論文

査読有り
2016年5月

Non-coding Double-stranded RNA and Antimicrobial Peptide LL-37 Induce Growth Factor Expression from Keratinocytes and Endothelial Cells

JOURNAL OF BIOLOGICAL CHEMISTRY
  • Christopher A. Adase
  • ,
  • Andrew W. Borkowski
  • ,
  • Ling-juan Zhang
  • ,
  • Michael R. Williams
  • ,
  • Emi Sato
  • ,
  • James A. Sanford
  • ,
  • Richard L. Gallo

291
22
開始ページ
11635
終了ページ
11646
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1074/jbc.M116.725317
出版者・発行元
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC

A critical function for skin is that when damaged it must simultaneously identify the nature of the injury, repair barrier function, and limit the intrusion of pathogenic organisms. These needs are carried out through the detection of damage-associated molecular patterns (DAMPs) and a response that includes secretion of cytokines, chemokines, growth factors, and antimicrobial peptides (AMPs). In this study, we analyzed how non-coding double-stranded RNA (dsRNAs) act as a DAMP in the skin and how the human cathelicidin AMP LL-37 might influence growth factor production in response to this DAMP. dsRNA alone significantly increased the expression of multiple growth factors in keratinocytes, endothelial cells, and fibroblasts. Furthermore, RNA sequencing transcriptome analysis found that multiple growth factors increase when cells are exposed to both LL-37 and dsRNA, a condition that mimics normal wounding. Quantitative PCR and/or ELISA validated that growth factors expressed by keratinocytes in these conditions included, but were not limited to, basic fibroblast growth factor (FGF2), heparin-binding EGF-like growth factor (HBEGF), vascular endothelial growth factor C (VEGFC), betacellulin (BTC), EGF, epiregulin (EREG), and other members of the transforming growth factor beta superfamily. These results identify a novel role for DAMPs and AMPs in the stimulation of repair and highlight the complex interactions involved in the wound environment.

Web of Science ® 被引用回数 : 11

リンク情報
DOI
https://doi.org/10.1074/jbc.M116.725317
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/27048655
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000377264800015&DestApp=WOS_CPL

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