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衰老的巨噬细胞释放炎性细胞因子和载有RNA的细胞外囊泡以规避成纤维细胞衰老。

Senescent Macrophages Release Inflammatory Cytokines and RNA-Loaded Extracellular Vesicles to Circumvent Fibroblast Senescence.

作者信息

Laliberté Camille, Bossé Bianca, Bourdeau Véronique, Prieto Luis I, Perron-Deshaies Genève, Vuong-Robillard Nhung, Igelmann Sebastian, Aguilar Lisbeth Carolina, Oeffinger Marlene, Baker Darren J, DesGroseillers Luc, Ferbeyre Gerardo

机构信息

Département de Biochimie et Médecine Moléculaire, Université de Montréal, Montréal, QC H3C 3J7, Canada.

Centre de Recherche du Centre, Hospitalier de l'Université de Montréal (CRCHUM), Montréal, QC H2X 0A9, Canada.

出版信息

Biomedicines. 2024 May 14;12(5):1089. doi: 10.3390/biomedicines12051089.

DOI:10.3390/biomedicines12051089
PMID:38791051
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11118806/
Abstract

Senescent cells, which accumulate with age, exhibit a pro-inflammatory senescence-associated secretory phenotype (SASP) that includes the secretion of cytokines, lipids, and extracellular vesicles (EVs). Here, we established an in vitro model of senescence induced by Raf-1 oncogene in RAW 264.7 murine macrophages (MΦ) and compared them to senescent MΦ found in mouse lung tumors or primary macrophages treated with hydrogen peroxide. The transcriptomic analysis of senescent MΦ revealed an important inflammatory signature regulated by NFkB. We observed an increased secretion of EVs in senescent MΦ, and these EVs presented an enrichment for ribosomal proteins, major vault protein, pro-inflammatory miRNAs, including miR-21a, miR-155, and miR-132, and several mRNAs. The secretion of senescent MΦ allowed senescent murine embryonic fibroblasts to restart cell proliferation. This antisenescence function of the macrophage secretome may explain their pro-tumorigenic activity and suggest that senolytic treatment to eliminate senescent MΦ could potentially prevent these deleterious effects.

摘要

衰老细胞会随着年龄的增长而积累，表现出一种促炎性衰老相关分泌表型（SASP），其中包括细胞因子、脂质和细胞外囊泡（EVs）的分泌。在此，我们建立了一种由Raf-1癌基因诱导RAW 264.7小鼠巨噬细胞（MΦ）衰老的体外模型，并将其与在小鼠肺肿瘤中发现的衰老MΦ或用过氧化氢处理的原代巨噬细胞进行比较。对衰老MΦ的转录组分析揭示了一种由NFkB调节的重要炎症特征。我们观察到衰老MΦ中EVs的分泌增加，并且这些EVs富含核糖体蛋白、主要穹窿蛋白、促炎性miRNA，包括miR-21a、miR-155和miR-132，以及几种mRNA。衰老MΦ的分泌使衰老的小鼠胚胎成纤维细胞重新开始细胞增殖。巨噬细胞分泌组的这种抗衰老功能可能解释了它们的促肿瘤活性，并表明消除衰老MΦ的衰老细胞溶解疗法可能潜在地预防这些有害影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e8d/11118806/efbd93beb4bc/biomedicines-12-01089-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e8d/11118806/edaebe7fb839/biomedicines-12-01089-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e8d/11118806/648b58b333e7/biomedicines-12-01089-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e8d/11118806/a72fc15ddc19/biomedicines-12-01089-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e8d/11118806/84b1684b2873/biomedicines-12-01089-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e8d/11118806/efbd93beb4bc/biomedicines-12-01089-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e8d/11118806/edaebe7fb839/biomedicines-12-01089-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e8d/11118806/648b58b333e7/biomedicines-12-01089-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e8d/11118806/a72fc15ddc19/biomedicines-12-01089-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e8d/11118806/84b1684b2873/biomedicines-12-01089-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e8d/11118806/efbd93beb4bc/biomedicines-12-01089-g005.jpg

相似文献

[1]
Senescent Macrophages Release Inflammatory Cytokines and RNA-Loaded Extracellular Vesicles to Circumvent Fibroblast Senescence.

Biomedicines. 2024-5-14

[2]
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[3]
P-MSC-derived extracellular vesicles facilitate diabetic wound healing via miR-145-5p/ CDKN1A-mediated functional improvements of high glucose-induced senescent fibroblasts.

Burns Trauma. 2023-10-18

[4]
Small extracellular vesicles and their miRNA cargo are anti-apoptotic members of the senescence-associated secretory phenotype.

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[5]
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Geroscience. 2022-12

[6]
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[7]
Network of extracellular vesicles surrounding senescent cells.

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[8]
Extracellular vesicles from senescent hepatic stellate cells promote cell viability of hepatoma cells through increasing EGF secretion from differentiated THP-1 cells.

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[9]
Senescent human hepatocytes express a unique secretory phenotype and promote macrophage migration.

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[10]
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引用本文的文献

[1]
Senescent macrophages in cancer: roles in tumor progression and treatment opportunities.

Cancer Biol Med. 2025-5-6

[2]
Human dermal fibroblast senescence in response to single and recurring oxidative stress.

Front Aging. 2025-3-28

[3]
Anti-senescence therapies: a new concept to address cardiovascular disease.

Cardiovasc Res. 2025-5-23

[4]
The Dual Role of Cellular Senescence in Macrophages: Unveiling the Hidden Driver of Age-Related Inflammation in Kidney Disease.

Int J Biol Sci. 2025-1-1

[5]
Major Vault Protein/Lung Resistance-Related Protein: A Novel Biomarker for Inflammation and Acute Infections.

Microorganisms. 2024-8-25

本文引用的文献

[1]
Senescent alveolar macrophages promote early-stage lung tumorigenesis.

Cancer Cell. 2023-7-10

[2]
Clearance of senescent macrophages ameliorates tumorigenesis in KRAS-driven lung cancer.

Cancer Cell. 2023-7-10

[3]
Cellular senescence and senolytics: the path to the clinic.

Nat Med. 2022-8

[4]
Quantitative proteomics identifies the core proteome of exosomes with syntenin-1 as the highest abundant protein and a putative universal biomarker.

Nat Cell Biol. 2021-6

[5]
Hypoxia-induced microRNA-155 overexpression in extracellular vesicles promotes renal cell carcinoma progression by targeting .

Aging (Albany NY). 2021-3-19

[6]
JUNB-FBXO21-ERK axis promotes cartilage degeneration in osteoarthritis by inhibiting autophagy.

Aging Cell. 2021-2

[7]
miR-21a in exosomes from Lewis lung carcinoma cells accelerates tumor growth through targeting PDCD4 to enhance expansion of myeloid-derived suppressor cells.

Oncogene. 2020-8-27

[8]
Attenuation of epigenetic regulator SMARCA4 and ERK-ETS signaling suppresses aging-related dopaminergic degeneration.

Aging Cell. 2020-9

[9]
Senolytic CAR T cells reverse senescence-associated pathologies.

Nature. 2020-6-17

[10]
An emerging focus on lipids in extracellular vesicles.

Adv Drug Deliv Rev. 2020

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