The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Cells migrating to sites of tissue damage in response to the danger signal HMGB1 require NF-κB activation
Open accessAbstract
Tissue damage is usually followed by healing, as both differentiated and stem cells migrate to replace dead or damaged cells. Mesoangioblasts (vessel-associated stem cells that can repair muscles) and fibroblasts migrate toward soluble factors released by damaged tissue. Two such factors are high mobility group box 1 (HMGB1), a nuclear protein that is released by cells undergoing unscheduled death (necrosis) but not by apoptotic cells, and stromal derived factor (SDF)–1/CXCL12. We find that HMGB1 activates the canonical nuclear factor κB (NF-κB) pathway via extracellular signal-regulated kinase phosphorylation. NF-κB signaling is necessary for chemotaxis toward HMGB1 and SDF-1/CXCL12, but not toward growth factor platelet-derived growth factor, formyl-met-leu-phe (a peptide that mimics bacterial invasion), or the archetypal NF-κB–activating signal tumor necrosis factor α. In dystrophic mice, mesoangioblasts injected into the general circulation ingress inefficiently into muscles if their NF-κB signaling pathway is disabled. These findings suggest that NF-κB signaling controls tissue regeneration in addition to early events in inflammation.
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Cites
Release of chromatin protein HMGB1 by necrotic cells triggers inflammation
Scaffidi, P., Misteli, T., & Bianchi, M. E. (2002) · Nature · doi:10.1038/nature00858 · Cited by 4,221
Self-citationDAMPs, PAMPs and alarmins: all we need to know about danger
Bianchi, M. E. (2007) · Journal of Leukocyte Biology · doi:10.1189/jlb.0306164 · Cited by 2,794
Self-citationThe two NF-κB activation pathways and their role in innate and adaptive immunity
Bonizzi, G., & Karin, M. (2004) · Trends in Immunology · doi:10.1016/j.it.2004.03.008 · Cited by 2,535
Understanding RAGE, the receptor for advanced glycation end products
Bierhaus, A., Humpert, P. M., Morcos, M., Wendt, T., Chavakis, T., Arnold, B., Stern, D. M., & Nawroth, P. P. (2005) · Journal of Molecular Medicine · doi:10.1007/s00109-005-0688-7 · Cited by 1,297
Minasi, M. G., Riminucci, M., De Angelis, L., Borello, U., Berarducci, B., Innocenzi, A., Caprioli, A., Sirabella, D., Baiocchi, M., De Maria, R., et al. (2002) · Development · doi:10.1242/dev.129.11.2773 · Cited by 514
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Cited by
HMGB1 is a therapeutic target for sterile inflammation and infection
Andersson, U., & Tracey, K. J. (2011) · Annual Review of Immunology · doi:10.1146/annurev-immunol-030409-101323 · Cited by 1,437
Neuroinflammation: friend and foe for ischemic stroke
Jayaraj, R. L., Azimullah, S., Beiram, R., Jalal, F. Y., & Rosenberg, G. A. (2019) · Journal of Neuroinflammation · doi:10.1186/s12974-019-1516-2 · Cited by 1,428
Kang, R., Chen, R., Zhang, Q., Hou, W., Wu, S., Cao, L., Huang, J., Yu, Y., Fan, X.-G., Yan, Z., et al. (2014) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2014.05.001 · Cited by 956
HMGB1: Endogenous Danger Signaling
Klune, J. R., Dhupar, R., Cardinal, J., Billiar, T. R., & Tsung, A. (2008) · Molecular Medicine · doi:10.2119/2008-00034.klune · Cited by 762
Mutually exclusive redox forms of HMGB1 promote cell recruitment or proinflammatory cytokine release
Venereau, E., Casalgrandi, M., Schiraldi, M., Antoine, D. J., Cattaneo, A., De Marchis, F., Liu, J., Antonelli, A., Preti, A., Raeli, L., et al. (2012) · Journal of Experimental Medicine · doi:10.1084/jem.20120189 · Cited by 720
“Fibroblasts, respond to lower concentrations of HMGB1 compared with leukocytes (Palumbo et al., 2007) and support their own migration by secreting CXCL12 both basally and in response to HMGB1 activation of the receptor for advanced glycation end products (RAGE; Schiraldi et al., 2012).”
BackgroundSelf-citation
Metadata
- Authors
- Palumbo, R., Galvez, B. G., Pusterla, T., De Marchis, F., Cossu, G., Marcu, K. B., & Bianchi, M. E.
- Venue
- The Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2007-10-08
- Volume
- 179
- Issue
- 1
- Pages
- 33-40
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- OpenAlex
- W2095609344
- Cited by
- 250
- References
- 5
- FWCI
- 6.54
- Type
- journal article
- Language
- en
- Open access
- green
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- Palumbo, R., Galvez, B. G., Pusterla, T., De Marchis, F., Cossu, G., Marcu, K. B., & Bianchi, M. E. (2007). Cells migrating to sites of tissue damage in response to the danger signal HMGB1 require NF-κB activation. The Journal of Cell Biology. https://doi.org/10.1083/jcb.200704015
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
