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Telomere dynamics in induced pluripotent stem cells:Potentials for Human disease modeling

Telomere dynamics in induced pluripotent stem cells:Potentials for Human disease modeling
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摘要 Recent advances in reprograming somatic cells from normal and diseased tissues into induced pluripotent stem cells (iPSCs) provide exciting possibilities for generating renewed tissues for disease modeling and therapy. However, questions remain on whether iPSCs still retain certain markers (e.g. aging) of the original somatic cells that could limit their replicative potential and utility. A reliable biological marker for measuring cellular aging is telomere length, which is maintained by a specialized form of cellular polymerase known as telomerase. Telomerase is composed of the cellular reverse transcriptase protein, the integral RNA component, and other cellular proteins (e.g. dyskerin). Mutations in any of these components of telomerase can lead to a severe form of marrow def iciency known as dyskeratosis congenita (DC). This review summarizes recent f indings on the effect of cellular reprograming via iPS of normal or DC patient-derived tissues on telomerase function and consequently on telomere length maintenance. The potentials and challenges of using iPSCs in a clinical setting will also be discussed. Recent advances in reprograming somatic cells from normal and diseased tissues into induced pluripotent stem cells (iPSCs) provide exciting possibilities for generating renewed tissues for disease modeling and therapy. However, questions remain on whether iPSCs still retain certain markers (e.g. aging) of the original somatic cells that could limit their replicative potential and utility. A reliable biological marker for measuring cellular aging is telomere length, which is maintained by a specialized form of cellular polymerase known as telomerase. Telomerase is composed of the cellular reverse transcriptase protein, the integral RNA component, and other cellular proteins (e.g. dyskerin). Mutations in any of these components of telomerase can lead to a severe form of marrow deficiency known as dyskeratosis congenita (DC). This review summarizes recent findings on the effect of cellular reprograming via iPS of normal or DC patient-derived tissues on telomerase function and consequently on telomere length maintenance. The potentials and challenges of using iPSCs in a clinical setting will also be discussed.
作者 Hinh Ly
出处 《World Journal of Stem Cells》 SCIE CAS 2011年第10期89-95,共7页 世界干细胞杂志(英文版)(电子版)
基金 Supported by A Research Scholar Grant of the American Cancer Society (RSG-06-162-01-GMC)
关键词 Induced PLURIPOTENT stem cells TELOMERES TELOMERASE Dyskeratosis congenita MARROW failure Induced pluripotent stem cells Telomeres, Telomerase Dyskeratosis congenita Marrow failure
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参考文献81

  • 1Stuart Knight,Tom Vulliamy,Ben Morgan,Koen Devriendt,Philip Mason,Inderjeet Dokal.Identification of novel DKC1 mutations in patients with dyskeratosis congenita: implications for pathophysiology and diagnosis[J]. Human Genetics . 2001 (4)
  • 2Xu D,Alipio Z,Fink LM,et al.Phenotypic correction of murine hemophilia A using an iPS cell-based therapyProceedings of the National Academy of Sciences of the United States of America,2009.
  • 3Autexier C,Lue NF.The structure and function of telomerase reverse transcriptase. Annual Review of Biochemistry . 2006
  • 4Alter BP,Giri N,Savage SA,Rosenberg PS.Cancer in dyskeratosis congenita. Blood . 2009
  • 5Alter BP,Baerlocher GM,Savage SA,Chanock SJ,Weksler BB,Willner JP,Peters JA,Giri N,Lansdorp PM.Very shorttelomere length by flow fluorescence in situ hybridizationidentifies patients with dyskeratosis congenita. Blood . 2007
  • 6Du HY,Pumbo E,Ivanovich J,An P,Maziarz RT,Reiss UM,Chirnomas D,Shimamura A,Vlachos A,Lipton JM,Goyal RK,Goldman F,Wilson DB,Mason PJ,Bessler M.TERC and TERT gene mutations in patients with bone marrow failure and the signif icance of telomere length measurements. Blood . 2009
  • 7Carroll KA,Ly H.Telomere dysfunction in human diseases: the long and short of it!. Int J Clin Exp Pathol . 2009
  • 8Walne AJ,Vulliamy T,Marrone A,Beswick R,Kirwan M,Masunari Y,Al-Qurashi FH,Aljurf M,Dokal I.Genetic het-erogeneity in autosomal recessive dyskeratosis congenita with one subtype due to mutations in the telomerase-associ-ated protein NOP10. Human Molecular Genetics . 2007
  • 9Zhong F,Savage SA,Shkreli M,Giri N,Jessop L,Myers T,Chen R,Alter BP,Artandi SE.Disruption of telomerase traf-fi cking by TCAB1 mutation causes dyskeratosis congenita. Genes and Development . 2011
  • 10Venteicher AS,Abreu EB,Meng Z,McCann KE,Terns RM,Veenstra TD,Terns MP,Artandi SE.A human telomerase holoenzyme protein required for Cajal body localization and telomere synthesis. Science . 2009

二级参考文献15

  • 1Hayflick L. The limited in vitro lifetime of human hiploid cell strains. Exp Cell Res 1965; 37:614-636.
  • 2Harley cB, Futcher AB, Greider CW. Telomeres shorten during ageing of human fibroblasts. Nature 1990; 345:458- 460.
  • 3Lanza RP, Cibelli JB, Blackwell C, et al. Extension of cell life-span and telomere length in animals cloned from senescent somatic cells. Science 2000; 288:665-669.
  • 4Takahashi K, Tanabe K, Ohnuki M, et al. Induction of pluripotent stem cells from adult human fibroblasts by defined factors. Cell 2007; 131:861-872.
  • 5Calado RT, Young NS. Telomere diseases. N Engl J Med 2009; 361:2353- 2365.
  • 6Agarwal S, Loh YH, McLoughlin EM, et al. Telomere elongation in induced pluripotent stem cells from dyskeratosis congenita patients. Nature 2010; 464:292-296.
  • 7Batista LF, Pech ME Zhong FL, et al. Telomere shortening and loss of selfrenewal in dyskeratosis congenita induced pluripotent stem cells. Nature 2011; 474:399-402.
  • 8Wong JM, Collins K. Telomerase RNA level limits telomere maintenance in X- linked dyskeratosis congenita. Genes Dev 2006; 20:2848-2858.
  • 9Venteicher AS, Abreu EB, Meng Z, et al. A human telomerase holoenzyme protein required for Cajal body localization and telomere synthesis. Science 2009; 323:644-648.
  • 10Suhr ST, Chang EA, Rodriguez RM, et al. Telomere dynamics in human cells reprogrammed to pluripotency. PLoS One 2009; 4:e8124.

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