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TβRII Regulates the Proliferation of Metanephric Mesenchyme Cells through Six2 In Vitro
The transforming growth factor-β (TGFβ) family signaling pathways play an important role in regulatory cellular networks and exert specific effects on developmental programs during embryo development. However, the function of TGFβ signaling pathways on the early kidney development remains unclear. I...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5412437/ https://www.ncbi.nlm.nih.gov/pubmed/28420207 http://dx.doi.org/10.3390/ijms18040853 |
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author | Mao, Zhaomin Lyu, Zhongshi Huang, Liyuan Zhou, Qin Weng, Yaguang |
author_facet | Mao, Zhaomin Lyu, Zhongshi Huang, Liyuan Zhou, Qin Weng, Yaguang |
author_sort | Mao, Zhaomin |
collection | PubMed |
description | The transforming growth factor-β (TGFβ) family signaling pathways play an important role in regulatory cellular networks and exert specific effects on developmental programs during embryo development. However, the function of TGFβ signaling pathways on the early kidney development remains unclear. In this work, we aim to detect the underlying role of TGFβ type II receptor (TβRII) in vitro, which has a similar expression pattern as the crucial regulator Six2 during early kidney development. Firstly, the 5-ethynyl-2′-deoxyuridine (EdU) assay showed knock down of TβRII significantly decreased the proliferation ratio of metanephric mesenchyme (MM) cells. Additionally, real-time Polymerase Chain Reaction (PCR) and Western blot together with immunofluorescence determined that the mRNA and protein levels of Six2 declined after TβRII knock down. Also, Six2 was observed to be able to partially rescue the proliferation phenotype caused by the depletion of TβRII. Moreover, bioinformatics analysis and luciferase assay indicated Smad3 could transcriptionally target Six2. Further, the EdU assay showed that Smad3 could also rescue the inhibition of proliferation caused by the knock down of TβRII. Taken together, these findings delineate the important function of the TGFβ signaling pathway in the early development of kidney and TβRII was shown to be able to promote the expression of Six2 through Smad3 mediating transcriptional regulation and in turn activate the proliferation of MM cells. |
format | Online Article Text |
id | pubmed-5412437 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-54124372017-05-05 TβRII Regulates the Proliferation of Metanephric Mesenchyme Cells through Six2 In Vitro Mao, Zhaomin Lyu, Zhongshi Huang, Liyuan Zhou, Qin Weng, Yaguang Int J Mol Sci Article The transforming growth factor-β (TGFβ) family signaling pathways play an important role in regulatory cellular networks and exert specific effects on developmental programs during embryo development. However, the function of TGFβ signaling pathways on the early kidney development remains unclear. In this work, we aim to detect the underlying role of TGFβ type II receptor (TβRII) in vitro, which has a similar expression pattern as the crucial regulator Six2 during early kidney development. Firstly, the 5-ethynyl-2′-deoxyuridine (EdU) assay showed knock down of TβRII significantly decreased the proliferation ratio of metanephric mesenchyme (MM) cells. Additionally, real-time Polymerase Chain Reaction (PCR) and Western blot together with immunofluorescence determined that the mRNA and protein levels of Six2 declined after TβRII knock down. Also, Six2 was observed to be able to partially rescue the proliferation phenotype caused by the depletion of TβRII. Moreover, bioinformatics analysis and luciferase assay indicated Smad3 could transcriptionally target Six2. Further, the EdU assay showed that Smad3 could also rescue the inhibition of proliferation caused by the knock down of TβRII. Taken together, these findings delineate the important function of the TGFβ signaling pathway in the early development of kidney and TβRII was shown to be able to promote the expression of Six2 through Smad3 mediating transcriptional regulation and in turn activate the proliferation of MM cells. MDPI 2017-04-18 /pmc/articles/PMC5412437/ /pubmed/28420207 http://dx.doi.org/10.3390/ijms18040853 Text en © 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Mao, Zhaomin Lyu, Zhongshi Huang, Liyuan Zhou, Qin Weng, Yaguang TβRII Regulates the Proliferation of Metanephric Mesenchyme Cells through Six2 In Vitro |
title | TβRII Regulates the Proliferation of Metanephric Mesenchyme Cells through Six2 In Vitro |
title_full | TβRII Regulates the Proliferation of Metanephric Mesenchyme Cells through Six2 In Vitro |
title_fullStr | TβRII Regulates the Proliferation of Metanephric Mesenchyme Cells through Six2 In Vitro |
title_full_unstemmed | TβRII Regulates the Proliferation of Metanephric Mesenchyme Cells through Six2 In Vitro |
title_short | TβRII Regulates the Proliferation of Metanephric Mesenchyme Cells through Six2 In Vitro |
title_sort | tβrii regulates the proliferation of metanephric mesenchyme cells through six2 in vitro |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5412437/ https://www.ncbi.nlm.nih.gov/pubmed/28420207 http://dx.doi.org/10.3390/ijms18040853 |
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