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Amelogenins modulate cytokine expression in LPS-challenged cultured human macrophages.

Artikel i vetenskaplig tidskrift
Författare Sofia Almqvist
Maria Werthén
S Petter Lyngstadaas
Christina Gretzer
Peter Thomsen
Publicerad i Cytokine
Volym 58
Nummer/häfte 2
Sidor 274-9
ISSN 1096-0023
Publiceringsår 2012
Publicerad vid Institutionen för kliniska vetenskaper, Avdelningen för biomaterialvetenskap
Sidor 274-9
Språk en
Länkar dx.doi.org/10.1016/j.cyto.2012.02.0...
Ämnesord Amelogenins; Extracellular matrix (ECM); Macrophage; Inflammation; Cytokine
Ämneskategorier Biomaterialvetenskap

Sammanfattning

Amelogenins are enamel matrix proteins with a proven ability to restore tissues in patients with advanced periodontitis and chronic skin wounds. To explore the mechanisms of action of amelogenins in wound inflammation, the in vitro effect on the expression of selected cell mediators involved in inflammation and tissue repair from human monocyte-derived macrophages was studied. Macrophages were treated with amelogenins in serum-enriched medium with simultaneous lipopolysaccharide (LPS) stimulation, for 6, 24 and 72 h, and the conditioned culture medium was analysed for 28 different cytokines. Amelogenin treatment directed the LPS-induced release of both pro- and anti-inflammatory cytokines towards an alternatively activated macrophage phenotype. This change in activation was also demonstrated by the amelogenin-induced secretion of alternative macrophage activation-associated CC chemokine-1 (AMAC-1, also known as CCL18; p<0.001), a well-documented marker of alternative activation. Amelogenins were also shown significantly to increase the macrophage expression of vascular endothelial growth factor and, to a lesser but significant extent, insulin-like growth factor-1 after 24h of culture. The results of the present in vitro study show that monocyte-derived macrophages stimulated by inflammatory agonist LPS respond to the treatment with amelogenins by reducing the pro-inflammatory activity and increasing the expression of tissue repair mediators.

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