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MYC Participates in Lipopolysaccharide-Induced Sepsis via Promoting Cell Proliferation and Inhibiting Apoptosis

OBJECTIVE: This study aimed to explore the potential mechanism of MYC proto-oncogene, BHLH Transcription Factor (MYC) gene, on sepsis. MATERIALS AND METHODS: In this experimental study, rat-derived H9C2 cardiomyocyte cells were cultured in vitro, followed by lipopolysaccharide (LPS) treatment with d...

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Autores principales: Li, Yin, Kong, Chengqi, Feng, Lei, Tang, Wenliang, Chen, Mengwei, Zheng, Zhiyuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Royan Institute 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7481895/
https://www.ncbi.nlm.nih.gov/pubmed/32779435
http://dx.doi.org/10.22074/cellj.2020.6961
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author Li, Yin
Kong, Chengqi
Feng, Lei
Tang, Wenliang
Chen, Mengwei
Zheng, Zhiyuan
author_facet Li, Yin
Kong, Chengqi
Feng, Lei
Tang, Wenliang
Chen, Mengwei
Zheng, Zhiyuan
author_sort Li, Yin
collection PubMed
description OBJECTIVE: This study aimed to explore the potential mechanism of MYC proto-oncogene, BHLH Transcription Factor (MYC) gene, on sepsis. MATERIALS AND METHODS: In this experimental study, rat-derived H9C2 cardiomyocyte cells were cultured in vitro, followed by lipopolysaccharide (LPS) treatment with different concentration gradients. The cholecystokinin octapeptide (CCK-8) assay, enzyme-linked immunoassay (ELISA) assay, quantitative reverse transcription polymerase chain reaction (qRT-PCR), cell transfection, Western blot and flow cytometry were used to observe the cellular apoptosis and proliferation of cells in both treated LPS groups and normal control group. RESULTS: The result of CCK-8 assay showed that silencing MYC inhibited cellular proliferation of sepsis in absence or presence of LPS treatment. ELISA assay showed that the expressions of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were decreased in MYC silenced group, but they were increased after LPS treatment. Moreover, Flow cytometry assay showed that MYC silencing contributed to the apoptosis of sepsis cells. Furthermore, the expression of inflammatory factors showed that MYC silencing elevated the expression of inflammation factors. CONCLUSION: MYC might take part in the process of LPS induced sepsis through suppressing apoptosis and inducing cell proliferation. Moreover, MYC might reduce inflammation during the progression of LPS induced sepsis.
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spelling pubmed-74818952020-09-15 MYC Participates in Lipopolysaccharide-Induced Sepsis via Promoting Cell Proliferation and Inhibiting Apoptosis Li, Yin Kong, Chengqi Feng, Lei Tang, Wenliang Chen, Mengwei Zheng, Zhiyuan Cell J Original Article OBJECTIVE: This study aimed to explore the potential mechanism of MYC proto-oncogene, BHLH Transcription Factor (MYC) gene, on sepsis. MATERIALS AND METHODS: In this experimental study, rat-derived H9C2 cardiomyocyte cells were cultured in vitro, followed by lipopolysaccharide (LPS) treatment with different concentration gradients. The cholecystokinin octapeptide (CCK-8) assay, enzyme-linked immunoassay (ELISA) assay, quantitative reverse transcription polymerase chain reaction (qRT-PCR), cell transfection, Western blot and flow cytometry were used to observe the cellular apoptosis and proliferation of cells in both treated LPS groups and normal control group. RESULTS: The result of CCK-8 assay showed that silencing MYC inhibited cellular proliferation of sepsis in absence or presence of LPS treatment. ELISA assay showed that the expressions of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were decreased in MYC silenced group, but they were increased after LPS treatment. Moreover, Flow cytometry assay showed that MYC silencing contributed to the apoptosis of sepsis cells. Furthermore, the expression of inflammatory factors showed that MYC silencing elevated the expression of inflammation factors. CONCLUSION: MYC might take part in the process of LPS induced sepsis through suppressing apoptosis and inducing cell proliferation. Moreover, MYC might reduce inflammation during the progression of LPS induced sepsis. Royan Institute 2020 2020-09-08 /pmc/articles/PMC7481895/ /pubmed/32779435 http://dx.doi.org/10.22074/cellj.2020.6961 Text en Any use, distribution, reproduction or abstract of this publication in any medium, with the exception of commercial purposes, is permitted provided the original work is properly cited http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Li, Yin
Kong, Chengqi
Feng, Lei
Tang, Wenliang
Chen, Mengwei
Zheng, Zhiyuan
MYC Participates in Lipopolysaccharide-Induced Sepsis via Promoting Cell Proliferation and Inhibiting Apoptosis
title MYC Participates in Lipopolysaccharide-Induced Sepsis via Promoting Cell Proliferation and Inhibiting Apoptosis
title_full MYC Participates in Lipopolysaccharide-Induced Sepsis via Promoting Cell Proliferation and Inhibiting Apoptosis
title_fullStr MYC Participates in Lipopolysaccharide-Induced Sepsis via Promoting Cell Proliferation and Inhibiting Apoptosis
title_full_unstemmed MYC Participates in Lipopolysaccharide-Induced Sepsis via Promoting Cell Proliferation and Inhibiting Apoptosis
title_short MYC Participates in Lipopolysaccharide-Induced Sepsis via Promoting Cell Proliferation and Inhibiting Apoptosis
title_sort myc participates in lipopolysaccharide-induced sepsis via promoting cell proliferation and inhibiting apoptosis
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7481895/
https://www.ncbi.nlm.nih.gov/pubmed/32779435
http://dx.doi.org/10.22074/cellj.2020.6961
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