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Identification of a transcriptional signature for the wound healing continuum.

Peake MA, Caley M, Giles PJ, Wall I, Enoch S, Davies LC, Kipling D, Thomas DW, Stephens P - Wound Repair Regen (2014 May-Jun)

Bottom Line: Central to these outcomes is the role of the fibroblast.Genes whose expression increases following serum exposure in the order OMF < NF < CWF are candidates for a negative/impaired healing phenotype (the dysfunctional healing group), whereas genes with the converse pattern are potentially associated with a positive/preferential healing phenotype (the enhanced healing group).Sixty-six genes in the enhanced healing group and 38 genes in the dysfunctional healing group were identified.

View Article: PubMed Central - PubMed

Affiliation: Wound Biology Group, Cardiff Institute of Tissue Engineering and Repair, Tissue Engineering and Reparative Dentistry, School of Dentistry.

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An overview of the cellular and clinical characteristics of the functional wound healing continuum. Key processes associated with scarless, scarring, and nonhealing wound repair are highlighted as they increase and decline across the repair spectrum. Critical to this is the role of the fibroblast and the “aging” transition from fetal fibroblasts, through adult fibroblasts to senescent fibroblasts.
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fig01: An overview of the cellular and clinical characteristics of the functional wound healing continuum. Key processes associated with scarless, scarring, and nonhealing wound repair are highlighted as they increase and decline across the repair spectrum. Critical to this is the role of the fibroblast and the “aging” transition from fetal fibroblasts, through adult fibroblasts to senescent fibroblasts.

Mentions: It is well established through in vitro investigations that oral mucosal fibroblasts (OMFs) (compared with patient-matched skin fibroblasts) exhibit a fetal-like phenotype.1,2 At the other end of this continuum is the impaired wound healing phenotype shown by senescent fibroblasts found within chronic (nonhealing) wounds of aged individuals. The response of these cells is impaired3,4 and in stark contrast to those from the oral mucosa. Interestingly, impaired wound healing is also a feature of certain premature aging conditions, for example, Werner's syndrome.5 Between these two extremes of tissue response, the normal wound healing response, as found in adult dermal tissues, features an intermediate rate of wound repair, which results ultimately in a repair of the tissue but inevitably the production of scar tissue (Figure 1).


Identification of a transcriptional signature for the wound healing continuum.

Peake MA, Caley M, Giles PJ, Wall I, Enoch S, Davies LC, Kipling D, Thomas DW, Stephens P - Wound Repair Regen (2014 May-Jun)

An overview of the cellular and clinical characteristics of the functional wound healing continuum. Key processes associated with scarless, scarring, and nonhealing wound repair are highlighted as they increase and decline across the repair spectrum. Critical to this is the role of the fibroblast and the “aging” transition from fetal fibroblasts, through adult fibroblasts to senescent fibroblasts.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4230470&req=5

fig01: An overview of the cellular and clinical characteristics of the functional wound healing continuum. Key processes associated with scarless, scarring, and nonhealing wound repair are highlighted as they increase and decline across the repair spectrum. Critical to this is the role of the fibroblast and the “aging” transition from fetal fibroblasts, through adult fibroblasts to senescent fibroblasts.
Mentions: It is well established through in vitro investigations that oral mucosal fibroblasts (OMFs) (compared with patient-matched skin fibroblasts) exhibit a fetal-like phenotype.1,2 At the other end of this continuum is the impaired wound healing phenotype shown by senescent fibroblasts found within chronic (nonhealing) wounds of aged individuals. The response of these cells is impaired3,4 and in stark contrast to those from the oral mucosa. Interestingly, impaired wound healing is also a feature of certain premature aging conditions, for example, Werner's syndrome.5 Between these two extremes of tissue response, the normal wound healing response, as found in adult dermal tissues, features an intermediate rate of wound repair, which results ultimately in a repair of the tissue but inevitably the production of scar tissue (Figure 1).

Bottom Line: Central to these outcomes is the role of the fibroblast.Genes whose expression increases following serum exposure in the order OMF < NF < CWF are candidates for a negative/impaired healing phenotype (the dysfunctional healing group), whereas genes with the converse pattern are potentially associated with a positive/preferential healing phenotype (the enhanced healing group).Sixty-six genes in the enhanced healing group and 38 genes in the dysfunctional healing group were identified.

View Article: PubMed Central - PubMed

Affiliation: Wound Biology Group, Cardiff Institute of Tissue Engineering and Repair, Tissue Engineering and Reparative Dentistry, School of Dentistry.

Show MeSH
Related in: MedlinePlus