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Cell fusion induced by ERVWE1 or measles virus causes cellular senescence

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...

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Autores principales: Chuprin, Anna, Gal, Hilah, Biron-Shental, Tal, Biran, Anat, Amiel, Aliza, Rozenblatt, Shmuel, Krizhanovsky, Valery
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cold Spring Harbor Laboratory Press 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3828521/
https://www.ncbi.nlm.nih.gov/pubmed/24186980
http://dx.doi.org/10.1101/gad.227512.113
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author Chuprin, Anna
Gal, Hilah
Biron-Shental, Tal
Biran, Anat
Amiel, Aliza
Rozenblatt, Shmuel
Krizhanovsky, Valery
author_facet Chuprin, Anna
Gal, Hilah
Biron-Shental, Tal
Biran, Anat
Amiel, Aliza
Rozenblatt, Shmuel
Krizhanovsky, Valery
author_sort Chuprin, Anna
collection PubMed
description 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.
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spelling pubmed-38285212014-05-01 Cell fusion induced by ERVWE1 or measles virus causes cellular senescence Chuprin, Anna Gal, Hilah Biron-Shental, Tal Biran, Anat Amiel, Aliza Rozenblatt, Shmuel Krizhanovsky, Valery Genes Dev Research Paper 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. Cold Spring Harbor Laboratory Press 2013-11-01 /pmc/articles/PMC3828521/ /pubmed/24186980 http://dx.doi.org/10.1101/gad.227512.113 Text en © 2013 Chuprin et al.; Published by Cold Spring Harbor Laboratory Press http://creativecommons.org/licenses/by-nc/3.0/ This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 3.0 Unported), as described at http://creativecommons.org/licenses/by-nc/3.0/.
spellingShingle Research Paper
Chuprin, Anna
Gal, Hilah
Biron-Shental, Tal
Biran, Anat
Amiel, Aliza
Rozenblatt, Shmuel
Krizhanovsky, Valery
Cell fusion induced by ERVWE1 or measles virus causes cellular senescence
title Cell fusion induced by ERVWE1 or measles virus causes cellular senescence
title_full Cell fusion induced by ERVWE1 or measles virus causes cellular senescence
title_fullStr Cell fusion induced by ERVWE1 or measles virus causes cellular senescence
title_full_unstemmed Cell fusion induced by ERVWE1 or measles virus causes cellular senescence
title_short Cell fusion induced by ERVWE1 or measles virus causes cellular senescence
title_sort cell fusion induced by ervwe1 or measles virus causes cellular senescence
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3828521/
https://www.ncbi.nlm.nih.gov/pubmed/24186980
http://dx.doi.org/10.1101/gad.227512.113
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