Eintrag weiter verarbeiten
Mir-21 Promotes Cardiac Fibrosis After Myocardial Infarction Via Targeting Smad7
Gespeichert in:
| Zeitschriftentitel: | Cellular Physiology and Biochemistry |
|---|---|
| Personen und Körperschaften: | , , , , , , , , , , , , , , |
| In: | Cellular Physiology and Biochemistry, 42, 2017, 6, S. 2207-2219 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
S. Karger AG
|
| Schlagwörter: |
| author_facet |
Yuan, Jinxia Chen, Hongtao Ge, Dawei Xu, Yu Xu, Haihua Yang, Yang Gu, Ming Zhou, Yuhe Zhu, Jingdong Ge, Ting Chen, Qun Gao, Yue Wang, Yanqing Li, Xiaowei Zhao, Yanfang Yuan, Jinxia Chen, Hongtao Ge, Dawei Xu, Yu Xu, Haihua Yang, Yang Gu, Ming Zhou, Yuhe Zhu, Jingdong Ge, Ting Chen, Qun Gao, Yue Wang, Yanqing Li, Xiaowei Zhao, Yanfang |
|---|---|
| author |
Yuan, Jinxia Chen, Hongtao Ge, Dawei Xu, Yu Xu, Haihua Yang, Yang Gu, Ming Zhou, Yuhe Zhu, Jingdong Ge, Ting Chen, Qun Gao, Yue Wang, Yanqing Li, Xiaowei Zhao, Yanfang |
| spellingShingle |
Yuan, Jinxia Chen, Hongtao Ge, Dawei Xu, Yu Xu, Haihua Yang, Yang Gu, Ming Zhou, Yuhe Zhu, Jingdong Ge, Ting Chen, Qun Gao, Yue Wang, Yanqing Li, Xiaowei Zhao, Yanfang Cellular Physiology and Biochemistry Mir-21 Promotes Cardiac Fibrosis After Myocardial Infarction Via Targeting Smad7 Physiology |
| author_sort |
yuan, jinxia |
| spelling |
Yuan, Jinxia Chen, Hongtao Ge, Dawei Xu, Yu Xu, Haihua Yang, Yang Gu, Ming Zhou, Yuhe Zhu, Jingdong Ge, Ting Chen, Qun Gao, Yue Wang, Yanqing Li, Xiaowei Zhao, Yanfang 1015-8987 1421-9778 S. Karger AG Physiology http://dx.doi.org/10.1159/000479995 <jats:p>Background/Aims: Cardiac fibrosis after myocardial infarction (MI) has been identified as an important factor in the deterioration of heart function. Previous studies have demonstrated that miR-21 plays an important role in various pathophysiological processes in the heart. However, the role of miR-21 in fibrosis regulation after MI remains unclear. Methods: To induce cardiac infarction, the left anterior descending coronary artery was permanently ligated of mice. First, we explored the expression of miR-21 in the infarcted zone in mice model of MI via RT-qPCR. Next, we examined the effects of TGF-β1 on miR-21 expression in cardiac fibroblasts (CFs). Then, CFs were infected with miR-21 mimics or miR-21 inhibitors to investigate the effects of miR-21 on the process of CFs activation in vitro. Further, bioinformatics analysis and luciferase reporter assay were performed to identify and validate the target gene of miR-21. At last, in-vivo study was done to confirm MiR-21 regulated myocardial fibrosis after MI in mice. Results: MiR-21 was up-regulated in the infarcted zone after MI in vivo. TGF-β1 treatment increased miR-21 expression in CFs. Overexpression of miR-21 promoted the effects of TGF-β1-induced activation of CFs, evidenced by increased expression of Col-1, α-SMA and F-actin, whereas inhibition of miR-21 attenuated the process of fibrosis. Bioinformatics, Western blot analysis and luciferase reporter assay demonstrated that Smad7 is a direct target of miR-21. In addition, in-vivo study revealed that MiR-21 regulated myocardial fibrosis after MI in mice. Conclusion: These findings suggested that miR-21 has a critical role in CF activation and cardiac fibrosis after MI through via TGF-β/Smad7 signaling pathway. Thus, miR-21 promises to be a potential therapy in treatment of cardiac fibrosis after MI.</jats:p> Mir-21 Promotes Cardiac Fibrosis After Myocardial Infarction Via Targeting Smad7 Cellular Physiology and Biochemistry |
| doi_str_mv |
10.1159/000479995 |
| facet_avail |
Online Free |
| finc_class_facet |
Biologie |
| format |
ElectronicArticle |
| fullrecord |
blob:ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTE1OS8wMDA0Nzk5OTU |
| id |
ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTE1OS8wMDA0Nzk5OTU |
| institution |
DE-Gla1 DE-Zi4 DE-15 DE-Pl11 DE-Rs1 DE-105 DE-14 DE-Ch1 DE-L229 DE-D275 DE-Bn3 DE-Brt1 DE-D161 DE-Zwi2 |
