Clinical and molecular effects on mature burn scars after treatment with a fractional CO(2)  laser.
OBJECTIVE
There have been several case reports of improvement in the appearance of mature burn scars following treatment with fractional CO(2) lasers. However, the biochemical mechanisms responsible for these improvements have not been elucidated.


METHODS
Ten patients with mature, full-thickness, hypertrophic burn scars received initial treatment with a fractional CO(2) laser. Clinical improvement was measured with Vancouver Scar Scale as well as Patient and Observer Scar Assessment Scale. Fresh tissue samples were obtained before the initial treatment and 48 hours after the first treatment for TaqMan Real-time RT-PCR analyses. Expressions of several scar-related biological markers, including types I and III procollagen, matrix metalloproteinase (MMP)-1, -13, transforming growth factor (TGF)-β1, β2, β3, and basic fibroblast growth factor (bFGF), as well as microRNA miR-17-92 cluster, were investigated.


RESULTS
There were significant improvements in both observer and subject ratings in all scales. Both types I and III procollagen mRNA levels were dramatically down-regulated after treatment, but the ratio of types I/III procollagen mRNA was not different. The expression of MMP-1 was significantly up-regulated after treatment, while TGF-β2, -β3, and bFGF levels were significantly down-regulated. Expression of miR-18a and miR-19a were dramatically up-regulated (P < 0.05) after treatment.


CONCLUSIONS
Our study indicated that fractional CO(2) resulted in clinical improvement of mature burn scar. Alteration of types I and III procollagen, MMP-1, TGF-β2, -β3, bFGF, as well as miRNAs miR-18a and miR-19a expression may be responsible for the clinical improvement after treatment. Our finding may have implications for novel treatments and further our understanding of fractional CO(2) laser treatment.
Henry Ford Immunology Program, Henry Ford Hospital, Detroit, Michigan, USA.
Le
L
Qu
Austin
A
Liu
Li
L
Zhou
Chundi
C
He
Peter H
PH
Grossman
Ronald L
RL
Moy
Qing-Sheng
QS
Mi
David
D
Ozog
D000328:Adult; D015415:Biomarkers / Q000378:metabolism; D002056:Burns / Q000150:complications*; D017439:Cicatrix, Hypertrophic / Q000209:etiology / Q000235:genetics / Q000378:metabolism / Q000601:surgery*; D015536:Down-Regulation; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000378:metabolism; D006801:Humans; D054020:Lasers, Gas / Q000627:therapeutic use*; D008297:Male; D020781:Matrix Metalloproteinase 1 / Q000378:metabolism; D053509:Matrix Metalloproteinase 13 / Q000378:metabolism; D035683:MicroRNAs / Q000378:metabolism; D008875:Middle Aged; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016212:Transforming Growth Factor beta / Q000378:metabolism; D016896:Treatment Outcome; D015854:Up-Regulation
D015415:Biomarkers; C524941:MIRN17 microRNA, human; D035683:MicroRNAs; D016212:Transforming Growth Factor beta; D016222:Fibroblast Growth Factor 2; D053509:Matrix Metalloproteinase 13; C522360:MMP1 protein, human; D020781:Matrix Metalloproteinase 1