Declining levels of the protein BubR1 occur when both people and animals age. This contributes to cell senescence or deterioration, weight loss, muscle wasting and cataracts.
Mayo Clinic researchers have shown that adult progenitor or stem cells -- important for repair and regeneration of skeletal muscle and maintenance of healthy fat tissue -- are subject to cellular senescence, and that clearance of these cells limits age-related deterioration of these tissues. The findings appear today online in the journal Cell Reports.
BubR1 is an essential part of the mitotic checkpoint, the mechanism controlling proper cell division or mitosis. Without sufficient levels of BubR1, chromosomal imbalance will occur, leading to premature aging and cancer. Using mutant mice that expressed low levels of BubR1, the researchers found development of dysfunctional tissue with impaired cell regeneration. In analyzing the progenitor populations in skeletal muscle and fat, they found that a subset of progenitors was senescent and that the tumor suppressor p53 was acting to prevent this from happening through activation of p21.
Not only do the findings contribute to knowledge on cell senescence as it relates to aging and related diseases, but understanding the mechanisms may lead to future therapies, say the researchers.