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SCAMP4 enhances the senescent cell secretome

The senescence-associated secretory phenotype (SASP) is a major trait of senescent cells, but the molecular regulators of SASP factor secretion are poorly understood. Mass spectrometry analysis revealed that secretory carrier membrane protein 4 (SCAMP4) levels were strikingly elevated on the surface...

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Autores principales: Kim, Kyoung Mi, Noh, Ji Heon, Bodogai, Monica, Martindale, Jennifer L., Pandey, Poonam R., Yang, Xiaoling, Biragyn, Arya, Abdelmohsen, Kotb, Gorospe, Myriam
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cold Spring Harbor Laboratory Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6075036/
https://www.ncbi.nlm.nih.gov/pubmed/29967290
http://dx.doi.org/10.1101/gad.313270.118
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author Kim, Kyoung Mi
Noh, Ji Heon
Bodogai, Monica
Martindale, Jennifer L.
Pandey, Poonam R.
Yang, Xiaoling
Biragyn, Arya
Abdelmohsen, Kotb
Gorospe, Myriam
author_facet Kim, Kyoung Mi
Noh, Ji Heon
Bodogai, Monica
Martindale, Jennifer L.
Pandey, Poonam R.
Yang, Xiaoling
Biragyn, Arya
Abdelmohsen, Kotb
Gorospe, Myriam
author_sort Kim, Kyoung Mi
collection PubMed
description The senescence-associated secretory phenotype (SASP) is a major trait of senescent cells, but the molecular regulators of SASP factor secretion are poorly understood. Mass spectrometry analysis revealed that secretory carrier membrane protein 4 (SCAMP4) levels were strikingly elevated on the surface of senescent cells compared with proliferating cells. Interestingly, silencing SCAMP4 in senescent fibroblasts reduced the secretion of SASP factors, including interleukin 6 (IL6), IL8, growth differentiation factor 15 (GDF-15), C-X-C motif chemokine ligand 1 (CXCL1), and IL7, while, conversely, SCAMP4 overexpression in proliferating fibroblasts increased SASP factor secretion. Our results indicate that SCAMP4 accumulates on the surface of senescent cells, promotes SASP factor secretion, and critically enhances the SASP phenotype.
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spelling pubmed-60750362019-01-01 SCAMP4 enhances the senescent cell secretome Kim, Kyoung Mi Noh, Ji Heon Bodogai, Monica Martindale, Jennifer L. Pandey, Poonam R. Yang, Xiaoling Biragyn, Arya Abdelmohsen, Kotb Gorospe, Myriam Genes Dev Research Communication The senescence-associated secretory phenotype (SASP) is a major trait of senescent cells, but the molecular regulators of SASP factor secretion are poorly understood. Mass spectrometry analysis revealed that secretory carrier membrane protein 4 (SCAMP4) levels were strikingly elevated on the surface of senescent cells compared with proliferating cells. Interestingly, silencing SCAMP4 in senescent fibroblasts reduced the secretion of SASP factors, including interleukin 6 (IL6), IL8, growth differentiation factor 15 (GDF-15), C-X-C motif chemokine ligand 1 (CXCL1), and IL7, while, conversely, SCAMP4 overexpression in proliferating fibroblasts increased SASP factor secretion. Our results indicate that SCAMP4 accumulates on the surface of senescent cells, promotes SASP factor secretion, and critically enhances the SASP phenotype. Cold Spring Harbor Laboratory Press 2018-07-01 /pmc/articles/PMC6075036/ /pubmed/29967290 http://dx.doi.org/10.1101/gad.313270.118 Text en Published by Cold Spring Harbor Laboratory Press http://creativecommons.org/licenses/by-nc/4.0/ This is a work of the US Government.
spellingShingle Research Communication
Kim, Kyoung Mi
Noh, Ji Heon
Bodogai, Monica
Martindale, Jennifer L.
Pandey, Poonam R.
Yang, Xiaoling
Biragyn, Arya
Abdelmohsen, Kotb
Gorospe, Myriam
SCAMP4 enhances the senescent cell secretome
title SCAMP4 enhances the senescent cell secretome
title_full SCAMP4 enhances the senescent cell secretome
title_fullStr SCAMP4 enhances the senescent cell secretome
title_full_unstemmed SCAMP4 enhances the senescent cell secretome
title_short SCAMP4 enhances the senescent cell secretome
title_sort scamp4 enhances the senescent cell secretome
topic Research Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6075036/
https://www.ncbi.nlm.nih.gov/pubmed/29967290
http://dx.doi.org/10.1101/gad.313270.118
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