Lamin B1 fluctuations have differential effects on cellular proliferation and senescence
Open accessAbstract
The nuclear lamina consists of A- and B-type lamins. Mutations in LMNA cause many human diseases, including progeria, a premature aging syndrome, whereas LMNB1 duplication causes adult-onset autosomal dominant leukodystrophy (ADLD). LMNB1 is reduced in cells from progeria patients, but the significance of this reduction is unclear. In this paper, we show that LMNB1 protein levels decline in senescent human dermal fibroblasts and keratinocytes, mediated by reduced transcription and inhibition of LMNB1 messenger ribonucleic acid (RNA) translation by miRNA-23a. This reduction is also observed in chronologically aged human skin tissue. To determine whether altered LMNB1 levels cause senescence, we either increased or reduced LMNB1. Both LMNB1 depletion and overexpression inhibited proliferation, but only LMNB1 overexpression induced senescence, which was prevented by telomerase expression or inactivation of p53. This phenotype was exacerbated by a simultaneous reduction of LMNA/C. Our results demonstrate that altering LMNB1 levels inhibits proliferation and are relevant to understanding the molecular pathology of ADLD.
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Reduction of LMNB1 has been confirmed in various senescent cell types.
“Since then, several studies have confirmed the reduction of LMNB1 in various senescent cell types (Barascu et al. 2012; Freund et al. 2012; Dreesen et al. 2013; Sadaie et al. 2013; Shah et al. 2013).”
From Cellular senescence and its effector programs (2014) · cites this paper as Dreesen et al. 2013
The fine balance between LMNB1 and LMNA may be differentially perturbed depending on the system.
“In addition to the aforementioned dual role of ROS in proliferation depending on its levels, the fine balance between LMNB1 and LMNA may also be differentially perturbed depending on the system (Hutchison 2012; Dreesen et al. 2013).”
From Cellular senescence and its effector programs (2014) · cites this paper as Dreesen et al. 2013
Overexpression of LMNB1 either delays or enhances senescence or exhibits minimal effect on proliferation, depending on study.
“Compared with LMNB1 depletion, phenotypes induced by ectopic LMNB1 were more heterogeneous between studies: Overexpression of LMNB1 either delays (Shimi et al. 2011) or enhances senescence (Barascu et al. 2012; Dreesen et al. 2013) or exhibits a minimal effect on proliferation (Sadaie et al. 2013).”
From Cellular senescence and its effector programs (2014) · cites this paper as Dreesen et al. 2013
RNAi-mediated depletion of LMNB1 is associated with reduced cell proliferation to various degrees in most studies.
“However, RNAi-mediated depletion of LMNB1 appears to be associated with reduced cell proliferation to various degrees in most (Shimi et al. 2011; Dreesen et al. 2013; Sadaie et al. 2013; Shah et al. 2013).”
From Cellular senescence and its effector programs (2014) · cites this paper as Dreesen et al. 2013
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- Authors
- Dreesen, O., Chojnowski, A., Ong, P. F., Zhao, T. Y., Common, J. E., Lunny, D., Lane, E. B., Lee, S. J., Vardy, L. A., Stewart, C. L., & Colman, A.
- Affiliations
- Institute of Medical Biology (SG)
- National University of Singapore (SG)
- Corresponding author
- Dreesen, Oliver
- Colman, Alan
- ORCID
- Venue
- Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2013-02-25
- Volume
- 200
- Issue
- 5
- Pages
- 605-617
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC3587829
- OpenAlex
- W2154140726
- Cited by
- 250
- References
- 6
- Citations by year
- 2026: 17 · 2025: 15 · 2024: 16 · 2023: 23 · 2022: 22 · 2021: 25 · 2020: 18 · 2019: 18 · 2018: 16 · 2017: 8 · 2016: 14 · 2015: 23 · 2014: 27 · 2013: 8
- FWCI
- 10.76
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Cell Biology (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- lamin B1, nuclear lamina, cellular senescence, cell proliferation, Hutchinson-Gilford progeria syndrome, lamin A/C, autosomal dominant leukodystrophy, protein synthesis inhibition, telomerase, p53, dermal fibroblasts, keratinocytes, skin aging
- MeSH terms
- Cell Differentiation, Cells, Cultured, DNA Damage, DNA-Binding Proteins, Fibroblasts, Genotype, Humans, Membrane Proteins, Phenotype, RNA, Messenger, Time Factors, Transcription, Genetic, Transfection, Down-Regulation, Skin Aging, Keratinocytes, Up-Regulation, Tumor Suppressor Protein p53, Cellular Senescence, Telomerase, Pelizaeus-Merzbacher Disease, RNA Interference, Nuclear Lamina, Lamin Type A, Lamin Type B, MicroRNAs, Cell Proliferation
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