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Inflammatory and alternatively activated human macrophages attract vessel-associated stem cells, relying on separate HMGB1- and MMP-9-dependent pathways

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Inflammatory and alternatively activated human macrophages attract vessel-associated stem cells, relying on separate HMGB1- and MMP-9-dependent pathways. / Lolmede, K.; Campana, L.; Vezzoli, M.; Bosurgi, L.; Tonlorenzi, R.; Clementi, E.; Bianchi, M.E.; Cossu, G.; Manfredi, A.A.; Brunelli, S.; Rovere-Querini, P.

in: J LEUKOCYTE BIOL, Jahrgang 85, Nr. 5, 2009, S. 779-87.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Lolmede, K, Campana, L, Vezzoli, M, Bosurgi, L, Tonlorenzi, R, Clementi, E, Bianchi, ME, Cossu, G, Manfredi, AA, Brunelli, S & Rovere-Querini, P 2009, 'Inflammatory and alternatively activated human macrophages attract vessel-associated stem cells, relying on separate HMGB1- and MMP-9-dependent pathways', J LEUKOCYTE BIOL, Jg. 85, Nr. 5, S. 779-87. https://doi.org/10.1189/jlb.0908579

APA

Lolmede, K., Campana, L., Vezzoli, M., Bosurgi, L., Tonlorenzi, R., Clementi, E., Bianchi, M. E., Cossu, G., Manfredi, A. A., Brunelli, S., & Rovere-Querini, P. (2009). Inflammatory and alternatively activated human macrophages attract vessel-associated stem cells, relying on separate HMGB1- and MMP-9-dependent pathways. J LEUKOCYTE BIOL, 85(5), 779-87. https://doi.org/10.1189/jlb.0908579

Vancouver

Lolmede K, Campana L, Vezzoli M, Bosurgi L, Tonlorenzi R, Clementi E et al. Inflammatory and alternatively activated human macrophages attract vessel-associated stem cells, relying on separate HMGB1- and MMP-9-dependent pathways. J LEUKOCYTE BIOL. 2009;85(5):779-87. https://doi.org/10.1189/jlb.0908579

Bibtex

@article{df0a5e0846c44f1bb17ef06af03e24c1,
title = "Inflammatory and alternatively activated human macrophages attract vessel-associated stem cells, relying on separate HMGB1- and MMP-9-dependent pathways",
abstract = "Inflammatory macrophages recruited at the site of damaged muscles progressively acquire an alternative activation profile. Inflammatory (M1) and alternatively activated (M2) macrophages exert various and even opposite functions. M1 cells amplify tissue damage, and M2 cells dispose of necrotic fibers and deliver survival signals to myogenic precursors, finally supporting healing. A critical step in muscle healing is the recruitment of myogenic stem cells, including vessel-associated stem cells (mesoangioblasts), which have been demonstrated to home to damaged skeletal muscle selectively and preferentially. Little information is available about the signals involved and the role played by infiltrating macrophages. Here, we report that the polarization of macrophages dramatically skews the secretion of high mobility group box 1 (HMGB1), TNF-α, vascular endothelial growth factor, and metalloproteinase 9 (MMP-9), molecules involved in the regulation of cell diapedesis and migration. All polarized macrophage populations were strikingly effective at inducing mesoangioblast migration. By means of specific inhibitors, we verified that the recruitment of mesoangioblasts requires the secretion of HMGB1 and TNF-α by M1 cells and of MMP-9 by M2 cells. Together, these data demonstrate a feature, unrecognized previously, of macrophages: their ability to attract stem cells, which is conserved throughout their polarization. Moreover, they open the possibility of novel strategies, aimed at interfering selectively with signals that recruit blood-derived stem cells toward pro- or anti-inflammatory macrophages.",
author = "K. Lolmede and L. Campana and M. Vezzoli and L. Bosurgi and R. Tonlorenzi and E. Clementi and M.E. Bianchi and G. Cossu and A.A. Manfredi and S. Brunelli and P. Rovere-Querini",
year = "2009",
doi = "10.1189/jlb.0908579",
language = "English",
volume = "85",
pages = "779--87",
journal = "J LEUKOCYTE BIOL",
issn = "0741-5400",
publisher = "FASEB",
number = "5",

}

RIS

TY - JOUR

T1 - Inflammatory and alternatively activated human macrophages attract vessel-associated stem cells, relying on separate HMGB1- and MMP-9-dependent pathways

AU - Lolmede, K.