| imprint |
S. Karger AG, 2017 |
| imprint_str_mv |
S. Karger AG, 2017 |
| issn |
1421-9778 1015-8987 |
| issn_str_mv |
1421-9778 1015-8987 |
| language |
English |
| mega_collection |
S. Karger AG (CrossRef) |
| match_str |
yuan2017mir21promotescardiacfibrosisaftermyocardialinfarctionviatargetingsmad7 |
| publishDateSort |
2017 |
| publisher |
S. Karger AG |
| recordtype |
ai |
| record_format |
ai |
| series |
Cellular Physiology and Biochemistry |
| source_id |
49 |
| title |
Mir-21 Promotes Cardiac Fibrosis After Myocardial Infarction Via Targeting Smad7 |
| title_unstemmed |
Mir-21 Promotes Cardiac Fibrosis After Myocardial Infarction Via Targeting Smad7 |
| title_full |
Mir-21 Promotes Cardiac Fibrosis After Myocardial Infarction Via Targeting Smad7 |
| title_fullStr |
Mir-21 Promotes Cardiac Fibrosis After Myocardial Infarction Via Targeting Smad7 |
| title_full_unstemmed |
Mir-21 Promotes Cardiac Fibrosis After Myocardial Infarction Via Targeting Smad7 |
| title_short |
Mir-21 Promotes Cardiac Fibrosis After Myocardial Infarction Via Targeting Smad7 |
| title_sort |
mir-21 promotes cardiac fibrosis after myocardial infarction via targeting smad7 |
| topic |
Physiology |
| url |
http://dx.doi.org/10.1159/000479995 |
| publishDate |
2017 |
| physical |
2207-2219 |
| description |
<jats:p>Background/Aims: Cardiac fibrosis after myocardial infarction (MI) has been identified as an important factor in the deterioration of heart function. Previous studies have demonstrated that miR-21 plays an important role in various pathophysiological processes in the heart. However, the role of miR-21 in fibrosis regulation after MI remains unclear. Methods: To induce cardiac infarction, the left anterior descending coronary artery was permanently ligated of mice. First, we explored the expression of miR-21 in the infarcted zone in mice model of MI via RT-qPCR. Next, we examined the effects of TGF-β1 on miR-21 expression in cardiac fibroblasts (CFs). Then, CFs were infected with miR-21 mimics or miR-21 inhibitors to investigate the effects of miR-21 on the process of CFs activation in vitro. Further, bioinformatics analysis and luciferase reporter assay were performed to identify and validate the target gene of miR-21. At last, in-vivo study was done to confirm MiR-21 regulated myocardial fibrosis after MI in mice. Results: MiR-21 was up-regulated in the infarcted zone after MI in vivo. TGF-β1 treatment increased miR-21 expression in CFs. Overexpression of miR-21 promoted the effects of TGF-β1-induced activation of CFs, evidenced by increased expression of Col-1, α-SMA and F-actin, whereas inhibition of miR-21 attenuated the process of fibrosis. Bioinformatics, Western blot analysis and luciferase reporter assay demonstrated that Smad7 is a direct target of miR-21. In addition, in-vivo study revealed that MiR-21 regulated myocardial fibrosis after MI in mice. Conclusion: These findings suggested that miR-21 has a critical role in CF activation and cardiac fibrosis after MI through via TGF-β/Smad7 signaling pathway. Thus, miR-21 promises to be a potential therapy in treatment of cardiac fibrosis after MI.</jats:p> |
| container_issue |
6 |
| container_start_page |
2207 |
| container_title |
Cellular Physiology and Biochemistry |
| container_volume |
42 |
| format_de105 |
Article, E-Article |
| format_de14 |
Article, E-Article |
| format_de15 |
Article, E-Article |
| format_de520 |
Article, E-Article |
| format_de540 |
Article, E-Article |
| format_dech1 |
Article, E-Article |
| format_ded117 |
Article, E-Article |
| format_degla1 |
E-Article |
| format_del152 |
Buch |
| format_del189 |
Article, E-Article |
| format_dezi4 |
Article |
| format_dezwi2 |
Article, E-Article |
| format_finc |
Article, E-Article |
| format_nrw |
Article, E-Article |
| _version_ |
1792348515328851975 |
| geogr_code |
not assigned |
| last_indexed |
2024-03-01T18:10:47.777Z |
| geogr_code_person |
not assigned |
| openURL |
