Loss of lamin B1 is a biomarker to quantify cellular senescence in photoaged skin
Open accessAbstract
Skin ageing is an inevitable consequence of life and accelerated by exposure to ultraviolet (UV) rays. Senescence is an irreversible growth arrest and senescent cells accumulate in ageing tissues, at sites of age-related pathologies and in pre-neoplastic lesions. Conventionally, senescent cells have been detected by senescence associated-β-galactosidase (SA-β-gal) staining, a procedure that requires enzymatic activity, which is lost in fixed tissue samples. We previously demonstrated that loss of lamin B1 is a novel marker to identify senescent cells. Here, we demonstrate that loss of lamin B1 facilitates the detection and quantification of senescent cells upon UV-exposure in vitro and upon chronic UV-exposure and skin regeneration in vivo. Taken together, this marker enables the study of environmental conditions on tissue ageing and regeneration in vivo, serves as a diagnostic tool to distinguish senescent from proliferating cells in pre-neoplastic lesions, and facilitates investigating the role of senescent cells in various age-related pathologies.
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Repeated UVB exposure in human keratinocytes and mouse epidermis results in loss of LMNB1.
“Repeated UVB exposure in human keratinocytes and mouse epidermis results in loss of LMNB1 (ref. 217).”
From SenNet recommendations for detecting senescent cells in different tissues (2024) · cites this paper as [217]
The Results section reports lamin B1 loss in human keratinocytes after UVB exposure and in mouse epidermis after irradiation for 10 consecutive days. The Methods describe a single irradiation of the keratinocyte cultures, so the source does not support repeated UVB exposure in human keratinocytes. (LLM, conf=0.88)
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- [3]He S Sharpless NE Senescence in Health and Disease Cell 2017 169 1000 1011 10.1016/j.cell.2017.05.015 28575665 PMC5643029 · DOI · Paper page
- [4]Ivanov A Lysosome-mediated processing of chromatin in senescence J. Cell Biol. 2013 202 129 143 10.1083/jcb.201212110 23816621 PMC3704985 · DOI · Paper page
- [5]Michaloglou C BRAFE600-associated senescence-like cell cycle arrest of human naevi Nature 2005 436 720 724 10.1038/nature03890 16079850 · DOI · Paper page
- [6]Dimri GP A biomarker that identifies senescent human cells in culture and in aging skin in vivo Proc Natl Acad Sci 1995 92 9363 9367 10.1073/pnas.92.20.9363 7568133 PMC40985 · DOI · Paper page
- [8]Kuilman T Michaloglou C Mooi WJ Peeper DS The essence of senescence Genes and Development 2010 24 2463 2479 10.1101/gad.1971610 21078816 PMC2975923 · DOI · Paper page
- [10]Dreesen O Lamin B1 fluctuations have differential effects on cellular proliferation and senescence J. Cell Biol. 2013 200 605 617 10.1083/jcb.201206121 23439683 PMC3587829 · DOI · Paper page
- [11]Dreesen O Ong PF Chojnowski A Colman A The contrasting roles of lamin B1 in cellular aging and human disease Nucleus 2013 4 283 90 10.4161/nucl.25808 23873483 PMC3810336 · DOI
- [12]Freund A Laberge R-M Demaria M Campisi J Lamin B1 loss is a senescence-associated biomarker Mol. Biol. Cell 2012 23 2066 75 10.1091/mbc.E11-10-0884 22496421 PMC3364172 · DOI · Paper page
- [13]Shimi T The role of nuclear lamin B1 in cell proliferation and senescence Genes Dev. 2011 25 2579 2593 10.1101/gad.179515.111 22155925 PMC3248680 · DOI · Paper page
- [14]Chojnowski A Progerin reduces LAP2??-telomere association in hutchinson-gilford progeria Elife 2015 4 1 21 10.7554/eLife.07759 PMC4565980 26312502 · DOI
- [15]Taimen P A progeria mutation reveals functions for lamin A in nuclear assembly, architecture, and chromosome organization Proc. Natl. Acad. Sci. USA 2009 106 20788 20793 10.1073/pnas.0911895106 19926845 PMC2779830 · DOI
- [17]Debacq-Chainiaux F Leduc C Verbeke A Toussaint O UV, stress and aging Dermatoendocrinol. 2012 4 236 240 10.4161/derm.23652 23467762 PMC3583883 · DOI · Paper page
- [18]Chou WC Direct migration of follicular melanocyte stem cells to the epidermis after wounding or UVB irradiation is dependent on Mc1r signaling Nat Med 2013 19 924 929 10.1038/nm.3194 23749232 PMC3859297 · DOI
- [19]Lin S-T Heng MY Ptáček LJ Fu Y-H Regulation of Myelination in the Central Nervous System by Nuclear Lamin B1 and Non-coding RNAs Transl. Neurodegener. 2014 3 4 10.1186/2047-9158-3-4 24495672 PMC3937061 · DOI · Paper page
- [20]Dou Z Autophagy mediates degradation of nuclear lamina Nature 2015 527 105 109 10.1038/nature15548 26524528 PMC4824414 · DOI · Paper page
- [21]Shah PP Lamin B1 depletion in senescent cells triggers large-scale changes in gene expression and the chromatin landscape Genes Dev. 2013 27 1787 1799 10.1101/gad.223834.113 23934658 PMC3759695 · DOI · Paper page
