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KLF13 promotes porcine adipocyte differentiation through PPARγ activation
BACKGROUND: Adipogenesis is tightly controlled by a complex network of transcription factors acting at different stages of differentiation. Kruppel-like factors (KLFs) as a family of zinc-finger transcription factors play diverse roles during cell differentiation and development in mammals. RESULTS:...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4469396/ https://www.ncbi.nlm.nih.gov/pubmed/26085920 http://dx.doi.org/10.1186/s13578-015-0016-z |
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author | Jiang, Shuzhong Wei, Hongkui Song, Tongxing Yang, Yang Zhang, Feng Zhou, Yuanfei Peng, Jian Jiang, Siwen |
author_facet | Jiang, Shuzhong Wei, Hongkui Song, Tongxing Yang, Yang Zhang, Feng Zhou, Yuanfei Peng, Jian Jiang, Siwen |
author_sort | Jiang, Shuzhong |
collection | PubMed |
description | BACKGROUND: Adipogenesis is tightly controlled by a complex network of transcription factors acting at different stages of differentiation. Kruppel-like factors (KLFs) as a family of zinc-finger transcription factors play diverse roles during cell differentiation and development in mammals. RESULTS: In the present study, we showed that KLF13 acts as a key regulator regulating porcine adipocyte differentiation. The expression of KLF13 was markedly up-regulated during the early stage of porcine adipocyte differentiation, which was followed by expression of PPARγ. Porcine adipocyte differentiation was significantly attenuated by the addition of siRNA against KLF13, whereas overexpression of KLF13 resulted in enhanced porcine adipocyte differentiation. Using promoter deletion and mutation analysis, we identified a KLF13-binding site within −593/-577 region of the porcine PPARγ proximal promoter, indicating that KLF13 directly interacts with porcine PPARγ promoter. However, inhibition of KLF13 by siRNA did not impair mouse adipocyte differentiation. In addition, knockdown and/or overexpression of KLF13 in 3 T3-L1 cells all did not influence expression of PPARγ2. CONCLUSIONS: Collectively, our results suggest that KLF13 exist as a key pro-adipogenic transcription factor through transactivating PPARγ expression in porcine adipocyte differentiation, whereas no such effect was detected in mouse adipocyte differentiation. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13578-015-0016-z) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-4469396 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-44693962015-06-18 KLF13 promotes porcine adipocyte differentiation through PPARγ activation Jiang, Shuzhong Wei, Hongkui Song, Tongxing Yang, Yang Zhang, Feng Zhou, Yuanfei Peng, Jian Jiang, Siwen Cell Biosci Research BACKGROUND: Adipogenesis is tightly controlled by a complex network of transcription factors acting at different stages of differentiation. Kruppel-like factors (KLFs) as a family of zinc-finger transcription factors play diverse roles during cell differentiation and development in mammals. RESULTS: In the present study, we showed that KLF13 acts as a key regulator regulating porcine adipocyte differentiation. The expression of KLF13 was markedly up-regulated during the early stage of porcine adipocyte differentiation, which was followed by expression of PPARγ. Porcine adipocyte differentiation was significantly attenuated by the addition of siRNA against KLF13, whereas overexpression of KLF13 resulted in enhanced porcine adipocyte differentiation. Using promoter deletion and mutation analysis, we identified a KLF13-binding site within −593/-577 region of the porcine PPARγ proximal promoter, indicating that KLF13 directly interacts with porcine PPARγ promoter. However, inhibition of KLF13 by siRNA did not impair mouse adipocyte differentiation. In addition, knockdown and/or overexpression of KLF13 in 3 T3-L1 cells all did not influence expression of PPARγ2. CONCLUSIONS: Collectively, our results suggest that KLF13 exist as a key pro-adipogenic transcription factor through transactivating PPARγ expression in porcine adipocyte differentiation, whereas no such effect was detected in mouse adipocyte differentiation. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13578-015-0016-z) contains supplementary material, which is available to authorized users. BioMed Central 2015-06-10 /pmc/articles/PMC4469396/ /pubmed/26085920 http://dx.doi.org/10.1186/s13578-015-0016-z Text en © Jiang et al. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Jiang, Shuzhong Wei, Hongkui Song, Tongxing Yang, Yang Zhang, Feng Zhou, Yuanfei Peng, Jian Jiang, Siwen KLF13 promotes porcine adipocyte differentiation through PPARγ activation |
title | KLF13 promotes porcine adipocyte differentiation through PPARγ activation |
title_full | KLF13 promotes porcine adipocyte differentiation through PPARγ activation |
title_fullStr | KLF13 promotes porcine adipocyte differentiation through PPARγ activation |
title_full_unstemmed | KLF13 promotes porcine adipocyte differentiation through PPARγ activation |
title_short | KLF13 promotes porcine adipocyte differentiation through PPARγ activation |
title_sort | klf13 promotes porcine adipocyte differentiation through pparγ activation |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4469396/ https://www.ncbi.nlm.nih.gov/pubmed/26085920 http://dx.doi.org/10.1186/s13578-015-0016-z |
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