Toll-like receptor 3 regulates cord blood-derived endothelial cell function in vitro and in vivo. Grelier, A., Cras, A., Balitrand, N., Delmau, C., Lecourt, S., Lepelletier, Y., Riesterer, H., Freida, D., Lataillade, J., Lebousse-Kerdiles, M., Cuccini, W., de Latour, R. P., Marolleau, J., Uzan, G., Larghero, J., & Vanneaux, V. Angiogenesis, 2013. doi abstract bibtex Circulating endothelial progenitor cells (cEPC) are capable of homing to neovascularisation sites, in which they proliferate and differentiate into endothelial cells. Transplantation of cEPC-derived cells, in particular those isolated from umbilical cord blood (UCB), has emerged as a promising approach in the treatment of cardio-vascular diseases. After in vivo transplantation, these cells may be exposed to local or systemic inflammation or pathogens, of which they are a common target. Because Toll-like receptors (TLR) are critical in detecting pathogens and in initiating inflammatory responses, we hypothesized that TLR may govern UCB cEPC-derived cells function. While these cells expressed almost all TLR, we found that only TLR3 dramatically impaired cell properties. TLR3 activation inhibited cell proliferation, modified cell cycle entry, impaired the in vitro angiogenic properties and induced pro-inflammatory cytokines production. The anti-angiogenic effect of TLR3 activation was confirmed in vivo in a hind-limb ischemic mice model. Moreover, TLR3 activation consistently leads to an upregulation of miR-29b, -146a and -155 and to a deregulation of cytoskeleton and cell cycle regulator. Hence, TLR3 activation is likely to be a key regulator of cEPC-derived cells properties.
@article{grelier_toll-like_2013,
title = {Toll-like receptor 3 regulates cord blood-derived endothelial cell function in vitro and in vivo},
issn = {1573-7209},
doi = {10.1007/s10456-013-9358-5},
abstract = {Circulating endothelial progenitor cells (cEPC) are capable of homing to neovascularisation sites, in which they proliferate and differentiate into endothelial cells. Transplantation of cEPC-derived cells, in particular those isolated from umbilical cord blood (UCB), has emerged as a promising approach in the treatment of cardio-vascular diseases. After in vivo transplantation, these cells may be exposed to local or systemic inflammation or pathogens, of which they are a common target. Because Toll-like receptors (TLR) are critical in detecting pathogens and in initiating inflammatory responses, we hypothesized that TLR may govern UCB cEPC-derived cells function. While these cells expressed almost all TLR, we found that only TLR3 dramatically impaired cell properties. TLR3 activation inhibited cell proliferation, modified cell cycle entry, impaired the in vitro angiogenic properties and induced pro-inflammatory cytokines production. The anti-angiogenic effect of TLR3 activation was confirmed in vivo in a hind-limb ischemic mice model. Moreover, TLR3 activation consistently leads to an upregulation of miR-29b, -146a and -155 and to a deregulation of cytoskeleton and cell cycle regulator. Hence, TLR3 activation is likely to be a key regulator of cEPC-derived cells properties.},
journal = {Angiogenesis},
author = {Grelier, Aurore and Cras, Audrey and Balitrand, Nicole and Delmau, Catherine and Lecourt, Séverine and Lepelletier, Yves and Riesterer, Hélène and Freida, Delphine and Lataillade, Jean-Jacques and Lebousse-Kerdiles, Marie-Caroline and Cuccini, Wendy and de Latour, Regis Peffault and Marolleau, Jean-Pierre and Uzan, Georges and Larghero, Jérôme and Vanneaux, Valérie},
year = {2013},
}