AU - Campana, L.

AU - Vezzoli, M.

AU - Bosurgi, L.

AU - Tonlorenzi, R.

AU - Clementi, E.

AU - Bianchi, M.E.

AU - Cossu, G.

AU - Manfredi, A.A.

AU - Brunelli, S.

AU - Rovere-Querini, P.

PY - 2009

Y1 - 2009

N2 - Inflammatory macrophages recruited at the site of damaged muscles progressively acquire an alternative activation profile. Inflammatory (M1) and alternatively activated (M2) macrophages exert various and even opposite functions. M1 cells amplify tissue damage, and M2 cells dispose of necrotic fibers and deliver survival signals to myogenic precursors, finally supporting healing. A critical step in muscle healing is the recruitment of myogenic stem cells, including vessel-associated stem cells (mesoangioblasts), which have been demonstrated to home to damaged skeletal muscle selectively and preferentially. Little information is available about the signals involved and the role played by infiltrating macrophages. Here, we report that the polarization of macrophages dramatically skews the secretion of high mobility group box 1 (HMGB1), TNF-α, vascular endothelial growth factor, and metalloproteinase 9 (MMP-9), molecules involved in the regulation of cell diapedesis and migration. All polarized macrophage populations were strikingly effective at inducing mesoangioblast migration. By means of specific inhibitors, we verified that the recruitment of mesoangioblasts requires the secretion of HMGB1 and TNF-α by M1 cells and of MMP-9 by M2 cells. Together, these data demonstrate a feature, unrecognized previously, of macrophages: their ability to attract stem cells, which is conserved throughout their polarization. Moreover, they open the possibility of novel strategies, aimed at interfering selectively with signals that recruit blood-derived stem cells toward pro- or anti-inflammatory macrophages.

AB - Inflammatory macrophages recruited at the site of damaged muscles progressively acquire an alternative activation profile. Inflammatory (M1) and alternatively activated (M2) macrophages exert various and even opposite functions. M1 cells amplify tissue damage, and M2 cells dispose of necrotic fibers and deliver survival signals to myogenic precursors, finally supporting healing. A critical step in muscle healing is the recruitment of myogenic stem cells, including vessel-associated stem cells (mesoangioblasts), which have been demonstrated to home to damaged skeletal muscle selectively and preferentially. Little information is available about the signals involved and the role played by infiltrating macrophages. Here, we report that the polarization of macrophages dramatically skews the secretion of high mobility group box 1 (HMGB1), TNF-α, vascular endothelial growth factor, and metalloproteinase 9 (MMP-9), molecules involved in the regulation of cell diapedesis and migration. All polarized macrophage populations were strikingly effective at inducing mesoangioblast migration. By means of specific inhibitors, we verified that the recruitment of mesoangioblasts requires the secretion of HMGB1 and TNF-α by M1 cells and of MMP-9 by M2 cells. Together, these data demonstrate a feature, unrecognized previously, of macrophages: their ability to attract stem cells, which is conserved throughout their polarization. Moreover, they open the possibility of novel strategies, aimed at interfering selectively with signals that recruit blood-derived stem cells toward pro- or anti-inflammatory macrophages.

UR - http://www.scopus.com/inward/record.url?eid=2-s2.0-65549151760&partnerID=MN8TOARS

U2 - 10.1189/jlb.0908579

DO - 10.1189/jlb.0908579

M3 - SCORING: Journal article

C2 - 19197071

VL - 85

SP - 779

EP - 787

JO - J LEUKOCYTE BIOL

JF - J LEUKOCYTE BIOL

SN - 0741-5400

IS - 5

ER -