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Bellidifolin Inhibits SRY-Related High Mobility Group-Box Gene 9 to Block TGF-β Signalling Activation to Ameliorate Myocardial Fibrosis

Myocardial fibrosis is the main morphological change of ventricular remodelling caused by cardiovascular diseases, mainly manifested due to the excessive production of collagen proteins. SRY-related high mobility group-box gene 9 (SOX9) is a new target regulating myocardial fibrosis. Bellidifolin (B...

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Autores principales: Yao, Ting-Ting, Yang, Hong-Xia, Sun, Jia-Huan, Zhang, Yue, Zhang, Yu, Song, Qiu-Hang, Liu, Wei-Zhe, Zhang, Juan-Juan, Li, Ai-Ying
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9110156/
https://www.ncbi.nlm.nih.gov/pubmed/35586685
http://dx.doi.org/10.1155/2022/6841276
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author Yao, Ting-Ting
Yang, Hong-Xia
Sun, Jia-Huan
Zhang, Yue
Zhang, Yu
Song, Qiu-Hang
Liu, Wei-Zhe
Zhang, Juan-Juan
Li, Ai-Ying
author_facet Yao, Ting-Ting
Yang, Hong-Xia
Sun, Jia-Huan
Zhang, Yue
Zhang, Yu
Song, Qiu-Hang
Liu, Wei-Zhe
Zhang, Juan-Juan
Li, Ai-Ying
author_sort Yao, Ting-Ting
collection PubMed
description Myocardial fibrosis is the main morphological change of ventricular remodelling caused by cardiovascular diseases, mainly manifested due to the excessive production of collagen proteins. SRY-related high mobility group-box gene 9 (SOX9) is a new target regulating myocardial fibrosis. Bellidifolin (BEL), the active component of G. acuta, can prevent heart damage. However, it is unclear whether BEL can regulate SOX9 to alleviate myocardial fibrosis. The mice were subjected to isoproterenol (ISO) to establish myocardial fibrosis, and human myocardial fibroblasts (HCFs) were activated by TGF-β1 in the present study. The pathological changes of cardiac tissue were observed by HE staining. Masson staining was applied to reveal the collagen deposition in the heart. The measurement for expression of fibrosis-related proteins, SOX9, and TGF-β1 signalling molecules adopted Western blot and immunohistochemistry. The effects of BEL on HCFs, activity were detected by CCK-8. The result showed that BEL did not affect cell viability. And, the data indicated that BEL inhibited the elevations in α-SMA, Collagen I, and Collagen III by decreasing SOX9 expression. Additionally, SOX9 suppression by siRNA downregulated the TGF-β1 expression and prevented Smad3 phosphorylation, as supported by reducing the expression of α-SMA, Collagen I, and Collagen III. In vivo study verified that BEL ameliorated myocardial fibrosis by inhibiting SOX9. Therefore, BEL inhibited SOX9 to block TGF-β1 signalling activation to ameliorate myocardial fibrosis.
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spelling pubmed-91101562022-05-17 Bellidifolin Inhibits SRY-Related High Mobility Group-Box Gene 9 to Block TGF-β Signalling Activation to Ameliorate Myocardial Fibrosis Yao, Ting-Ting Yang, Hong-Xia Sun, Jia-Huan Zhang, Yue Zhang, Yu Song, Qiu-Hang Liu, Wei-Zhe Zhang, Juan-Juan Li, Ai-Ying Evid Based Complement Alternat Med Research Article Myocardial fibrosis is the main morphological change of ventricular remodelling caused by cardiovascular diseases, mainly manifested due to the excessive production of collagen proteins. SRY-related high mobility group-box gene 9 (SOX9) is a new target regulating myocardial fibrosis. Bellidifolin (BEL), the active component of G. acuta, can prevent heart damage. However, it is unclear whether BEL can regulate SOX9 to alleviate myocardial fibrosis. The mice were subjected to isoproterenol (ISO) to establish myocardial fibrosis, and human myocardial fibroblasts (HCFs) were activated by TGF-β1 in the present study. The pathological changes of cardiac tissue were observed by HE staining. Masson staining was applied to reveal the collagen deposition in the heart. The measurement for expression of fibrosis-related proteins, SOX9, and TGF-β1 signalling molecules adopted Western blot and immunohistochemistry. The effects of BEL on HCFs, activity were detected by CCK-8. The result showed that BEL did not affect cell viability. And, the data indicated that BEL inhibited the elevations in α-SMA, Collagen I, and Collagen III by decreasing SOX9 expression. Additionally, SOX9 suppression by siRNA downregulated the TGF-β1 expression and prevented Smad3 phosphorylation, as supported by reducing the expression of α-SMA, Collagen I, and Collagen III. In vivo study verified that BEL ameliorated myocardial fibrosis by inhibiting SOX9. Therefore, BEL inhibited SOX9 to block TGF-β1 signalling activation to ameliorate myocardial fibrosis. Hindawi 2022-05-09 /pmc/articles/PMC9110156/ /pubmed/35586685 http://dx.doi.org/10.1155/2022/6841276 Text en Copyright © 2022 Ting-Ting Yao et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Yao, Ting-Ting
Yang, Hong-Xia
Sun, Jia-Huan
Zhang, Yue
Zhang, Yu
Song, Qiu-Hang
Liu, Wei-Zhe
Zhang, Juan-Juan
Li, Ai-Ying
Bellidifolin Inhibits SRY-Related High Mobility Group-Box Gene 9 to Block TGF-β Signalling Activation to Ameliorate Myocardial Fibrosis
title Bellidifolin Inhibits SRY-Related High Mobility Group-Box Gene 9 to Block TGF-β Signalling Activation to Ameliorate Myocardial Fibrosis
title_full Bellidifolin Inhibits SRY-Related High Mobility Group-Box Gene 9 to Block TGF-β Signalling Activation to Ameliorate Myocardial Fibrosis
title_fullStr Bellidifolin Inhibits SRY-Related High Mobility Group-Box Gene 9 to Block TGF-β Signalling Activation to Ameliorate Myocardial Fibrosis
title_full_unstemmed Bellidifolin Inhibits SRY-Related High Mobility Group-Box Gene 9 to Block TGF-β Signalling Activation to Ameliorate Myocardial Fibrosis
title_short Bellidifolin Inhibits SRY-Related High Mobility Group-Box Gene 9 to Block TGF-β Signalling Activation to Ameliorate Myocardial Fibrosis
title_sort bellidifolin inhibits sry-related high mobility group-box gene 9 to block tgf-β signalling activation to ameliorate myocardial fibrosis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9110156/
https://www.ncbi.nlm.nih.gov/pubmed/35586685
http://dx.doi.org/10.1155/2022/6841276
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