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Transplantation of cEPC-derived cells, in particular those isolated from umbilical cord blood (UCB), has emerged as a promising approach in the treatment of cardio-vascular diseases. After in vivo transplantation, these cells may be exposed to local or systemic inflammation or pathogens, of which they are a common target. Because Toll-like receptors (TLR) are critical in detecting pathogens and in initiating inflammatory responses, we hypothesized that TLR may govern UCB cEPC-derived cells function. While these cells expressed almost all TLR, we found that only TLR3 dramatically impaired cell properties. TLR3 activation inhibited cell proliferation, modified cell cycle entry, impaired the in vitro angiogenic properties and induced pro-inflammatory cytokines production. The anti-angiogenic effect of TLR3 activation was confirmed in vivo in a hind-limb ischemic mice model. Moreover, TLR3 activation consistently leads to an upregulation of miR-29b, -146a and -155 and to a deregulation of cytoskeleton and cell cycle regulator. Hence, TLR3 activation is likely to be a key regulator of cEPC-derived cells properties.","journal":"Angiogenesis","author":[{"propositions":[],"lastnames":["Grelier"],"firstnames":["Aurore"],"suffixes":[]},{"propositions":[],"lastnames":["Cras"],"firstnames":["Audrey"],"suffixes":[]},{"propositions":[],"lastnames":["Balitrand"],"firstnames":["Nicole"],"suffixes":[]},{"propositions":[],"lastnames":["Delmau"],"firstnames":["Catherine"],"suffixes":[]},{"propositions":[],"lastnames":["Lecourt"],"firstnames":["Séverine"],"suffixes":[]},{"propositions":[],"lastnames":["Lepelletier"],"firstnames":["Yves"],"suffixes":[]},{"propositions":[],"lastnames":["Riesterer"],"firstnames":["Hélène"],"suffixes":[]},{"propositions":[],"lastnames":["Freida"],"firstnames":["Delphine"],"suffixes":[]},{"propositions":[],"lastnames":["Lataillade"],"firstnames":["Jean-Jacques"],"suffixes":[]},{"propositions":[],"lastnames":["Lebousse-Kerdiles"],"firstnames":["Marie-Caroline"],"suffixes":[]},{"propositions":[],"lastnames":["Cuccini"],"firstnames":["Wendy"],"suffixes":[]},{"propositions":["de"],"lastnames":["Latour"],"firstnames":["Regis","Peffault"],"suffixes":[]},{"propositions":[],"lastnames":["Marolleau"],"firstnames":["Jean-Pierre"],"suffixes":[]},{"propositions":[],"lastnames":["Uzan"],"firstnames":["Georges"],"suffixes":[]},{"propositions":[],"lastnames":["Larghero"],"firstnames":["Jérôme"],"suffixes":[]},{"propositions":[],"lastnames":["Vanneaux"],"firstnames":["Valérie"],"suffixes":[]}],"year":"2013","bibtex":"@article{grelier_toll-like_2013,\n\ttitle = {Toll-like receptor 3 regulates cord blood-derived endothelial cell function in vitro and in vivo},\n\tissn = {1573-7209},\n\tdoi = {10.1007/s10456-013-9358-5},\n\tabstract = {Circulating endothelial progenitor cells (cEPC) are capable of homing to neovascularisation sites, in which they proliferate and differentiate into endothelial cells. Transplantation of cEPC-derived cells, in particular those isolated from umbilical cord blood (UCB), has emerged as a promising approach in the treatment of cardio-vascular diseases. After in vivo transplantation, these cells may be exposed to local or systemic inflammation or pathogens, of which they are a common target. Because Toll-like receptors (TLR) are critical in detecting pathogens and in initiating inflammatory responses, we hypothesized that TLR may govern UCB cEPC-derived cells function. While these cells expressed almost all TLR, we found that only TLR3 dramatically impaired cell properties. TLR3 activation inhibited cell proliferation, modified cell cycle entry, impaired the in vitro angiogenic properties and induced pro-inflammatory cytokines production. The anti-angiogenic effect of TLR3 activation was confirmed in vivo in a hind-limb ischemic mice model. Moreover, TLR3 activation consistently leads to an upregulation of miR-29b, -146a and -155 and to a deregulation of cytoskeleton and cell cycle regulator. Hence, TLR3 activation is likely to be a key regulator of cEPC-derived cells properties.},\n\tjournal = {Angiogenesis},\n\tauthor = {Grelier, Aurore and Cras, Audrey and Balitrand, Nicole and Delmau, Catherine and Lecourt, Séverine and Lepelletier, Yves and Riesterer, Hélène and Freida, Delphine and Lataillade, Jean-Jacques and Lebousse-Kerdiles, Marie-Caroline and Cuccini, Wendy and de Latour, Regis Peffault and Marolleau, Jean-Pierre and Uzan, Georges and Larghero, Jérôme and Vanneaux, Valérie},\n\tyear = {2013},\n}\n\n\n\n","author_short":["Grelier, A.","Cras, A.","Balitrand, N.","Delmau, C.","Lecourt, S.","Lepelletier, Y.","Riesterer, H.","Freida, D.","Lataillade, J.","Lebousse-Kerdiles, M.","Cuccini, W.","de Latour, R. 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