenchymal spindle shape to a small round-to-polygonal cell, one of the characteristics of EFT. EWS/ETS also induced immunophenotypic changes in MPCs, including the disappearance of the mesenchyme-positive markers CD10 and CD13 and the up-regulation of the EFT-positive markers CD54, CD99, CD117, and CD271. Furthermore, a prominent shift from the gene expression profile of MPCs to that of EFT was observed in the presence of EWS/ETS. Together with the observation that EWS/ETS enhances the ability of cells to invade Matrigel, these results suggest that EWS/ETS proteins contribute to alterations of cellular features and confer an EFT-like phenotype to human MPCs.Ewing's family tumor (EFT) is a rare childhood cancer arising mainly in bone and soft tissue. Since EFT has a poor prognosis, it is important to elucidate the underlying pathogenic mechanisms for establishing a more effective therapeutic strategy. EFT is characterized by the presence of chimeric genes composed of EWS and ets transcription factor genes (ETS) formed by specific chromosomal translocations, i.e., EWS/FLI1, t(11;22)(q24;q12); EWS/ERG, t(21;22)(q12;q12); EWS/ETV1, t(7;22)(p22;q12); EWS/E1AF, t(17;22)(q12;q12); and EWS/FEV, t(2;22)(q33;q12) (26). The products of these chimeric genes behave as aberrant transcriptional regulators and are believed to play a crucial role in the onset and progression of EFT (3,36). Indeed, recent studies have revealed that the induction of EWS/FLI1 proteins can trigger transformation in certain cell types, including NIH 3T3 cells (36), C2C12 myoblasts (12), and murine primary bone marrow-derived mesenchymal progenitor cells (MPCs) (6, 45, 52). However, studies have also indicated that overexpression of EWS/ FLI1 provokes apoptosis and growth arrest in mouse normal embryonic fibroblasts and primary human fibroblasts (10, 31), hence hampering understanding of the precise role of EWS/ ETS proteins in the development of EFT. The function of EWS/ETS proteins would be greatly influenced by cell type, and thus the cells that can originate EFTs might be more susceptible to the tumorigenic effects of EWS/ETS.Although the cell origin of EFT is still unknown, the expression of neuronal markers in spite of the occurrence in bone and soft tissues has kept open the debate as to a potential mesenchymal or neuroectodermal origin. As described ...

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“…Ainsi, le tri par cytométrie en flux de la population STRO-1 fort permet d'enrichir (x 950 fois) en CFU-F la suspension de cellules mononucléées et les cellules coexprimant STRO-1 et CD106 (vascular cell adhesion molecule, VCAM) repré-sentent une population très purifiée de CSM [8]. Mais d'autres antigè-nes peuvent être utilisés avec des résultats performants : le CD49a ou le CD271 [9]. Le CD49a (ou chaîne alpha 1 des intégrines) est exprimé par les CSM et toutes les CFU-F sont présentes dans la fraction CD49a + des cellules médullaires [10].…”

unclassified

Cellules souches mésenchymateuses

Sensebé

Bourin

2011

Med Sci (Paris)

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Isolation of bone marrow mesenchymal stem cells by anti-nerve growth factor receptor antibodies

Cited by 511 publications

References 33 publications

Necrotic cell-derived high mobility group box 1 attracts antigen-presenting cells but inhibits hepatocyte growth factor-mediated tropism of mesenchymal stem cells for apoptotic cell death

Necrotic cell-derived high mobility group box 1 attracts antigen-presenting cells but inhibits hepatocyte growth factor-mediated tropism of mesenchymal stem cells for apoptotic cell death

Inducible Expression of Chimeric EWS/ETS Proteins Confers Ewing's Family Tumor-Like Phenotypes to Human Mesenchymal Progenitor Cells

Cellules souches mésenchymateuses

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