FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2135149410> ?p ?o ?g. }

• W2135149410 endingPage "e27352" @default.
• W2135149410 startingPage "e27352" @default.
• W2135149410 abstract "Somatic cells reprogrammed into induced pluripotent stem cells (iPSCs) acquire features of human embryonic stem cells (hESCs) and thus represent a promising source for cellular therapy of debilitating diseases, such as age-related disorders. However, reprogrammed cell lines have been found to harbor various genomic alterations. In addition, we recently discovered that the mitochondrial DNA of human fibroblasts also undergoes random mutational events upon reprogramming. Aged somatic cells might possess high susceptibility to nuclear and mitochondrial genome instability. Hence, concerns over the oncogenic potential of reprogrammed cells due to the lack of genomic integrity may hinder the applicability of iPSC-based therapies for age-associated conditions. Here, we investigated whether aged reprogrammed cells harboring chromosomal abnormalities show resistance to apoptotic cell death or mitochondrial-associated oxidative stress, both hallmarks of cancer transformation. Four iPSC lines were generated from dermal fibroblasts derived from an 84-year-old woman, representing the oldest human donor so far reprogrammed to pluripotency. Despite the presence of karyotype aberrations, all aged-iPSCs were able to differentiate into neurons, re-establish telomerase activity, and reconfigure mitochondrial ultra-structure and functionality to a hESC-like state. Importantly, aged-iPSCs exhibited high sensitivity to drug-induced apoptosis and low levels of oxidative stress and DNA damage, in a similar fashion as iPSCs derived from young donors and hESCs. Thus, the occurrence of chromosomal abnormalities within aged reprogrammed cells might not be sufficient to over-ride the cellular surveillance machinery and induce malignant transformation through the alteration of mitochondrial-associated cell death. Taken together, we unveiled that cellular reprogramming is capable of reversing aging-related features in somatic cells from a very old subject, despite the presence of genomic alterations. Nevertheless, we believe it will be essential to develop reprogramming protocols capable of safeguarding the integrity of the genome of aged somatic cells, before employing iPSC-based therapy for age-associated disorders." @default.
• W2135149410 created "2016-06-24" @default.
• W2135149410 creator A5000535666 @default.
• W2135149410 creator A5001429713 @default.
• W2135149410 creator A5006595878 @default.
• W2135149410 creator A5007042386 @default.
• W2135149410 creator A5007313625 @default.
• W2135149410 creator A5019720850 @default.
• W2135149410 creator A5027351514 @default.
• W2135149410 creator A5035076884 @default.
• W2135149410 creator A5063828019 @default.
• W2135149410 creator A5070055681 @default.
• W2135149410 creator A5082517458 @default.
• W2135149410 date "2011-11-14" @default.
• W2135149410 modified "2023-10-01" @default.
• W2135149410 title "Mitochondrial-Associated Cell Death Mechanisms Are Reset to an Embryonic-Like State in Aged Donor-Derived iPS Cells Harboring Chromosomal Aberrations" @default.
• W2135149410 cites W1522323234 @default.
• W2135149410 cites W1574694350 @default.
• W2135149410 cites W1612842202 @default.
• W2135149410 cites W1963842583 @default.
• W2135149410 cites W1970449040 @default.
• W2135149410 cites W1971453554 @default.
• W2135149410 cites W1975230462 @default.
• W2135149410 cites W1977049211 @default.
• W2135149410 cites W1982692107 @default.
• W2135149410 cites W1982882278 @default.
• W2135149410 cites W1983594275 @default.
• W2135149410 cites W1986371962 @default.
• W2135149410 cites W1999034879 @default.
• W2135149410 cites W2000210729 @default.
• W2135149410 cites W2005097929 @default.
• W2135149410 cites W2007462861 @default.
• W2135149410 cites W2019019085 @default.
• W2135149410 cites W2022936555 @default.
• W2135149410 cites W2025192477 @default.
• W2135149410 cites W2025738240 @default.
• W2135149410 cites W2036140173 @default.
• W2135149410 cites W2037146644 @default.
• W2135149410 cites W2037338370 @default.
• W2135149410 cites W2039605728 @default.
• W2135149410 cites W2054791794 @default.
• W2135149410 cites W2058981318 @default.
• W2135149410 cites W2059378220 @default.
• W2135149410 cites W2061821048 @default.
• W2135149410 cites W2066571367 @default.
• W2135149410 cites W2070041362 @default.
• W2135149410 cites W2071850731 @default.
• W2135149410 cites W2073610802 @default.
• W2135149410 cites W2075084906 @default.
• W2135149410 cites W2075270655 @default.
• W2135149410 cites W2081970735 @default.
• W2135149410 cites W2087470701 @default.
• W2135149410 cites W2105754268 @default.
• W2135149410 cites W2109705859 @default.
• W2135149410 cites W2113896242 @default.
• W2135149410 cites W2118843707 @default.
• W2135149410 cites W2121966499 @default.
• W2135149410 cites W2124098526 @default.
• W2135149410 cites W2124482905 @default.
• W2135149410 cites W2128353741 @default.
• W2135149410 cites W2129298171 @default.
• W2135149410 cites W2129534676 @default.
• W2135149410 cites W2136541538 @default.
• W2135149410 cites W2138977668 @default.
• W2135149410 cites W2142046859 @default.
• W2135149410 cites W2146447597 @default.
• W2135149410 cites W2152288884 @default.
• W2135149410 cites W2162757786 @default.
• W2135149410 cites W2163404991 @default.
• W2135149410 cites W2171813756 @default.
• W2135149410 doi "https://doi.org/10.1371/journal.pone.0027352" @default.
• W2135149410 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3215709" @default.
• W2135149410 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22110631" @default.
• W2135149410 hasPublicationYear "2011" @default.
• W2135149410 type Work @default.
• W2135149410 sameAs 2135149410 @default.
• W2135149410 citedByCount "100" @default.
• W2135149410 countsByYear W21351494102012 @default.
• W2135149410 countsByYear W21351494102013 @default.
• W2135149410 countsByYear W21351494102014 @default.
• W2135149410 countsByYear W21351494102015 @default.
• W2135149410 countsByYear W21351494102016 @default.
• W2135149410 countsByYear W21351494102017 @default.
• W2135149410 countsByYear W21351494102018 @default.
• W2135149410 countsByYear W21351494102019 @default.
• W2135149410 countsByYear W21351494102020 @default.
• W2135149410 countsByYear W21351494102021 @default.
• W2135149410 countsByYear W21351494102022 @default.
• W2135149410 countsByYear W21351494102023 @default.
• W2135149410 crossrefType "journal-article" @default.
• W2135149410 hasAuthorship W2135149410A5000535666 @default.
• W2135149410 hasAuthorship W2135149410A5001429713 @default.
• W2135149410 hasAuthorship W2135149410A5006595878 @default.
• W2135149410 hasAuthorship W2135149410A5007042386 @default.
• W2135149410 hasAuthorship W2135149410A5007313625 @default.
• W2135149410 hasAuthorship W2135149410A5019720850 @default.
• W2135149410 hasAuthorship W2135149410A5027351514 @default.
• W2135149410 hasAuthorship W2135149410A5035076884 @default.

• next