Tissue Eng Regen Med.  2017 Jun;14(3):267-277. 10.1007/s13770-017-0034-5.

Epidermal Growth Factor (EGF)-Like Repeats and Discoidin I-Like Domains 3 (EDIL3): A Potential New Therapeutic Tool for the Treatment of Keloid Scars

• Ryu YH
• Lee YJ
• Kim KJ
• Lee SJ
• Han YN
• Rhie JW

• KMID: 2395083
• DOI: http://doi.org/10.1007/s13770-017-0034-5

Abstract

In keloids, the mechanism underlying the excessive accumulation of extracellular matrix after injury of the skin is unclear, and there is no effective treatment because of the incomplete understanding of their pathogenesis; thus, a high recurrence rate is observed. We studied a new marker of keloids to determine a new treatment strategy. First, the keloid gene expression profile (GSE44270) was analyzed (downloaded from the Gene Expression Omnibus database) and the new keloid marker candidate, epidermal growth factor (EGF)-like repeats and discoidin I-like domains 3 (EDIL3) which were upregulated in keloid samples was identified. Knockdown of EDIL3 is known to suppresses angiogenesis by downregulating relevant inhibitory factors that can limit the supply of survival factors to tumor cells from the circulation via the vascular endothelial cells. In keloids, the mechanism of action of EDIL3 may be similar to that in tumors; the inhibition of apoptosis in tumor cells via a reduction in the apoptosis of blood vessels by upregulating an angiogenic factor. To determine whether EDIL3 is involved in keloid formation, we performed knockdown of EDIL3 in keloid fibroblasts in vitro by transfection with anti-EDIL3 small interfering RNA (via microporation). EDIL3 was upregulated in keloid fibroblasts compared with normal fibroblasts in collagen type I, II and III. Our results indicate the control of EDIL3 expression may be a new promising treatment of keloid disease also the molecular targeting of EDIL3 may improve the quality of treatment and reduce the formation of keloids.

Keyword

Keloid scar; EDIL3; Collagen; siRNA; Transfection

MeSH Terms

Angiogenesis Inducing Agents
Apoptosis
Blood Vessels
Cicatrix*
Collagen
Collagen Type I
Endothelial Cells
Epidermal Growth Factor*
Extracellular Matrix
Fibroblasts
Gene Expression
In Vitro Techniques
Keloid*
Recurrence
RNA, Small Interfering
Skin
Transcriptome
Transfection
Angiogenesis Inducing Agents
Collagen
Collagen Type I
Epidermal Growth Factor
RNA, Small Interfering