Induction by innate defence regulator peptide 1018 of pro-angiogenic molecules and endothelial cell migration in a high glucose environment
Copyright © 2018 Elsevier Inc. All rights reserved..
Synthetic innate defence regulator (IDR) peptides such as IDR-1018 modulate immunity to promote key protective functions including chemotaxis, wound healing, and anti-infective activity, while suppressing pro-inflammatory responses to non-pathological levels. Here we demonstrated that IDR-1018 induced, by up to 75-fold, pro-angiogenic VEGF-165 in keratinocytes but suppressed this isoform in endothelial cells. It also induced early angiogenin and prolonged anti-inflammatory TGFβ expression on endothelial cells, while suppressing early pro-inflammatory IL-1β expression levels. IDR-1018 also down-regulated the hypoxia induced transcription factor HIF-1α in both keratinocytes and endothelial cells. Consistent with these data, in an in vitro wound healing scratch assay, IDR-1018 induced migration of endothelial cells under conditions of hypoxia while in epithelial cells migration increased only under conditions of normoxia.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2018 |
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Erschienen: |
2018 |
Enthalten in: |
Zur Gesamtaufnahme - volume:101 |
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Enthalten in: |
Peptides - 101(2018) vom: 06. März, Seite 135-144 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Marin-Luevano, Paulina [VerfasserIn] |
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Links: |
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Anmerkungen: |
Date Completed 26.12.2018 Date Revised 26.12.2018 published: Print-Electronic Citation Status MEDLINE |
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doi: |
10.1016/j.peptides.2018.01.010 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM280147732 |
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520 | |a Copyright © 2018 Elsevier Inc. All rights reserved. | ||
520 | |a Synthetic innate defence regulator (IDR) peptides such as IDR-1018 modulate immunity to promote key protective functions including chemotaxis, wound healing, and anti-infective activity, while suppressing pro-inflammatory responses to non-pathological levels. Here we demonstrated that IDR-1018 induced, by up to 75-fold, pro-angiogenic VEGF-165 in keratinocytes but suppressed this isoform in endothelial cells. It also induced early angiogenin and prolonged anti-inflammatory TGFβ expression on endothelial cells, while suppressing early pro-inflammatory IL-1β expression levels. IDR-1018 also down-regulated the hypoxia induced transcription factor HIF-1α in both keratinocytes and endothelial cells. Consistent with these data, in an in vitro wound healing scratch assay, IDR-1018 induced migration of endothelial cells under conditions of hypoxia while in epithelial cells migration increased only under conditions of normoxia | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a Research Support, Non-U.S. Gov't | |
650 | 4 | |a Angiogenesis | |
650 | 4 | |a Angiogenin | |
650 | 4 | |a Diabetic foot ulcer | |
650 | 4 | |a IDR-1018 | |
650 | 4 | |a VGF | |
650 | 4 | |a Wound healing | |
650 | 7 | |a Angiogenesis Inducing Agents |2 NLM | |
650 | 7 | |a Antimicrobial Cationic Peptides |2 NLM | |
650 | 7 | |a HIF1A protein, human |2 NLM | |
650 | 7 | |a Hypoxia-Inducible Factor 1, alpha Subunit |2 NLM | |
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650 | 7 | |a Interleukin-1beta |2 NLM | |
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700 | 1 | |a Trujillo, Valentin |e verfasserin |4 aut | |
700 | 1 | |a Rodriguez-Carlos, Adrian |e verfasserin |4 aut | |
700 | 1 | |a González-Curiel, Irma |e verfasserin |4 aut | |
700 | 1 | |a Enciso-Moreno, Jose A |e verfasserin |4 aut | |
700 | 1 | |a Hancock, Robert E W |e verfasserin |4 aut | |
700 | 1 | |a Rivas-Santiago, Bruno |e verfasserin |4 aut | |
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