Inflammatory Gene Expression of Human Perivascular Adipose Tissue in Abdominal Aortic Aneurysms.


Journal

European journal of vascular and endovascular surgery : the official journal of the European Society for Vascular Surgery
ISSN: 1532-2165
Titre abrégé: Eur J Vasc Endovasc Surg
Pays: England
ID NLM: 9512728

Informations de publication

Date de publication:
06 2021
Historique:
received: 13 04 2020
revised: 15 02 2021
accepted: 20 02 2021
pubmed: 17 4 2021
medline: 17 8 2021
entrez: 16 4 2021
Statut: ppublish

Résumé

Perivascular adipose tissue (PVAT) contributes to vascular homeostasis and is increasingly linked to vascular pathology. PVAT density and volume were associated with abdominal aortic aneurysm (AAA) presence and dimensions on imaging. However, mechanisms underlying the role of PVAT in AAA have not been clarified. This study aimed to explore differences in PVAT from AAA using gene expression and functional tests. Human aortic PVAT and control subcutaneous adipose tissue were collected during open AAA surgery. Gene analyses and functional tests were performed. The control group consisted of healthy aorta from non-living renal transplant donors. Gene expression tests were performed to study genes potentially involved in various inflammatory processes and AAA related genes. Live PVAT and subcutaneous adipose tissue (SAT) from AAA were used for ex vivo co-culture with smooth muscle cells (SMCs) retrieved from non-pathological aortas. Adipose tissue was harvested from 27 AAA patients (n [gene expression] = 22, n [functional tests] = 5) and five control patients. An increased inflammatory gene expression of PTPRC (p = .008), CXCL8 (p = .033), LCK (p = .003), CCL5 (p = .004) and an increase in extracellular matrix breakdown marker MMP9 (p = .016) were found in AAA compared with controls. Also, there was a decreased anti-inflammatory gene expression of PPARG in AAA compared with controls (p = .040). SMC co-cultures from non-pathological aortas with PVAT from AAA showed increased MMP9 (p = .033) and SMTN (p = .008) expression and SAT increased SMTN expression in these SMC. The data revealed that PVAT from AAA shows an increased pro-inflammatory and matrix metallopeptidase gene expression and decreased anti-inflammatory gene expression. Furthermore, increased expression of genes involved in aneurysm formation was found in healthy SMC co-culture with PVAT of AAA patients. Therefore, PVAT from AAA might contribute to inflammation of the adjacent aortic wall and thereby plays a possible role in AAA pathophysiology. These proposed pathways of inflammatory induction could reveal new therapeutic targets in AAA treatment.

Identifiants

pubmed: 33858751
pii: S1078-5884(21)00186-6
doi: 10.1016/j.ejvs.2021.02.034
pii:
doi:

Substances chimiques

CCL5 protein, human 0
CXCL8 protein, human 0
Chemokine CCL5 0
Cytoskeletal Proteins 0
Interleukin-8 0
Muscle Proteins 0
PPAR gamma 0
PPARG protein, human 0
RNA, Messenger 0
SMTN protein, human 0
LCK protein, human EC 2.7.10.2
Lymphocyte Specific Protein Tyrosine Kinase p56(lck) EC 2.7.10.2
Leukocyte Common Antigens EC 3.1.3.48
PTPRC protein, human EC 3.1.3.48
MMP9 protein, human EC 3.4.24.35
Matrix Metalloproteinase 9 EC 3.4.24.35

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1008-1016

Informations de copyright

Copyright © 2021 The Author(s). Published by Elsevier B.V. All rights reserved.

Auteurs

Jorn P Meekel (JP)

Department of Vascular Surgery, Amsterdam University Medical Centres, location VUmc, Amsterdam, the Netherlands; Department of Physiology, Amsterdam University Medical Centres, Amsterdam Cardiovascular Sciences, Amsterdam, the Netherlands; Department of Surgery, Zaans Medisch Centrum, Zaandam, the Netherlands.

Marina Dias-Neto (M)

Department of Angiology and Vascular Surgery, São João University Hospital Centre, Porto, Portugal; Department of Surgery and Physiology, Cardiovascular Research Unit, Faculty of Medicine, University of Porto, Portugal.

Natalija Bogunovic (N)

Department of Vascular Surgery, Amsterdam University Medical Centres, location VUmc, Amsterdam, the Netherlands; Department of Physiology, Amsterdam University Medical Centres, Amsterdam Cardiovascular Sciences, Amsterdam, the Netherlands.

Gloria Conceição (G)

Department of Surgery and Physiology, Cardiovascular Research Unit, Faculty of Medicine, University of Porto, Portugal.

Claudia Sousa-Mendes (C)

Department of Surgery and Physiology, Cardiovascular Research Unit, Faculty of Medicine, University of Porto, Portugal.

Gawin R Stoll (GR)

Department of Physiology, Amsterdam University Medical Centres, Amsterdam Cardiovascular Sciences, Amsterdam, the Netherlands.

Adelino Leite-Moreira (A)

Department of Surgery and Physiology, Cardiovascular Research Unit, Faculty of Medicine, University of Porto, Portugal.

Jennifer Huynh (J)

Department of Vascular Surgery, Amsterdam University Medical Centres, location VUmc, Amsterdam, the Netherlands; Department of Physiology, Amsterdam University Medical Centres, Amsterdam Cardiovascular Sciences, Amsterdam, the Netherlands.

Dimitra Micha (D)

Department of Clinical Genetics, Amsterdam University Medical Centres, location VUmc, Amsterdam, the Netherlands.

Etto C Eringa (EC)

Department of Physiology, Amsterdam University Medical Centres, Amsterdam Cardiovascular Sciences, Amsterdam, the Netherlands.

Ron Balm (R)

Department of Vascular Surgery, Amsterdam University Medical Centres, location AMC, Amsterdam, the Netherlands.

Jan D Blankensteijn (JD)

Department of Vascular Surgery, Amsterdam University Medical Centres, location VUmc, Amsterdam, the Netherlands.

Kak K Yeung (KK)

Department of Vascular Surgery, Amsterdam University Medical Centres, location VUmc, Amsterdam, the Netherlands; Department of Physiology, Amsterdam University Medical Centres, Amsterdam Cardiovascular Sciences, Amsterdam, the Netherlands; Department of Vascular Surgery, Amsterdam University Medical Centres, location AMC, Amsterdam, the Netherlands. Electronic address: k.yeung@amsterdamumc.nl.

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Classifications MeSH