ArticleThe journals of gerontology. Series A, Biological sciences and medical sciences2013
Small molecule inhibition of p38 MAP kinase extends the replicative life span of human ATR-Seckel syndrome fibroblasts.
Article in The journals of gerontology. Series A, Biological sciences and medical sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Isolating and Validating Fibroblast-like Cells from the Skeletal Muscle of the Siamese Crocodile (Veterinary sciences · 2026Article
- Protein expression of nucleolar protein 12 in the retina and its implication in protection of retina from UV irradiation damage.Cell death discovery · 2024Article
- p16Frontiers in immunology · 2021Article
- CSB promoter downregulation via histone H3 hypoacetylation is an early determinant of replicative senescence.Nature communications · 2019Article
- Mapping out p38MAPK.American journal of reproductive immunology (New York, N.Y. : 1989) · 2017Review
- Article
- ATR-mediated regulation of nuclear and cellular plasticity.DNA repair · 2016Review
- Hallmarks of progeroid syndromes: lessons from mice and reprogrammed cells.Disease models & mechanisms · 2016Review
- Primordial dwarfism: overview of clinical and genetic aspects.Molecular genetics and genomics : MGG · 2016Review
- Nijmegen breakage syndrome fibroblasts expressing the C-terminal truncated NBN(p70) protein undergo p38/MK2-dependent premature senescence.Biogerontology · 2015Article
- Rejuvenation of the muscle stem cell population restores strength to injured aged muscles.Nature medicine · 2014Article
- Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Ataxia-telangiectasia and rad3 (ATR)-related Seckel syndrome is associated with growth retardation and premature aging features. ATR-Seckel fibroblasts have a reduced replicative capacity in vitro and an aged morphology that is associated with activation of stress-associated p38 mitogen-activated protein kinase and phosphorylated HSP27. These phenotypes are prevented using p38 inhibitors, with replicative capacity restored to the normal range. However, this stressed phenotype is retained in telomerase-immortalized ATR-Seckel fibroblasts, indicating that it is independent of telomere erosion. As with normal fibroblasts, senescence in ATR-Seckel is bypassed by p53 abrogation. Young ATR-Seckel fibroblasts show elevated levels of p21(WAF1), p16(INK4A), phosphorylated actin-binding protein cofilin, and phosphorylated caveolin-1, with small molecule drug inhibition of p38 reducing p16(INK4A) and caveolin-1 phosphorylation. In conclusion, ATR-Seckel fibroblasts undergo accelerated aging via stress-induced premature senescence and p38 activation that may underlie certain clinical features of Seckel syndrome, and our data suggest a novel target for pharmacological intervention in this human syndrome.
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