The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
MicroRNA-101 Inhibited Postinfarct Cardiac Fibrosis and Improved Left Ventricular Compliance via the FBJ Osteosarcoma Oncogene/Transforming Growth Factor-β1 Pathway
Open accessAbstract
Background—: Cardiac interstitial fibrosis is a major cause of the deteriorated performance of the heart in patients with chronic myocardial infarction. MicroRNAs (miRs) have recently been proven to be a novel class of regulators of cardiovascular diseases, including those associated with cardiac fibrosis. This study aimed to explore the role of miR-101 in cardiac fibrosis and the underlying mechanisms. Methods and Results—: Four weeks after coronary artery ligation of rats, the expression of miR-101a and miR-101b (miR-101a/b) in the peri-infarct area was decreased. Treatment of cultured rat neonatal cardiac fibroblasts with angiotensin II also suppressed the expression of miR-101a/b. Forced expression of miR-101a/b suppressed the proliferation and collagen production in rat neonatal cardiac fibroblasts, as revealed by cell counting, MTT assay, and quantitative reverse transcription–polymerase chain reaction. The effect was abrogated by cotransfection with AMO-101a/b, the antisense inhibitors of miR-101a/b. c-Fos was found to be a target of miR-101a because overexpression of miR-101a decreased the protein and mRNA levels of c-Fos and its downstream protein transforming growth factor-β1. Silencing c-Fos by siRNA mimicked the antifibrotic action of miR-101a, whereas forced expression of c-Fos protein canceled the effect of miR-101a in cultured cardiac fibroblasts. Strikingly, echocardiography and hemodynamic measurements indicated remarkable improvement of the cardiac performance 4 weeks after adenovirus-mediated overexpression of miR-101a in rats with chronic myocardial infarction. Furthermore, the interstitial fibrosis was alleviated and the expression of c-Fos and transforming growth factor-β1 was inhibited. Conclusion—: Overexpression of miR-101a can mitigate interstitial fibrosis and the deterioration of cardiac performance in postinfarct rats, indicating the therapeutic potential of miR-101a for cardiac disease associated with fibrosis.
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Cites
MicroRNA-21 contributes to myocardial disease by stimulating MAP kinase signalling in fibroblasts
Thum, T., Gross, C., Fiedler, J., Fischer, T., Kissler, S., Bussen, M., Galuppo, P., Just, S., Rottbauer, W., Frantz, S., et al. (2008) · Nature · doi:10.1038/nature07511 · Cited by 2,349
Cited by
TGF-β: the master regulator of fibrosis
Meng, X.-M., Nikolic-Paterson, D. J., & Lan, H. Y. (2016) · Nature Reviews Nephrology · doi:10.1038/nrneph.2016.48 · Cited by 3,528
Frangogiannis, N. G. (2021) · Cardiovascular Research · doi:10.1093/cvr/cvaa324 · Cited by 1,229
Scioli, M. G., Storti, G., D’Amico, F., Rodríguez Guzmán, R., Centofanti, F., Doldo, E., Céspedes Miranda, E. M., & Orlandi, A. (2020) · Journal of Clinical Medicine · doi:10.3390/jcm9061995 · Cited by 281
Cell type–specific microRNA therapies for myocardial infarction
Liu, B., Wang, B., Zhang, X., Lock, R., Nash, T., & Vunjak-Novakovic, G. (2021) · Science Translational Medicine · doi:10.1126/scitranslmed.abd0914 · Cited by 53
Metadata
- Authors
- Pan, Z., Sun, X., Shan, H., Wang, N., Wang, J., Ren, J., Feng, S., Xie, L., Lu, C., Yuan, Y., Zhang, Y., Wang, Y., Lu, Y., & Yang, B.
- Venue
- Circulation
- Published
- 2012-08-14
- Volume
- 126
- Issue
- 7
- Pages
- 840-850
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2023560350
- Cited by
- 312
- References
- 1
- FWCI
- 16.50
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Pan, Z., Sun, X., Shan, H., Wang, N., Wang, J., Ren, J., Feng, S., Xie, L., Lu, C., Yuan, Y., Zhang, Y., Wang, Y., Lu, Y., & Yang, B. (2012). MicroRNA-101 Inhibited Postinfarct Cardiac Fibrosis and Improved Left Ventricular Compliance via the FBJ Osteosarcoma Oncogene/Transforming Growth Factor-β1 Pathway. Circulation. https://doi.org/10.1161/circulationaha.112.094524
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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