Does Malformed Lamin A Produce Enough Cellular Senescence to Contribute Meaningfully to the Progression of Aging?

In this study, we identified that paracrine senescence is triggered in senescent hMSCs with abnormal nuclear structures by increasing the expression of MCP-1 and that inhibition of MCP-1 decreases the SASP. Furthermore, we found that GATA4 mediates the senescence of hMSCs induced by defective lamin A. We assessed whether down-regulation of GATA4 disturbs the progerin- or prelamin A-dependent senescence phenotype. Elucidating how GATA4 regulates senescence in hMSCs with nuclear defects may aid in understanding the etiology of complex aging disorders. We show that inhibition of GATA4 expression protects hMSCs from cellular senescence, implying unique therapeutic opportunity against progeroid syndromes and physiological aging.
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs