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- Title
Cells migrating to sites of tissue damage in response to the danger signal HMGB1 require NF-kappaB activation.
- Authors
Palumbo, Roberta; Galvez, Beatriz G; Pusterla, Tobias; De Marchis, Francesco; Cossu, Giulio; Marcu, Kenneth B; Bianchi, Marco E
- Abstract
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 kappaB (NF-kappaB) pathway via extracellular signal-regulated kinase phosphorylation. NF-kappaB 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-kappaB-activating signal tumor necrosis factor alpha. In dystrophic mice, mesoangioblasts injected into the general circulation ingress inefficiently into muscles if their NF-kappaB signaling pathway is disabled. These findings suggest that NF-kappaB signaling controls tissue regeneration in addition to early events in inflammation.
- Publication
The Journal of cell biology, 2007, Vol 179, Issue 1, p33
- ISSN
0021-9525
- Publication type
Journal Article
- DOI
10.1083/jcb.200704015