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Lactoferrin Stimulates Mouse Macrophage to Express BAFF via Smad3 Pathway

B cell-activating factor belonging to the TNF family (BAFF) is primarily expressed by macrophages and stimulates B cell proliferation, differentiation, survival, and Ig production. In this study, we explored the effect of lactoferrin (LF) on BAFF expression by murine macrophages. We determined the l...

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Detalles Bibliográficos
Autores principales: Chang, HeynKeyung, Jin, Bo-Ra, Jang, Young-Saeng, Kim, Woan-Sub, Kim, Pyeung-Hyeun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Association of Immunologists 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3422713/
https://www.ncbi.nlm.nih.gov/pubmed/22916043
http://dx.doi.org/10.4110/in.2012.12.3.84
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author Chang, HeynKeyung
Jin, Bo-Ra
Jang, Young-Saeng
Kim, Woan-Sub
Kim, Pyeung-Hyeun
author_facet Chang, HeynKeyung
Jin, Bo-Ra
Jang, Young-Saeng
Kim, Woan-Sub
Kim, Pyeung-Hyeun
author_sort Chang, HeynKeyung
collection PubMed
description B cell-activating factor belonging to the TNF family (BAFF) is primarily expressed by macrophages and stimulates B cell proliferation, differentiation, survival, and Ig production. In this study, we explored the effect of lactoferrin (LF) on BAFF expression by murine macrophages. We determined the level of BAFF expression at the transcriptional and protein levels using RT-PCR and ELISA, respectively. LF markedly enhanced BAFF expression in mouse macrophages at both the transcriptional and protein levels. Overexpression of Smad3/4 further increased LF-induced BAFF transcription while DN-Smad3 abolished the LF-induced BAFF expression. These results demonstrate that LF can enhance BAFF expression through Smad3/4 pathway.
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spelling pubmed-34227132012-08-22 Lactoferrin Stimulates Mouse Macrophage to Express BAFF via Smad3 Pathway Chang, HeynKeyung Jin, Bo-Ra Jang, Young-Saeng Kim, Woan-Sub Kim, Pyeung-Hyeun Immune Netw Original Article B cell-activating factor belonging to the TNF family (BAFF) is primarily expressed by macrophages and stimulates B cell proliferation, differentiation, survival, and Ig production. In this study, we explored the effect of lactoferrin (LF) on BAFF expression by murine macrophages. We determined the level of BAFF expression at the transcriptional and protein levels using RT-PCR and ELISA, respectively. LF markedly enhanced BAFF expression in mouse macrophages at both the transcriptional and protein levels. Overexpression of Smad3/4 further increased LF-induced BAFF transcription while DN-Smad3 abolished the LF-induced BAFF expression. These results demonstrate that LF can enhance BAFF expression through Smad3/4 pathway. The Korean Association of Immunologists 2012-06 2012-06-30 /pmc/articles/PMC3422713/ /pubmed/22916043 http://dx.doi.org/10.4110/in.2012.12.3.84 Text en Copyright © 2012 The Korean Association of Immunologists http://creativecommons.org/licenses/by-nc/3.0 This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Chang, HeynKeyung
Jin, Bo-Ra
Jang, Young-Saeng
Kim, Woan-Sub
Kim, Pyeung-Hyeun
Lactoferrin Stimulates Mouse Macrophage to Express BAFF via Smad3 Pathway
title Lactoferrin Stimulates Mouse Macrophage to Express BAFF via Smad3 Pathway
title_full Lactoferrin Stimulates Mouse Macrophage to Express BAFF via Smad3 Pathway
title_fullStr Lactoferrin Stimulates Mouse Macrophage to Express BAFF via Smad3 Pathway
title_full_unstemmed Lactoferrin Stimulates Mouse Macrophage to Express BAFF via Smad3 Pathway
title_short Lactoferrin Stimulates Mouse Macrophage to Express BAFF via Smad3 Pathway
title_sort lactoferrin stimulates mouse macrophage to express baff via smad3 pathway
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3422713/
https://www.ncbi.nlm.nih.gov/pubmed/22916043
http://dx.doi.org/10.4110/in.2012.12.3.84
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