Senescence associated secretory phenotype profile from primary lung mice fibroblasts depends on the senescence induction stimuli.
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Cellular senescence is a multifactorial phenomenon of growth arrest and distorted function, which has been recognized as an important feature during tumor suppression mechanisms and a contributor to aging. Senescent cells have an altered secretion pattern called Senescence-Associated Secretory Phenotype (SASP) that comprises a complex mix of factors including cytokines, growth factors, chemokines, and matrix metalloproteinases. SASP has been related with local inflammation that leads to cellular transformation and neurodegenerative diseases. Various pathways for senescence induction have been proposed; the most studied is replicative senescence due to telomere attrition called replicative senescence (RS). However, senescence can be prematurely achieved when cells are exposed to diverse stimuli such as oxidative stress (stress-induced premature senescence, SIPS) or proteasome inhibition (proteasome inhibition-induced premature senescence, PIIPS). SASP has been characterized in RS and SIPS but not in PIIPS. Hence, our aim was to determine SASP components in primary lung fibroblasts obtained from CD-1 mice induced to senescence by PIIPS and compare them to RS and SIPS. Our results showed important variations in the 62 cytokines analyzed, while SIPS and RS showed an increase in the secretion of most cytokines, and in PIIPS only 13 were incremented. Variations in glutathione-redox balance were also observed in SIPS and RS, and not in PIIPS. All senescence types SASP displayed a pro-inflammatory profile and increased proliferation in L929 mice fibroblasts exposed to SASP. However, the behavior observed was not exactly the same, suggesting that the senescence induction pathway might encompass dissimilar responses in adjacent cells and promote different outcomes.
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The senescence-associated secretory phenotype involves senescent cells secreting pro-inflammatory factors that may propagate senescence and dysregulated signalling in neighbouring cells, potentially disrupting tissue homeostasis.
“A notable feature of ageing is the senescence-associated secretory phenotype (SASP), wherein senescent cells secrete pro-inflammatory factors that may propagate senescence and dysregulated signalling in neighbouring cells, potentially disrupting tissue homeostasis [7].”
From Quantitative profiling of lifespan-dependent cell-cell communication potential reveals dynamic ligand-receptor network shifts across mouse tissues (2026) · cites this paper as [7]
The Introduction (page not available) defines SASP as secretion of factors with paracrine activity and says accumulated SASP can alter the cellular microenvironment and tissue structure. The Discussion (page not available) reports effects on adjacent cells. However, our copy does not say that SASP propagates senescence to neighbouring cells; the measured adjacent-cell effect was increased proliferation in a transformed cell line. (LLM, conf=0.84)
Experimental — accuracy not yet measuredp21 and p16 are both associated with the induction of senescence, but they do not always occur together in senescence.
“p21 and p16 are both associated with the induction of senescence, but they do not always occur together in senescence. Multiple in vitro studies have shown that their presence and expression can vary depending on the senescence-inducing stimuli, the cell type, and the specific context (Maciel-Barón et al, 2016).”
From Distinct senotypes in p16- and p21-positive cells across human and mouse aging tissues (2025) · cites this paper as Maciel-Barón et al, 2016
The Introduction (page unavailable) describes p53/p21 and/or pRB/p16 as pathways to senescence, supporting the point that both are associated with senescence but need not occur together. The study measures p16 and β-galactosidase in mouse lung fibroblasts under different senescence-inducing conditions; it does not measure p21 or establish how p21 and p16 expression varies by stimulus or cell type. (LLM, conf=0.82)
Experimental — accuracy not yet measuredAged 3xTg-AD male mice exhibit elevated plasma levels of known SASP factors, including IL-12, IL-10, IL-6, CXCL2, CXCL1, and G-CSF.
