Not exact matches
David Frescas et al (2017) Murine mesenchymal
cells that express elevated
levels of the CDK inhibitor p16 (Ink4a) in vivo are not necessarily
senescent (http://www.tandfonline.com/doi/full/10.1080/15384101.2017.1339850)
(6) However, it would be useful to see a more thorough analysis of the effect of ablating p16Ink4a - expressing
senescent cells, and whether there may instead be evidence of a short - term rejuvenation of tissue function that is slowly lost over time to rising
levels of other kinds of aging damage that INK - ATTAC activation does not address.
(6) Following this initial test of abrogating the early, age - related rise in p16Ink4a - expressing
cell burden, the investigators probed the effects of leaving BubR1H / H; INK - ATTAC to undergo 5 months of rapid «premature aging» (and thus, to the attendant accumulation of high
levels of p16Ink4a - positive
cells and onset of «early - aging» phenotypes), and only then inducing ablation of
senescent cells with the INK - ATTAC drug - activated system (see Figure 2 (g) below).
Dr. Campisi has found instead that a minority of
senescent cells evade destruction by secreting high
levels of matrix metalloproteinases (MMPs), which cleave MICA / B ligands and thereby prevent NKG2D binding.
Rather, the defective checkpoint system was left to proceed, and one of its downstream consequences, which was still under normal regulation — and one known to be directly induced by the normal degenerative aging process — was reversed at the structural
level, by clearing out the p16Ink4a - positive
senescent cells that had accumulated to an abnormal degree in their tissues.