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Cited by 144

The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.

Nuclear envelope defects cause stem cell dysfunction in premature-aging mice

Espada, Jesús, Varela, Ignacio, Flores, Ignacio, Ugalde, Alejandro P., Cadiñanos, Juan, Pendás, Alberto M., Stewart, Colin L., Tryggvason, Karl, Blasco, María A., Freije, José M.P., López-Otín, Carlos·2008·The Journal of Cell Biology
DOI 10.1083/jcb.200801096PMC PMC2287278
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Abstract

Nuclear lamina alterations occur in physiological aging and in premature aging syndromes. Because aging is also associated with abnormal stem cell homeostasis, we hypothesize that nuclear envelope alterations could have an important impact on stem cell compartments. To evaluate this hypothesis, we examined the number and functional competence of stem cells in Zmpste24-null progeroid mice, which exhibit nuclear lamina defects. We show that Zmpste24 deficiency causes an alteration in the number and proliferative capacity of epidermal stem cells. These changes are associated with an aberrant nuclear architecture of bulge cells and an increase in apoptosis of their supporting cells in the hair bulb region. These alterations are rescued in Zmpste24−/−Lmna+/− mutant mice, which do not manifest progeroid symptoms. We also report that molecular signaling pathways implicated in the regulation of stem cell behavior, such as Wnt and microphthalmia transcription factor, are altered in Zmpste24−/− mice. These findings establish a link between age-related nuclear envelope defects and stem cell dysfunction.

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Crossref · 10.1083/jcb.200801096

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  • Stress pathways elicited by aberrations in the nuclear lamina characteristic of HGPS include activation of p53, deregulation of the somatotrophic axis, and attrition of adult stem cells.

    “These pathways include the activation of p53 (Varela et al., 2005), deregulation of the somatotrophic axis (Marino et al., 2010), and attrition of adult stem cells (Espada et al., 2008; Scaffidi and Misteli, 2008).”

    From The Hallmarks of Aging (2013) · cites this paper as Espada et al., 2008

    The Results and discussion report impaired proliferative capacity of adult epidermal stem cells in Zmpste24-deficient mice, supporting stem-cell dysfunction linked to nuclear-envelope defects. But the same section reports an increase—not attrition—in stem-cell markers in the hair-follicle bulge. This citation is attached only to the adult-stem-cell part of the sentence, not the p53 or somatotrophic-axis claims. (LLM, conf=0.87)

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Research works printed but not linked: 29

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Metadata

Authors
Espada, J., Varela, I., Flores, I., Ugalde, A. P., Cadiñanos, J., Pendás, A. M., Stewart, C. L., Tryggvason, K., Blasco, M. A., Freije, J. M. P., & López-Otín, C.
Affiliations
  • 1Departamento de Bioquímica y Biología Molecular, Facultad de Medicina, Instituto Universitario de Oncología, Universidad de Oviedo, 33006 Oviedo, Spain
  • 2Telomeres and Telomerase Group, Molecular Oncology Program, Spanish National Cancer Research Center, 28029 Madrid, Spain
  • 3National Cancer Institute, Frederick, MD 21702
  • 4Division of Matrix Biology, Department of Biochemistry and Biophysics, Karolinska Institutet, SE-171 77 Stockholm, Sweden
Venue
The Journal of Cell Biology
Publisher
Rockefeller University Press
Published
2008-03-31
Volume
181
Issue
1
Pages
27-35
ISSN
  • 1540-8140
  • 0021-9525
DOI
10.1083/jcb.200801096
PMC
PMC2287278
Cited by
144
References
8
Language
en

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