url_ver=Z39.88-2004&ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fvufind.svn.sourceforge.net%3Agenerator&rft.title=Mir-21+Promotes+Cardiac+Fibrosis+After+Myocardial+Infarction+Via+Targeting+Smad7&rft.date=2017-01-01&genre=article&issn=1421-9778&volume=42&issue=6&spage=2207&epage=2219&pages=2207-2219&jtitle=Cellular+Physiology+and+Biochemistry&atitle=Mir-21+Promotes+Cardiac+Fibrosis+After+Myocardial+Infarction+Via+Targeting+Smad7&aulast=Zhao&aufirst=Yanfang&rft_id=info%3Adoi%2F10.1159%2F000479995&rft.language%5B0%5D=eng |
| SOLR | |
| _version_ | 1792348515328851975 |
| author | Yuan, Jinxia, Chen, Hongtao, Ge, Dawei, Xu, Yu, Xu, Haihua, Yang, Yang, Gu, Ming, Zhou, Yuhe, Zhu, Jingdong, Ge, Ting, Chen, Qun, Gao, Yue, Wang, Yanqing, Li, Xiaowei, Zhao, Yanfang |
| author_facet | Yuan, Jinxia, Chen, Hongtao, Ge, Dawei, Xu, Yu, Xu, Haihua, Yang, Yang, Gu, Ming, Zhou, Yuhe, Zhu, Jingdong, Ge, Ting, Chen, Qun, Gao, Yue, Wang, Yanqing, Li, Xiaowei, Zhao, Yanfang, Yuan, Jinxia, Chen, Hongtao, Ge, Dawei, Xu, Yu, Xu, Haihua, Yang, Yang, Gu, Ming, Zhou, Yuhe, Zhu, Jingdong, Ge, Ting, Chen, Qun, Gao, Yue, Wang, Yanqing, Li, Xiaowei, Zhao, Yanfang |
| author_sort | yuan, jinxia |
| container_issue | 6 |
| container_start_page | 2207 |
| container_title | Cellular Physiology and Biochemistry |
| container_volume | 42 |
| description | <jats:p>Background/Aims: Cardiac fibrosis after myocardial infarction (MI) has been identified as an important factor in the deterioration of heart function. Previous studies have demonstrated that miR-21 plays an important role in various pathophysiological processes in the heart. However, the role of miR-21 in fibrosis regulation after MI remains unclear. Methods: To induce cardiac infarction, the left anterior descending coronary artery was permanently ligated of mice. First, we explored the expression of miR-21 in the infarcted zone in mice model of MI via RT-qPCR. Next, we examined the effects of TGF-β1 on miR-21 expression in cardiac fibroblasts (CFs). Then, CFs were infected with miR-21 mimics or miR-21 inhibitors to investigate the effects of miR-21 on the process of CFs activation in vitro. Further, bioinformatics analysis and luciferase reporter assay were performed to identify and validate the target gene of miR-21. At last, in-vivo study was done to confirm MiR-21 regulated myocardial fibrosis after MI in mice. Results: MiR-21 was up-regulated in the infarcted zone after MI in vivo. TGF-β1 treatment increased miR-21 expression in CFs. Overexpression of miR-21 promoted the effects of TGF-β1-induced activation of CFs, evidenced by increased expression of Col-1, α-SMA and F-actin, whereas inhibition of miR-21 attenuated the process of fibrosis. Bioinformatics, Western blot analysis and luciferase reporter assay demonstrated that Smad7 is a direct target of miR-21. In addition, in-vivo study revealed that MiR-21 regulated myocardial fibrosis after MI in mice. Conclusion: These findings suggested that miR-21 has a critical role in CF activation and cardiac fibrosis after MI through via TGF-β/Smad7 signaling pathway. Thus, miR-21 promises to be a potential therapy in treatment of cardiac fibrosis after MI.</jats:p> |
| doi_str_mv | 10.1159/000479995 |
| facet_avail | Online, Free |
| finc_class_facet | Biologie |
| format | ElectronicArticle |
| format_de105 | Article, E-Article |
| format_de14 | Article, E-Article |
| format_de15 | Article, E-Article |
| format_de520 | Article, E-Article |
| format_de540 | Article, E-Article |
| format_dech1 | Article, E-Article |
| format_ded117 | Article, E-Article |
| format_degla1 | E-Article |
| format_del152 | Buch |
| format_del189 | Article, E-Article |
| format_dezi4 | Article |
| format_dezwi2 | Article, E-Article |
| format_finc | Article, E-Article |
| format_nrw | Article, E-Article |
| geogr_code | not assigned |
| geogr_code_person | not assigned |
| id | ai-49-aHR0cDovL2R4LmRvaS5vcmcvMTAuMTE1OS8wMDA0Nzk5OTU |
| imprint | S. Karger AG, 2017 |
