Age-related changes in monocytes exacerbate neointimal hyperplasia after vascular injury

Laisel Martinez, Camilo Gomez, Roberto I Vazquez-Padron

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Neointimal hyperplasia is the leading cause of restenosis after endovascular interventions. It is characterized by the accumulation of myofibroblast-like cells and extracellular matrix in the innermost layer of the wall and is exacerbated by inflammation. Monocytes from either young or aged rats were applied perivascularly to injured vascular walls of young recipient animals. Monocytes from aged rats, but not young donors, increased neointima thickness. Accordingly, the gene expression profiles of CD11b+ monocytes from aged rats showed significant up-regulation of genes involved in cellular adhesion, lipid degradation, cytotoxicity, differentiation, and inflammation. These included cadherin 13 (Cdh13), colony stimulating factor 1 (Csf1), chemokine C-X-C motif ligand 1 (Cxcl1), endothelial cell-selective adhesion molecule (Esam), and interferon gamma (Ifng). In conclusion, our results suggest that the increased inflammatory and adhesive profile of monocytes contributes to pathological wall remodeling in aged-related vascular diseases.

Original languageEnglish (US)
Pages (from-to)17054-17064
Number of pages11
JournalOncotarget
Volume6
Issue number19
StatePublished - 2015

Fingerprint

Vascular System Injuries
Hyperplasia
Monocytes
Chemokine CXCL1
Inflammation
Neointima
Macrophage Colony-Stimulating Factor
Myofibroblasts
Cell Adhesion Molecules
Vascular Diseases
Transcriptome
Adhesives
Interferon-gamma
Extracellular Matrix
Blood Vessels
Up-Regulation
Endothelial Cells
Lipids
Genes

Keywords

  • Age
  • Balloon injury
  • Gene expression
  • Monocytes
  • Neointimal hyperplasia

ASJC Scopus subject areas

  • Oncology

Cite this

Age-related changes in monocytes exacerbate neointimal hyperplasia after vascular injury. / Martinez, Laisel; Gomez, Camilo; Vazquez-Padron, Roberto I.

In: Oncotarget, Vol. 6, No. 19, 2015, p. 17054-17064.

Research output: Contribution to journalArticle

@article{59e2c9cc768647c3b32849e88a2d8343,
title = "Age-related changes in monocytes exacerbate neointimal hyperplasia after vascular injury",
abstract = "Neointimal hyperplasia is the leading cause of restenosis after endovascular interventions. It is characterized by the accumulation of myofibroblast-like cells and extracellular matrix in the innermost layer of the wall and is exacerbated by inflammation. Monocytes from either young or aged rats were applied perivascularly to injured vascular walls of young recipient animals. Monocytes from aged rats, but not young donors, increased neointima thickness. Accordingly, the gene expression profiles of CD11b+ monocytes from aged rats showed significant up-regulation of genes involved in cellular adhesion, lipid degradation, cytotoxicity, differentiation, and inflammation. These included cadherin 13 (Cdh13), colony stimulating factor 1 (Csf1), chemokine C-X-C motif ligand 1 (Cxcl1), endothelial cell-selective adhesion molecule (Esam), and interferon gamma (Ifng). In conclusion, our results suggest that the increased inflammatory and adhesive profile of monocytes contributes to pathological wall remodeling in aged-related vascular diseases.",
keywords = "Age, Balloon injury, Gene expression, Monocytes, Neointimal hyperplasia",
author = "Laisel Martinez and Camilo Gomez and Vazquez-Padron, {Roberto I}",
year = "2015",
language = "English (US)",
volume = "6",
pages = "17054--17064",
journal = "Oncotarget",
issn = "1949-2553",
publisher = "Impact Journals",
number = "19",

}

TY - JOUR

T1 - Age-related changes in monocytes exacerbate neointimal hyperplasia after vascular injury

AU - Martinez, Laisel

AU - Gomez, Camilo

AU - Vazquez-Padron, Roberto I

PY - 2015

Y1 - 2015

N2 - Neointimal hyperplasia is the leading cause of restenosis after endovascular interventions. It is characterized by the accumulation of myofibroblast-like cells and extracellular matrix in the innermost layer of the wall and is exacerbated by inflammation. Monocytes from either young or aged rats were applied perivascularly to injured vascular walls of young recipient animals. Monocytes from aged rats, but not young donors, increased neointima thickness. Accordingly, the gene expression profiles of CD11b+ monocytes from aged rats showed significant up-regulation of genes involved in cellular adhesion, lipid degradation, cytotoxicity, differentiation, and inflammation. These included cadherin 13 (Cdh13), colony stimulating factor 1 (Csf1), chemokine C-X-C motif ligand 1 (Cxcl1), endothelial cell-selective adhesion molecule (Esam), and interferon gamma (Ifng). In conclusion, our results suggest that the increased inflammatory and adhesive profile of monocytes contributes to pathological wall remodeling in aged-related vascular diseases.

AB - Neointimal hyperplasia is the leading cause of restenosis after endovascular interventions. It is characterized by the accumulation of myofibroblast-like cells and extracellular matrix in the innermost layer of the wall and is exacerbated by inflammation. Monocytes from either young or aged rats were applied perivascularly to injured vascular walls of young recipient animals. Monocytes from aged rats, but not young donors, increased neointima thickness. Accordingly, the gene expression profiles of CD11b+ monocytes from aged rats showed significant up-regulation of genes involved in cellular adhesion, lipid degradation, cytotoxicity, differentiation, and inflammation. These included cadherin 13 (Cdh13), colony stimulating factor 1 (Csf1), chemokine C-X-C motif ligand 1 (Cxcl1), endothelial cell-selective adhesion molecule (Esam), and interferon gamma (Ifng). In conclusion, our results suggest that the increased inflammatory and adhesive profile of monocytes contributes to pathological wall remodeling in aged-related vascular diseases.

KW - Age

KW - Balloon injury

KW - Gene expression

KW - Monocytes

KW - Neointimal hyperplasia

UR - http://www.scopus.com/inward/record.url?scp=84938280713&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84938280713&partnerID=8YFLogxK

M3 - Article

C2 - 25965835

AN - SCOPUS:84938280713

VL - 6

SP - 17054

EP - 17064

JO - Oncotarget

JF - Oncotarget

SN - 1949-2553

IS - 19

ER -