Abstract:
:Cellular senescence limits proliferation of potentially detrimental cells, preventing tumorigenesis and restricting tissue damage. However, the function of senescence in nonpathological conditions is unknown. We found that the human placental syncytiotrophoblast exhibited the phenotype and expressed molecular markers of cellular senescence. During embryonic development, ERVWE1-mediated cell fusion results in formation of the syncytiotrophoblast, which serves as the maternal/fetal interface at the placenta. Expression of ERVWE1 caused cell fusion in normal and cancer cells, leading to formation of hyperploid syncytia exhibiting features of cellular senescence. Infection by the measles virus, which leads to cell fusion, also induced cellular senescence in normal and cancer cells. The fused cells activated the main molecular pathways of senescence, the p53- and p16-pRb-dependent pathways; the senescence-associated secretory phenotype; and immune surveillance-related proteins. Thus, fusion-induced senescence might be needed for proper syncytiotrophoblast function during embryonic development, and reuse of this senescence program later in life protects against pathological expression of endogenous fusogens and fusogenic viral infections.
journal_name
Genes Devjournal_title
Genes & developmentauthors
Chuprin A,Gal H,Biron-Shental T,Biran A,Amiel A,Rozenblatt S,Krizhanovsky Vdoi
10.1101/gad.227512.113subject
Has Abstractpub_date
2013-11-01 00:00:00pages
2356-66issue
21eissn
0890-9369issn
1549-5477pii
27/21/2356journal_volume
27pub_type
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