- [22]Sadaie M Redistribution of the Lamin B1 genomic binding profile affects rearrangement of heterochromatic domains and SAHF formation during senescence Genes Dev. 2013 27 1800 1808 10.1101/gad.217281.113 23964094 PMC3759696 · DOI · Paper page
- [23]Chandra T Global reorganization of the nuclear landscape in senescent cells Cell Rep. 2015 10 471 484 10.1016/j.celrep.2014.12.055 25640177 PMC4542308 · DOI · Paper page
- [24]Shin, J. W. et al. The co-expression pattern of p63 and HDAC1: A potential way to disclose stem cells in interfollicular epidermis. Int. J. Mol. Sci. 18 (2017). PMC5535853 28672879
- [25]Keyes WM Mills AA A new link between senescence and aging Cell Cycle 2006 5 260 265 10.4161/cc.5.3.2415 16434880 · DOI
- [26]Liefer KM Down-regulation of p63 is required for epidermal UV-B-induced apoptosis Cancer Res. 2000 60 4016 4020 10945600
- [27]Rapisarda, V. et al. p63 transcription factor regulates nuclear shape and expression of nuclear envelope-associated genes in epidermal keratinocytes. J. Invest. Dermatol. 10.1016/j.jid.2017.05.013 (2017). PMC5610935 28595999 · DOI
- [28]Keyes WM p63 deficiency activates a program of cellular senescence and leads to accelerated aging Genes Dev. 2005 19 1986 1999 10.1101/gad.342305 16107615 PMC1199570 · DOI
- [29]Agin PP Rose AP Lane CC Akin FJ Sayre RM Changes in epidermal forward scattering absorption after UVA or UVA-UVB irradiation J. Invest. Dermatol. 1981 76 174 177 10.1111/1523-1747.ep12525676 7240785 · DOI
- [30]Pearse aD Gaskell SA Marks R Epidermal changes in human skin following irradiation with either UVB or UVA J. Invest. Dermatol. 1987 88 83 7 10.1111/1523-1747.ep12465094 3794392 · DOI
- [31]Sagelius H Targeted transgenic expression of the mutation causing Hutchinson-Gilford progeria syndrome leads to proliferative and degenerative epidermal disease J. Cell Sci. 2008 121 969 978 10.1242/jcs.022913 18334552 · DOI
- [32]McKenna T Embryonic expression of the common progeroid lamin A splice mutation arrests postnatal skin development Aging Cell 2014 13 292 302 10.1111/acel.12173 24305605 PMC4331787 · DOI
- [33]Mounkes LC Kozlov S Hernandez L Sullivan T Stewart CL A progeroid syndrome in mice is caused by defects in A-type lamins Nature 2003 423 298 301 10.1038/nature01631 12748643 · DOI
- [34]Solovei I LBR and lamin A/C sequentially tether peripheral heterochromatin and inversely regulate differentiation Cell 2013 152 584 598 10.1016/j.cell.2013.01.009 23374351 · DOI · Paper page
- [35]Hanif, M., Rosengardten, Y., Sagelius, H., Rozell, B. & Eriksson, M. Differential expression of A-type and B-type lamins during hair cycling. PLoS One4, (2009). PMC2606029 19122810
- [36]Zhang J A human iPSC model of hutchinson gilford progeria reveals vascular smooth muscle and mesenchymal stem cell defects Cell Stem Cell 2011 8 31 45 10.1016/j.stem.2010.12.002 21185252 · DOI
- [37]Swift J Nuclear Lamin-A Scales with Tissue Stiffness and Enhances Matrix-Directed Differentiation Science (80-.). 2013 341 1240104 1240104 10.1126/science.1240104 PMC3976548 23990565 · DOI
- [38]Constantinescu D Gray HL Sammak PJ Schatten GP Csoka AB Lamin A/C expression is a marker of mouse and human embryonic stem cell differentiation Stem Cells 2006 24 177 85 10.1634/stemcells.2004-0159 16179429 · DOI
- [39]Debacq-Chainiaux F Erusalimsky JD Campisi J Toussaint O Protocols to detect senescence-associated beta-galactosidase (SA-betagal) activity, a biomarker of senescent cells in culture and in vivo Nat. Protoc. 2009 4 1798 806 10.1038/nprot.2009.191 20010931 · DOI · Paper page
- [40]Jensen KB Driskell RR Watt FM Assaying proliferation and differentiation capacity of stem cells using disaggregated adult mouse epidermis Nat. Protoc. 2010 5 898 911 10.1038/nprot.2010.39 20431535 · DOI · Paper page
- Authors
- Wang, A. S., Ong, P. F., Chojnowski, A., Clavel, C., & Dreesen, O.
- Affiliations
- Institute of Medical Biology (SG)
- Corresponding author
- Clavel, Carlos
- Dreesen, Oliver
- Venue
- Scientific Reports
- Published
- 2017-11-15
- Volume
- 7
- Issue
- 1
- Pages
- 15678-15678
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC5688158
- OpenAlex
- W2767885122
- Cited by
- 131
- References
- 42
- Citations by year
- 2026: 8 · 2025: 20 · 2024: 19 · 2023: 19 · 2022: 14 · 2021: 19 · 2020: 23 · 2019: 8 · 2018: 1
- FWCI
- 6.48
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Biomedical Research Council
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- lamin B1, cellular senescence, photodamaged skin, skin aging, UV exposure, senescence biomarkers, senescence-associated β-galactosidase, skin regeneration, pre-neoplastic lesions, age-related diseases
- MeSH terms
- beta-Galactosidase, Humans, Regeneration, Skin, Ultraviolet Rays, Biomarkers, Skin Aging, Keratinocytes, Cellular Senescence, Lamin Type B, Cell Proliferation, Primary Cell Culture
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