Plac8 regulates the fibrogenic ability of cardiac fibroblasts in mice with myocardial infarction
Cardiac fibroblasts (CFs) are of vital importance for post-myocardial infarction (MI) remodeling. This study explored the role of Placenta specific 8 (Plac8) in MI on the basis of single-cell RNA-Seq (scRNA-Seq) data (GSE136088) and micro-array data (GSE153485). Through bioinformatics analysis, Plac...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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Taylor & Francis Group
2024-12-01
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| Series: | All Life |
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| Online Access: | http://dx.doi.org/10.1080/26895293.2023.2299569 |
| _version_ | 1797366048895270912 |
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| author | Ting Fu Jianping Gong Lei Xu Ningning Ji |
| author_facet | Ting Fu Jianping Gong Lei Xu Ningning Ji |
| author_sort | Ting Fu |
| collection | DOAJ |
| description | Cardiac fibroblasts (CFs) are of vital importance for post-myocardial infarction (MI) remodeling. This study explored the role of Placenta specific 8 (Plac8) in MI on the basis of single-cell RNA-Seq (scRNA-Seq) data (GSE136088) and micro-array data (GSE153485). Through bioinformatics analysis, Plac8 was finally identified as a key gene related to fibroblasts. In addition, primary CFs of the neonatal mice were isolated, cultured and treated with hypoxia for in vitro cell model construction. Hydroxyproline assay demonstrated enhanced collagen production in hypoxic CFs, and qRT-PCR revealed increased relative contents of type I and type III collagen (Col1a1 and Col3a1). Western blot showed increased protein expression level of α-smooth muscle actin (α-SMA), and transwell assay and wound-healing assay collectively suggested enhanced cell migration. Moreover, Plac8 was found to be upregulated in hypoxic CFs. Then, after transfection with siNC or siPlac8, it was revealed that down-regulating Plac8 protein expression in hypoxic CFs reduced the levels of collagen secretion, the number of activated CFs and the degree of cell migration, indicating the regulation of Plac8 on hypoxic CFs’ transformation into myofibroblasts, cell migration and collagen deposition. Excessive myocardial fibrosis can cause adverse cardiac remodeling, leading to malignant arrhythmia and even heart failure. |
| first_indexed | 2024-03-08T16:58:38Z |
| format | Article |
| id | doaj.art-3696d0e81f7b4f319961c3b68ae90c5b |
| institution | Directory Open Access Journal |
| issn | 2689-5307 |
| language | English |
| last_indexed | 2024-03-08T16:58:38Z |
| publishDate | 2024-12-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | All Life |
| spelling | doaj.art-3696d0e81f7b4f319961c3b68ae90c5b2024-01-04T15:59:10ZengTaylor & Francis GroupAll Life2689-53072024-12-0117110.1080/26895293.2023.22995692299569Plac8 regulates the fibrogenic ability of cardiac fibroblasts in mice with myocardial infarctionTing Fu0Jianping Gong1Lei Xu2Ningning Ji3Department of Cardiology, Yiwu Central HospitalDepartment of Cardiology, Yiwu Central HospitalDepartment of Cardiology, Yiwu Central HospitalDepartment of Cardiology, Yiwu Central HospitalCardiac fibroblasts (CFs) are of vital importance for post-myocardial infarction (MI) remodeling. This study explored the role of Placenta specific 8 (Plac8) in MI on the basis of single-cell RNA-Seq (scRNA-Seq) data (GSE136088) and micro-array data (GSE153485). Through bioinformatics analysis, Plac8 was finally identified as a key gene related to fibroblasts. In addition, primary CFs of the neonatal mice were isolated, cultured and treated with hypoxia for in vitro cell model construction. Hydroxyproline assay demonstrated enhanced collagen production in hypoxic CFs, and qRT-PCR revealed increased relative contents of type I and type III collagen (Col1a1 and Col3a1). Western blot showed increased protein expression level of α-smooth muscle actin (α-SMA), and transwell assay and wound-healing assay collectively suggested enhanced cell migration. Moreover, Plac8 was found to be upregulated in hypoxic CFs. Then, after transfection with siNC or siPlac8, it was revealed that down-regulating Plac8 protein expression in hypoxic CFs reduced the levels of collagen secretion, the number of activated CFs and the degree of cell migration, indicating the regulation of Plac8 on hypoxic CFs’ transformation into myofibroblasts, cell migration and collagen deposition. Excessive myocardial fibrosis can cause adverse cardiac remodeling, leading to malignant arrhythmia and even heart failure.http://dx.doi.org/10.1080/26895293.2023.2299569plac8myocardial infarction (mi)cardiac fibroblasts (cfs)wgcna |
| spellingShingle | Ting Fu Jianping Gong Lei Xu Ningning Ji Plac8 regulates the fibrogenic ability of cardiac fibroblasts in mice with myocardial infarction All Life plac8 myocardial infarction (mi) cardiac fibroblasts (cfs) wgcna |
| title | Plac8 regulates the fibrogenic ability of cardiac fibroblasts in mice with myocardial infarction |
| title_full | Plac8 regulates the fibrogenic ability of cardiac fibroblasts in mice with myocardial infarction |
| title_fullStr | Plac8 regulates the fibrogenic ability of cardiac fibroblasts in mice with myocardial infarction |
| title_full_unstemmed | Plac8 regulates the fibrogenic ability of cardiac fibroblasts in mice with myocardial infarction |
| title_short | Plac8 regulates the fibrogenic ability of cardiac fibroblasts in mice with myocardial infarction |
| title_sort | plac8 regulates the fibrogenic ability of cardiac fibroblasts in mice with myocardial infarction |
| topic | plac8 myocardial infarction (mi) cardiac fibroblasts (cfs) wgcna |
| url | http://dx.doi.org/10.1080/26895293.2023.2299569 |
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