Effects of antisense oligodeoxynucleotide to type I collagen gene on hypertrophic scars in the transplanted nude mouse model

Background:  Antisense nucleic acids are effective in inhibiting harmful or uncontrolled gene expression. We had previously proved that the antisense DNA to type I collagen could effectively inhibit the synthesis of collagen type I in cultured hypertrophic scar fibroblasts, suggesting a potential ro...

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Bibliographic Details
Published in:Journal of cutaneous pathology 2009-11, Vol.36 (11), p.1146-1150
Main Authors: Xie, Julin, Qi, Shaohai, Yuan, Jishan, Xu, Yinbing, Li, Tianzeng, Li, Houdong, Liu, Xusheng, Shu, Bin, Liang, Huizeng
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Blotting, Western
Cicatrix, Hypertrophic - genetics
Cicatrix, Hypertrophic - prevention & control
Collagen Type I - genetics
Dermatology
Down-Regulation
Enzyme-Linked Immunosorbent Assay
Gene Expression - drug effects
Humans
Medical sciences
Mice
Mice, Nude
Oligodeoxyribonucleotides, Antisense - pharmacology
Reverse Transcriptase Polymerase Chain Reaction
Skin Transplantation
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Summary:Background:  Antisense nucleic acids are effective in inhibiting harmful or uncontrolled gene expression. We had previously proved that the antisense DNA to type I collagen could effectively inhibit the synthesis of collagen type I in cultured hypertrophic scar fibroblasts, suggesting a potential role in anti‐scarring, but there are no published reports of its effect on scar in the transplanted nude mouse model. Aims:  To investigate the effects of antisense oligodeoxynucleotide (ASODN) to type I collagen gene on hypertrophic scars in the transplanted nude mouse model and clarify the potential of ASODN for the treatment of scars. Methods:  The nude mouse model of hypertrophic scar was created and subjected to daily injections with ASODN and Lipofectamine™ for 2 ,4 or 6 weeks. We then examined the scars for changes in histopathological characteristics. The effects of ASODN on type I collagen gene expression were examined by reverse transcription‐polymerase chain reaction and Western blots. Results:  The ASODN could remarkably alleviate the scar in the nude mouse model and consistently inhibit type I collagen gene expression at both the mRNA and protein levels. Conclusion:  ASODN was effective in downregulating type I collagen gene expression and could prove to be useful in the treatment of scars.
ISSN:0303-6987
1600-0560
DOI:10.1111/j.1600-0560.2009.01246.x