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JCI online early table of contents: June 13, 2011
Date:6/13/2011

ge of 12 years. It is caused by mutations in the LMNA gene that lead to the production of a mutant protein known as progerin. Recently, progerin was found at low levels in normal human cells and tissues, but whether it has a role in normal aging has not been determined. Collins and colleagues have now found that progerin production is triggered in normal human cells undergoing senescence the process by which normal cells lose their capacity to divide and by which they have their lifespan limited. Importantly, progerin production was only triggered during cellular senescence induced by shortening of telomeres the specialized structures at the ends of chromosomes, gradual loss of which activates senescence. These data indicate that telomere dysfunction and progerin production cooperate during the induction of cell senescence, demonstrating that understanding of the premature aging processes in individuals with HGPS is likely to provide insight into the normal aging process.

TITLE: Progerin and telomere dysfunction collaborate to trigger cellular senescence in normal human fibroblast cells

AUTHOR CONTACT:
Francis S. Collins
National Human Genome Research Institute, NIH, Bethesda, Maryland, USA.
Phone: 301.496.2433; Fax: 301.402.2700; E-mail: Francis.Collins@nih.gov.

View this article at: http://www.jci.org/articles/view/43578?key=3aae23e4a04eb4ff6781


INFLAMMATION: To be M1 or to be M2: the protein KLF4 decides for macrophages

Macrophages are cells critical for both immune defense against invading microbes and inflammation. They are currently classified as either M1 or M2, with M1 macrophages being considered pro-inflammatory and M2 macrophages anti-inflammatory. A team of researchers, led by Mukesh Jain, at Case Western Reserve University, Cleveland, has now identified
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Contact: Karen Honey
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Journal of Clinical Investigation
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