ArticleExperimental dermatology2010
Proliferative defects in dyskeratosis congenita skin keratinocytes are corrected by expression of the telomerase reverse transcriptase, TERT, or by activation of endogenous telomerase through expression of papillomavirus E6/E7 or the telomerase RNA component, TERC.
Article in Experimental dermatology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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24 citing papers in PubMed, 40 citations in OpenAlex.
- Article
- Identification of functional non-coding variants associated with orofacial cleft.Nature communications · 2025Article
- Multiple cell types support productive infection and dynamic translocation of infectious Ebola virus to the surface of human skin.Science advances · 2025Article
- Telomeres and Telomerase in the Control of Stem Cells.Biomedicines · 2022Review
- Tieing together loose ends: telomere instability in cancer and aging.Molecular oncology · 2022Review
- Human Keratinocyte Response to Superantigens.mSphere · 2020Article
- The potential of RNA as a target for national screening of pre-cancer.Journal of public health in Africa · 2018Article
- Differential Activation of Human Keratinocytes by Leishmania Species Causing Localized or Disseminated Disease.The Journal of investigative dermatology · 2017Article
- Effects of PCB126 and PCB153 on telomerase activity and telomere length in undifferentiated and differentiated HL-60 cells.Environmental science and pollution research international · 2016Article
- Novel Staphylococcus aureus Secreted Protein Alters Keratinocyte Proliferation and Elicits a Proinflammatory Response In Vitro and In Vivo.Biochemistry · 2015Article
- PCB126 inhibits adipogenesis of human preadipocytes.Toxicology in vitro : an international journal published in association with BIBRA · 2015Article
- Ectopic expression of Zmiz1 induces cutaneous squamous cell malignancies in a mouse model of cancer.The Journal of investigative dermatology · 2013Article
- Staphylococcal superantigens stimulate immortalized human adipocytes to produce chemokines.PloS one · 2013Article
- Article
- Article
- Dyskeratosis Congenita Dermal Fibroblasts are Defective in Supporting the Clonogenic Growth of Epidermal Keratinocytes.Aging and disease · 2012Article
- Three novel truncating TINF2 mutations causing severe dyskeratosis congenita in early childhood.Clinical genetics · 2012Article
- Native gel electrophoresis of human telomerase distinguishes active complexes with or without dyskerin.Nucleic acids research · 2012Article
- The role of telomeres in the ageing of human skin.Experimental dermatology · 2011Review
- The p53/p21(WAF/CIP) pathway mediates oxidative stress and senescence in dyskeratosis congenita cells with telomerase insufficiency.Antioxidants & redox signaling · 2011Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Dyskeratosis congenita (DC) is characterized by the triad of reticulate skin pigmentation, nail dystrophy and leukoplakia. Epidermal atrophy, hair growth defects, bone marrow failure and increased risk of cancer are also common in DC patients. DC is caused by mutations in genes encoding for telomerase complex factors. Although there is an association of epidermal abnormalities with DC, epidermal cells from DC donors have not been previously characterized. We have isolated skin keratinocytes from affected members of a family with an autosomal dominant form of DC that is caused by a mutation in the RNA component of telomerase, TERC. Here, we demonstrate that, similar to DC fibroblasts from these donors, DC keratinocytes have short telomeres and a short lifespan. DC keratinocytes also exhibited impaired colony forming efficiency (CFE) and migration capacity. Exogenous expression of the reverse transcriptase (RT) component of telomerase, TERT, activated telomerase levels to half that of TERT expressing normal cells and maintained telomeres at a short length with concomitant extension of lifespan. Unlike fibroblasts, transduction of human papillomavirus type 16 E6/E7 genes into DC keratinocytes activated telomerase to half that of E6/E7 expressing normal cells, and robust proliferation was observed. While expression of TERC has no measurable effect on telomerase in fibroblasts, expression of TERC in keratinocytes upregulated telomerase activity and, rarely, allowed rescue of proliferative defects. Our results point to important differences between DC fibroblasts and keratinocytes and show, for the first time, that expression of TERC can increase the lifespan of primary human epithelial cells.
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