| imprint_str_mv | S. Karger AG, 2017 |
| institution | DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-D161, DE-Zwi2 |
| issn | 1421-9778, 1015-8987 |
| issn_str_mv | 1421-9778, 1015-8987 |
| language | English |
| last_indexed | 2024-03-01T18:10:47.777Z |
| match_str | yuan2017mir21promotescardiacfibrosisaftermyocardialinfarctionviatargetingsmad7 |
| mega_collection | S. Karger AG (CrossRef) |
| physical | 2207-2219 |
| publishDate | 2017 |
| publishDateSort | 2017 |
| publisher | S. Karger AG |
| record_format | ai |
| recordtype | ai |
| series | Cellular Physiology and Biochemistry |
| source_id | 49 |
| spelling | Yuan, Jinxia Chen, Hongtao Ge, Dawei Xu, Yu Xu, Haihua Yang, Yang Gu, Ming Zhou, Yuhe Zhu, Jingdong Ge, Ting Chen, Qun Gao, Yue Wang, Yanqing Li, Xiaowei Zhao, Yanfang 1015-8987 1421-9778 S. Karger AG Physiology http://dx.doi.org/10.1159/000479995 <jats:p>Background/Aims: Cardiac fibrosis after myocardial infarction (MI) has been identified as an important factor in the deterioration of heart function. Previous studies have demonstrated that miR-21 plays an important role in various pathophysiological processes in the heart. However, the role of miR-21 in fibrosis regulation after MI remains unclear. Methods: To induce cardiac infarction, the left anterior descending coronary artery was permanently ligated of mice. First, we explored the expression of miR-21 in the infarcted zone in mice model of MI via RT-qPCR. Next, we examined the effects of TGF-β1 on miR-21 expression in cardiac fibroblasts (CFs). Then, CFs were infected with miR-21 mimics or miR-21 inhibitors to investigate the effects of miR-21 on the process of CFs activation in vitro. Further, bioinformatics analysis and luciferase reporter assay were performed to identify and validate the target gene of miR-21. At last, in-vivo study was done to confirm MiR-21 regulated myocardial fibrosis after MI in mice. Results: MiR-21 was up-regulated in the infarcted zone after MI in vivo. TGF-β1 treatment increased miR-21 expression in CFs. Overexpression of miR-21 promoted the effects of TGF-β1-induced activation of CFs, evidenced by increased expression of Col-1, α-SMA and F-actin, whereas inhibition of miR-21 attenuated the process of fibrosis. Bioinformatics, Western blot analysis and luciferase reporter assay demonstrated that Smad7 is a direct target of miR-21. In addition, in-vivo study revealed that MiR-21 regulated myocardial fibrosis after MI in mice. Conclusion: These findings suggested that miR-21 has a critical role in CF activation and cardiac fibrosis after MI through via TGF-β/Smad7 signaling pathway. Thus, miR-21 promises to be a potential therapy in treatment of cardiac fibrosis after MI.</jats:p> Mir-21 Promotes Cardiac Fibrosis After Myocardial Infarction Via Targeting Smad7 Cellular Physiology and Biochemistry |
| spellingShingle | Yuan, Jinxia, Chen, Hongtao, Ge, Dawei, Xu, Yu, Xu, Haihua, Yang, Yang, Gu, Ming, Zhou, Yuhe, Zhu, Jingdong, Ge, Ting, Chen, Qun, Gao, Yue, Wang, Yanqing, Li, Xiaowei, Zhao, Yanfang, Cellular Physiology and Biochemistry, Mir-21 Promotes Cardiac Fibrosis After Myocardial Infarction Via Targeting Smad7, Physiology |
| title | Mir-21 Promotes Cardiac Fibrosis After Myocardial Infarction Via Targeting Smad7 |
| title_full | Mir-21 Promotes Cardiac Fibrosis After Myocardial Infarction Via Targeting Smad7 |
| title_fullStr | Mir-21 Promotes Cardiac Fibrosis After Myocardial Infarction Via Targeting Smad7 |
| title_full_unstemmed | Mir-21 Promotes Cardiac Fibrosis After Myocardial Infarction Via Targeting Smad7 |
| title_short | Mir-21 Promotes Cardiac Fibrosis After Myocardial Infarction Via Targeting Smad7 |
| title_sort | mir-21 promotes cardiac fibrosis after myocardial infarction via targeting smad7 |
| title_unstemmed | Mir-21 Promotes Cardiac Fibrosis After Myocardial Infarction Via Targeting Smad7 |
| topic | Physiology |
| url | http://dx.doi.org/10.1159/000479995 |