THURSDAY, April 27 (HealthDay News) -- A splicing defect in the lamin A gene is known to cause premature aging diseases, and the same defect has now been linked to the normal process of cellular aging, according to a report published April 27 in Sciencexpress, the early online edition of Science. Reversing the defect causes fibroblasts to lose some age-related characteristics, and cells from 80- and 90-year-olds proliferate more like a child's.
Paola Scaffidi, Ph.D., and Tom Misteli, Ph.D., from the U.S. National Cancer Institute in Bethesda, Md., found that a splicing mutation that causes a shortened lamin A (LMNA) protein and is linked to the premature aging disease, Hutchinson-Gilford Progeria syndrome (HGPS), occurs sporadically in the cells of normally aging people.
The investigators found that the normally aging cells display nuclear characteristics similar to those from HGPS patients, including condensed chromatin and unrepaired DNA damage. Blocking the mutant splice site in healthy fibroblasts from normal individuals in their 80s and 90s reversed some of these nuclear defects and brought their proliferative rate back to the level of cells from a child.
"Given our finding that several nuclear defects in aged cells are reversible upon inhibition of the aberrant splicing event in LMNA, it will be interesting to determine whether other cellular features of aging respond to such treatment and whether organismal aging can be modulated by interference with lamin A," the authors write.
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