“We showed that aged 3xTg-AD male mice in particular, exhibit elevated plasma levels of known SASP factors [65, 66], including IL-12, IL-10, IL-6, CXCL2, CXCL1, and G-CSF”
From Age, sex and Alzheimer’s disease: a longitudinal study of 3xTg-AD mice reveals sex-specific disease trajectories and inflammatory responses mirrored in postmortem brains from Alzheimer’s patients (2024) · cites this paper as [65]
The Results section (page unavailable) identifies IL-6, IL-12, IL-10, and MIP-2 as studied SASP components; the Introduction also lists GROα. The citation follows “known SASP factors,” so the citing authors’ statement about plasma levels in aged 3xTg-AD mice is not attributed to this source. Our copy does not identify G-CSF as a SASP factor, leaving the full list only partly supported. (LLM, conf=0.84)
Experimental — accuracy not yet measuredSASP composition and strength varies substantially depending on inducer of senescence, duration, environment and cell type.
“The SASP composition and strength varies substantially, depending on the inducer of senescence, duration of senescence, environment and cell type (Coppé et al., 2008, 2011; Maciel-Barón et al., 2016).”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Maciel-Barón et al., 2016
The SASP can vary significantly in terms of the quantity and quality of secreted proteins and other factors, depending on the insult used to trigger cell senescence.
“However, we must to understand that the SASP can vary significantly in terms of the quantity and quality of secreted proteins and other factors, depending on the insult used to trigger cell senescence (Maciel‐Baron et al., 2016; Wiley et al., 2016); therefore, the composition of the SASP may be vary depending on the tissue and the insult.”
From Rapamycin inhibits the secretory phenotype of senescent cells by a Nrf2-independent mechanism (2017) · cites this paper as Maciel‐Baron et al., 2016
The composition and intensity of the SASP response can be affected by the senescence-inducing mechanism, cell type, and time since senescence initiation, indicating that there is no singular SASP.
“The composition and intensity of the SASP response can be affected by several factors including the senescence-inducing mechanism, cell type, and the amount of time passed since senescence initiation, indicating that there is no singular SASP.12–17”
From Paracrine roles of cellular senescence in promoting tumourigenesis (2018) · cites this paper as [13]
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Distinct senotypes in p16- and p21-positive cells across human and mouse aging tissues
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Mine, Y., Takahashi, T., & Okamoto, T. (2021) · Journal of Clinical Biochemistry and Nutrition · doi:10.3164/jcbn.20-185 · Cited by 5 · see citing works
Wei, B., Troendle, E. P., Simpson, D. A., & Stitt, A. W. (2026) · PLoS ONE · doi:10.1371/journal.pone.0345045
- Authors
- Maciel-Barón, L. A., Morales-Rosales, S. L., Aquino-Cruz, A. A., Triana-Martínez, F., Galván-Arzate, S., Luna-López, A., González-Puertos, V. Y., López-Díazguerrero, N. E., Torres, C., & Königsberg, M.
- Affiliations
- Universidad Autónoma Metropolitana (MX)
- Drexel University (US)
- Corresponding author
- Königsberg, Mina
- Venue
- AGE
- Published
- 2016-02
- Volume
- 38
- Issue
- 1
- Pages
- 26-26
- ISSN
- 0161-9152 (ISSN-L)
- 1574-4647
- PMC
- PMC5005892
- OpenAlex
- W2328126338
- Cited by
- 128
- References
- 59
- Citations by year
- 2026: 7 · 2025: 10 · 2024: 24 · 2023: 16 · 2022: 9 · 2021: 10 · 2020: 11 · 2019: 9 · 2018: 11 · 2017: 14 · 2016: 6 · 2015: 1
- FWCI
- 10.72
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- AGE (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- CONACYT (CB-2012-1-178349)
- Red tematica de enevejecimiento, salud y desarrollo (without number)
- INGER (DI-PI004/2012)
- 1RO (1RO1NS078283)
- R2 (R21AG046943)
- Commonwealth of Pennsylvania Universal Research Enhancement Grant (no number)
- CONACYT scholarship (265781)
- 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 › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Keywords
- senescence-associated secretory phenotype, cellular senescence, replicative senescence, stress-induced premature senescence, lung fibroblasts, cytokine production, glutathione redox balance, L929 fibroblasts
- MeSH terms
- Aging, Animals, Animals, Newborn, Cells, Cultured, DNA Damage, Fibroblasts, Lung, Phenotype, Cytokines, Telomere, Cellular Senescence, Oxidative Stress, Cell Proliferation, Mice
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