In vivo evidence of increased vascular endothelial growth factor in patients with major depressive disorder.

Astrocyte Astrocyte-derived extracellular vesicle Blood-brain barrier Major depressive disorder Vascular endothelial growth factor

Journal

Journal of affective disorders
ISSN: 1573-2517
Titre abrégé: J Affect Disord
Pays: Netherlands
ID NLM: 7906073

Informations de publication

Date de publication:
13 Sep 2024
Historique:
received: 21 05 2024
revised: 10 09 2024
accepted: 12 09 2024
medline: 16 9 2024
pubmed: 16 9 2024
entrez: 15 9 2024
Statut: aheadofprint

Résumé

Vascular endothelial growth factor (VEGF) is a candidate mediator of blood-brain barrier (BBB) disruption in depression. However, previous studies have mainly focused on peripheral blood VEGF levels, and the results are heterogeneous. Here we use astrocyte-derived extracellular vesicles (ADEVs) isolated from plasma to explore the in vivo changes of VEGF levels in patients with major depressive disorder (MDD). Thirty-five unmedicated patients with MDD and 35 healthy controls (HCs) were enrolled, and plasma ADEVs were isolated from each participant. VEGF levels in ADEVs and glial fibrillary acidic protein (GFAP) in plasma were measured. Additionally, Alix and CD81, two established extracellular vesicle markers, were quantified in ADEVs. At baseline, MDD patients exhibited significantly increased levels of VEGF in ADEVs and GFAP in plasma. Following four weeks of selective serotonin reuptake inhibitor treatment, these target protein levels did not significantly change. ROC curve analysis revealed an AUC of 0.711 for VEGF in ADEVs. In exploratory analysis, VEGF levels in ADEVs were positively correlated with Alix and CD81. Multiple factors regulate BBB permeability. This study focused solely on VEGF and the sample size for longitudinal analysis was relatively small. Our study is the first to confirm increased ADEV-derived VEGF levels in patients with MDD, thereby providing preliminary evidence supporting the hypothesis that the BBB is disrupted in depression.

Sections du résumé

BACKGROUND BACKGROUND
Vascular endothelial growth factor (VEGF) is a candidate mediator of blood-brain barrier (BBB) disruption in depression. However, previous studies have mainly focused on peripheral blood VEGF levels, and the results are heterogeneous. Here we use astrocyte-derived extracellular vesicles (ADEVs) isolated from plasma to explore the in vivo changes of VEGF levels in patients with major depressive disorder (MDD).
METHODS METHODS
Thirty-five unmedicated patients with MDD and 35 healthy controls (HCs) were enrolled, and plasma ADEVs were isolated from each participant. VEGF levels in ADEVs and glial fibrillary acidic protein (GFAP) in plasma were measured. Additionally, Alix and CD81, two established extracellular vesicle markers, were quantified in ADEVs.
RESULTS RESULTS
At baseline, MDD patients exhibited significantly increased levels of VEGF in ADEVs and GFAP in plasma. Following four weeks of selective serotonin reuptake inhibitor treatment, these target protein levels did not significantly change. ROC curve analysis revealed an AUC of 0.711 for VEGF in ADEVs. In exploratory analysis, VEGF levels in ADEVs were positively correlated with Alix and CD81.
LIMITATIONS CONCLUSIONS
Multiple factors regulate BBB permeability. This study focused solely on VEGF and the sample size for longitudinal analysis was relatively small.
CONCLUSION CONCLUSIONS
Our study is the first to confirm increased ADEV-derived VEGF levels in patients with MDD, thereby providing preliminary evidence supporting the hypothesis that the BBB is disrupted in depression.

Identifiants

pubmed: 39278472
pii: S0165-0327(24)01561-1
doi: 10.1016/j.jad.2024.09.073
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024. Published by Elsevier B.V.

Déclaration de conflit d'intérêts

Declaration of competing interest All authors declare that they have no conflicts of interest.

Auteurs

Kun Li (K)

Department of Psychiatry, Renmin Hospital of Wuhan University, Wuhan, Hubei, China; Clinical Laboratory, Affiliated Hospital of West Anhui Health Vocational College, Lu'an, Anhui, China.

Kun Wang (K)

Department of Psychiatry, Affied Hospital of West Anhui Health Vocational College, Lu'an, Anhui, China.

Shu-Xian Xu (SX)

Department of Psychiatry, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.

Xin-Hui Xie (XH)

Department of Psychiatry, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.

Yan Tang (Y)

Department of Psychiatry, Affied Hospital of West Anhui Health Vocational College, Lu'an, Anhui, China.

Lihong Zhang (L)

Clinical Laboratory, Affiliated Hospital of West Anhui Health Vocational College, Lu'an, Anhui, China.

Zhongchun Liu (Z)

Department of Psychiatry, Renmin Hospital of Wuhan University, Wuhan, Hubei, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China. Electronic address: zcliu6@whu.edu.cn.

Classifications MeSH