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Peptides. 2018 Mar;101:135-144. doi: 10.1016/j.peptides.2018.01.010. Epub 2018 Jan 17.

Induction by innate defence regulator peptide 1018 of pro-angiogenic molecules and endothelial cell migration in a high glucose environment.

Author information

1
Medical Research Unit-Zacatecas, Mexican Institute for Social Security-IMSS, Zacatecas, Mexico; Department of Immunology, School of Medicine, Universidad Autonoma de San Luis Potosi, Mexico.
2
Medical Research Unit-Zacatecas, Mexican Institute for Social Security-IMSS, Zacatecas, Mexico.
3
Faculty of Chemistry, Autonomous University of Zacatecas, Mexico.
4
Centre for Microbial Diseases and Immunity Research, University of British Columbia, 2259 Lower Mall Research Station, Vancouver, BC, Canada.
5
Medical Research Unit-Zacatecas, Mexican Institute for Social Security-IMSS, Zacatecas, Mexico. Electronic address: rondo_vm@yahoo.com.

Abstract

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.

KEYWORDS:

Angiogenesis; Angiogenin; Diabetic foot ulcer; IDR-1018; VGF; Wound healing

PMID:
29353019
DOI:
10.1016/j.peptides.2018.01.010
[Indexed for MEDLINE]

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