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Three papers published online in Nature help answer a fundamental question in mammalian ageing: why progenitor cells gradually lose their ability to divide and generate new cells as they grow old. They show that a protein called p16INK4a limits the regenerative abilities of such cells in ageing bone marrow, brain and pancreas.
p16INK4a is a protein involved in cell cycle control, and is already known to suppress cancer. The teams show that the activity of the p16INK4a gene increases as progenitor cells in the three mouse tissues lose their ability to self-renew. Sean Morrison and his colleagues studied neural progenitors in the mouse forebrain; Norman Sharpless and his team studied progenitors in the pancreatic islets that make insulin-secreting beta-cells; and David Scadden and his group examined haematopoietic bone marrow cells that make blood. The teams genetically engineered mice that lacked p16INK4a and then examined them when they reached old age, some 18 months later. Progenitor cells in these mice cling onto their youth - they do not show the normal age-dependent decline in proliferation. The work also suggests that type 2 diabetes might partly be explained by the failure of the pancreatic islets to renew with ageing, and perhaps that blocking this protein in certain tissues might combat certain effects of ageing. CONTACT Author paper [1]
Sean Morrison (University of Michigan, Ann Arbor, MI, USA)
E-mail: seanjm@umich.edu Author paper [2]
Norman Sharpless (University of North Carolina School of Medicine,
Chapel Hill, NC, USA)
E-mail: NES@med.unc.edu Author paper [3]
David Scadden (Harvard Stem Cell Institute, Boston, MA, USA)
E-mail: scadden.david@mgh.harvard.edu N&V author
Judith Campisi (Lawrence Berkeley National Laboratory, Berkeley, CA, USA)
E-mail: jcampisi@lbl.gov Abstracts available online:
Paper 1.
Paper 2.
Paper 3. (C) Nature press release.
Message posted by: Trevor M. D'Souza
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