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Cited by 22Telomeres, Telomerase, and SenescenceGenetics, Aging, and Longevity in Model OrganismsAutophagy in Disease and Therapy

Migrasomes trigger innate immune activation and mediate transmission of senescence signals across human cells

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Liu, Xiaoqian, Jiao, Haifeng, Zhang, Baohu, Zhang, Sheng, Yan, Kaowen, Qu, Jing, Zhang, Weiqi, Yu, Li +1 more·2023·Life Medicine
DOI 10.1093/lifemedi/lnad050PMC PMC11749555
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Abstract

Aging is a complex and heterogeneous process, raising important questions about how aging is differently impacted by underlying genetics and external factors. Recently, migrasomes, newly discovered organelles, have been identified to play important roles in various physiological and pathological processes by facilitating cell-to-cell communication. Thus far, their involvement in cellular senescence and aging remains largely unexplored. In this study, we aimed to investigate how migrasomes impact on cellular aging by leveraging multiple cellular senescence models, including replicatively senescent (RS), pathologically senescent and stress-induced senescent human mesenchymal stem cells (hMSCs), as well as RS human primary fibroblasts. In all cellular aging models, we detected an enhanced formation of migrasomes. Notably, migrasomes in senescent cells exhibited an accumulation of numerous aging hallmarks, such as dysfunctional mitochondria, endogenous retroviruses, and senescence-associated pro-inflammatory cytokines. Furthermore, we discovered that migrasomes derived from senescent cells can be taken up by young cells, thereby transferring aging signals and subsequently causing premature senescence phenotypes in recipient cells. Mechanistically, we found that treatment with migrasomes derived from senescent cells activated the innate immune response. Thus, our study sheds light on a pivotal role of migrasomes in mediating the contagiousness of aging.

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  • IgG induces senescence in macrophages derived from bone marrow, spleen, and peritoneal cavity, as indicated by increased SA-β-Gal activity, P21 expression, upregulated MMTV-positive cells, aggresome formation, and decreased H3K9me3 and lamin B1 levels.

    “Our data revealed that IgG induced senescence in these macrophages, as indicated by an increase in SA-β-Gal activity and P21 expression, along with upregulated MMTV-positive cells, aggresome formation, and decreased H3K9me3 and lamin B1 levels46”

    From Spatial transcriptomic landscape unveils immunoglobin-associated senescence as a hallmark of aging (2024) · cites this paper as [50]

    The Results section, “Migrasomes mediated the transfer of aging signals in a paracrine manner” (page unavailable), reports increased SA-β-gal positivity and p21 in human mesenchymal stem cells treated with migrasomes. It does not establish the claimed IgG effect in macrophages or report the specified MMTV-positive cells, aggresomes, H3K9me3, and lamin B1 changes. (LLM, conf=0.83)

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Cited by

Sorted by citations

Authors
Liu, X., Jiao, H., Zhang, B., Zhang, S., Yan, K., Qu, J., Zhang, W., Yu, L., & Liu, G.-H.
Affiliations
  • Chinese Academy of Sciences (CN)
  • Peking University (CN)
  • Capital Medical University (CN)
Corresponding author
  • Qu, Jing
  • Zhang, Weiqi
  • Yu, Li
  • Liu, Guang-Hui
ORCID
Venue
Life Medicine
Publisher
Oxford University Press (OUP)
Published
2023-12-01
Volume
2
Issue
6
Pages
lnad050-lnad050
ISSN
2755-1733 (ISSN-L)
DOI
10.1093/lifemedi/lnad050
PMC
PMC11749555
OpenAlex
W4389514288
Cited by
22
References
12
Citations by year
2026: 5 · 2025: 10 · 2024: 6 · 2023: 1
FWCI
3.89
Type
journal article
Language
en
Open access
Licence
Locations
  • Life Medicine (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Greater South Information System
Funders
  • National Natural Science Foundation of China (92168201, 32121001, 92149301, 32030023, 92049116, 81921006, 91949209, 92049304, YSBR-012, 82192863, 82125011, XDA16000000, 32330025)
  • Chinese Academy of Sciences (CAS-WX2021SF-0301, XDA16000000, YSBR-012, YSBR‐076, CAS-WX2021SF-0101, CAS-WX2022SDC-XK14)
  • Tsinghua University
  • National Key Research and Development Program of China ((2020YFA0112200, 2021YFF1201000, 2022YFA1103700, 2020YFA0804000)
  • Youth Innovation Promotion Association (E1CAZW0401)
  • Institute of Biophysics, Chinese Academy of Sciences
Topics
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
migrasomes, cellular senescence, aging, cell-to-cell communication, replicative senescence, stress-induced senescence, mesenchymal stem cells, fibroblasts, mitochondrial dysfunction, endogenous retroviruses, inflammatory cytokines, innate immune activation, premature senescence

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