Cells migrating to sites of tissue damage in response to the danger signal HMGB1 require NF-kappaB activation.

Cells migrating to sites of tissue damage in response to the danger signal HMGB1 require NF-kappaB activation. Research Abstract Details 

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Cells migrating to sites of tissue damage in response to the danger signal HMGB1 require NF-kappaB activation. Abstract Text:

Roberta Palumbo,Beatriz G Galvez,Tobias Pusterla,Francesco De Marchis,Giulio Cossu,Kenneth B Marcu,Marco E Bianchi,Roberta Palumbo,Beatriz G Galvez,Tobias Pusterla,Francesco De Marchis,Giulio Cossu,Kenneth B Marcu,Marco E Bianchi,Roberta Palumbo,Beatriz G Galvez,Tobias Pusterla,Francesco De Marchis,Giulio Cossu,Kenneth B Marcu,Marco E Bianchi,

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.

Cells migrating to sites of tissue damage in response to the danger signal HMGB1 require NF-kappaB activation. Publishing Authors By Initials

R Palumbo,BG Galvez,T Pusterla,F De Marchis,G Cossu,KB Marcu,ME Bianchi,R Palumbo,BG Galvez,T Pusterla,F De Marchis,G Cossu,KB Marcu,ME Bianchi,R Palumbo,BG Galvez,T Pusterla,F De Marchis,G Cossu,KB Marcu,ME Bianchi,

For similar biological phenomena, cell phenomena, and immunity: cell physiology: cell communication: signal transduction research abstracts see: biological phenomena, cell phenomena, and immunity: cell physiology: cell communication: signal transduction research

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Cells migrating to sites of tissue damage in response to the danger signal HMGB1 require NF-kappaB activation. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Journal of cell biology

VOLUME: 179

Page Numbers: 33-40

Journal Abbreviation: J. Cell Biol.

ISSN: 0021-9525

DAY: 8

MONTH: Oct

YEAR: 2007

Cells migrating to sites of tissue damage in response to the danger signal HMGB1 require NF-kappaB activation. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 375356

Cells migrating to sites of tissue damage in response to the danger signal HMGB1 require NF-kappaB activation. Keywords Mesh Terms:

KEYWORDS: Signal Transduction

MESH TERMS: analysis

Chemical & Substance for Abstract: Cells migrating to sites of tissue damage in response to the danger signal HMGB1 require NF-kappaB activation. Information

Substance Name: Mitogen-Activated Protein Kinases

Registry Number: EC 2.7.1.37

Grant and Affiliation Information for Cells migrating to sites of tissue damage in response to the danger signal HMGB1 require NF-kappaB activation.

AFFILIATION: Chromatin Dynamics Unit, Stem Cell Research Institute, Istituto Scientifico San Raffaele, 20132 Milan, Italy.

Country: United States

AGENCY: United States NIGMS

GRANT: R01-GM066882

ACRONYM: GM

MEDLINETA: J Cell Biol

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