The telomeric length and heterogeneity decrease with age in normal human oral keratinocytes

Kang, Mo K.; Swee, Jerry; Kim, Reuben H.; Baluda, M A; Park, No-Hee

doi:10.1016/s0047-6374(01)00407-9

Cited by 21 publications

(12 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Interestingly, EMT conversion in NHEK by ⌬Np63␣ led to telomere length extension in the absence of telomerase activation. This observation may be viewed as an appearance of the EMT phenotype because mesenchymal cells generally have longer telomeres than do epithelial cells (43). Because telomere length appeared to be elongated in NHEK/ ⌬Np63␣-M cells compared with that of parental NHEK in the absence of telomerase activation, EMT may have occurred selectively in cells that possessed longer telomeres, such as undifferentiated keratinocyte stem cells.…”

Section: Discussionmentioning

confidence: 99%

ΔNp63α Protein Triggers Epithelial-Mesenchymal Transition and Confers Stem Cell Properties in Normal Human Keratinocytes

Kim

Shin

et al. 2011

Journal of Biological Chemistry

Self Cite

View full text Add to dashboard Cite

Background: ⌬Np63␣ is an isoform of p63 that is predominantly expressed in normal epidermis. Results: Retroviral transduction of ⌬Np63␣ into rapidly proliferating primary human epidermal keratinocytes led to epithelialmesenchymal transition (EMT) and acquisition of stemlike properties. Conclusion: ⌬Np63␣ regulates EMT in primary human keratinocytes in a TGF-␤-dependent manner. Significance: Altering p63 level in NHEK may be a novel method to generate "induced mesenchymal stem cells" with multipotent capacity.

show abstract

Section: Discussionmentioning

confidence: 99%

ΔNp63α Protein Triggers Epithelial-Mesenchymal Transition and Confers Stem Cell Properties in Normal Human Keratinocytes

Kim

Shin

et al. 2011

Journal of Biological Chemistry

Self Cite

View full text Add to dashboard Cite

show abstract

“…We measured telomere length in both the epidermis and the dermis and found that the telomere length in the dermis was longer than in the epidermis. A previous study using oral mucosa [13] showed that the telomere length of exponentially replicating oral keratinocytes explanted from 28 donors between the ages of 21 and 84 yr was significantly shorter than that of normal human oral fibroblasts (5.3 AE 0.8 kbp versus 8.9 AE 1.0 kbp). Although the dermis is composed of various types of cells including endothelial cells, inflammatory cells and fibroblasts, fibroblasts are the major source of dermal DNA, thus our results showing the longer telomere length in the dermis agree well with this study of oral mucosa.…”

Section: Discussionmentioning

confidence: 89%

Telomere length of the skin in association with chronological aging and photoaging

Sugimoto¹,

Yamashita²,

Ueda

2006

Journal of Dermatological Science

View full text Add to dashboard Cite

“…Interestingly, the senescenceassociated loss of telomerase activity in vitro is not paralleled by the shortening of telomeres, or the accumulation of p53 or p16 [84]. However in vivo both telomerase activity and telomere length in the epidermis are reduced with age [85,86].…”

Section: Skin Ageingmentioning

confidence: 99%

Telomeres as Biomarkers for Ageing and Age-Related Diseases

Zglinicki¹,

Martin-Ruiz²

2005

CMM

353

232

View full text Add to dashboard Cite

Telomeres in telomerase-negative cells shorten during DNA replication in vitro due to numerous causes including the inability of DNA polymerases to fully copy the lagging strand, DNA end processing and random damage, often caused by oxidative stress. Short telomeres activate replicative senescence, an irreversible cell cycle arrest. Thus, telomere length is an indicator of replicative history, of the probability of cell senescence, and of the cumulative history of oxidative stress. Telomeres in most human cells shorten during ageing in vivo as well, suggesting that telomere length could be a biomarker of ageing and age-related morbidity. There are two distinct possibilities: First, in a tissue-specific fashion, short telomeres might indicate senescence of (stem) cells, and this might contribute to age-related functional attenuation in this tissue. Second, short telomeres in one tissue might cause systemic effects or might simply indicate a history of high stress and damage in the individual and could thus act as risk markers for age-related disease residing in a completely different tissue. In recent years, data have been published to support both approaches, and we will review these. While they together paint a fairly promising picture, it needs to be pointed out that until now most of the evidence is correlative, that much of it comes from underpowered studies, and that causal evidence for essential pathways, for instance for the impact of cell senescence on tissue ageing in vivo, is still very weak.

show abstract

The telomeric length and heterogeneity decrease with age in normal human oral keratinocytes

Cited by 21 publications

References 28 publications

ΔNp63α Protein Triggers Epithelial-Mesenchymal Transition and Confers Stem Cell Properties in Normal Human Keratinocytes

ΔNp63α Protein Triggers Epithelial-Mesenchymal Transition and Confers Stem Cell Properties in Normal Human Keratinocytes

Telomere length of the skin in association with chronological aging and photoaging

Telomeres as Biomarkers for Ageing and Age-Related Diseases

Contact Info

Product

Resources

About