The DOI matches its Crossref record; 60 of the 60 references it cites were found in a registry or an index.
Experimental myocardial infarction triggers canonical Wnt signaling and endothelial-to-mesenchymal transition
Open accessAbstract
SUMMARY: Despite available therapies, myocardial infarction (MI) remains a leading cause of death worldwide. Better understanding of the molecular and cellular mechanisms that regulate cardiac repair should help to improve the clinical outcome of MI patients. Using the reporter mouse line TOPGAL, we show that canonical (β-catenin-dependent) Wnt signaling is induced 4 days after experimental MI in subepicardial endothelial cells and perivascular smooth muscle actin (SMA)-positive (SMA+) cells. At 1 week after ischemic injury, a large number of canonical-Wnt-positive cells accumulated in the infarct area during granulation tissue formation. Coincidently with canonical Wnt activation, endothelial-to-mesenchymal transition (EndMT) was also triggered after MI. Using cell lineage tracing, we show that a significant portion of the canonical-Wnt-marked SMA+ mesenchymal cells is derived from endothelial cells. Canonical Wnt signaling induces mesenchymal characteristics in cultured endothelial cells, suggesting a direct role in EndMT. In conclusion, our study demonstrates that canonical Wnt activation and EndMT are molecular and cellular responses to MI and that canonical Wnt signaling activity is a characteristic property of EndMT-derived mesenchymal cells that take part in cardiac tissue repair after MI. These findings could lead to new strategies to improve the course of cardiac repair by temporal and cell-type-specific manipulation of canonical Wnt signaling.
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1 retracted
Lahat, G., Zhu, Q.-S., Huang, K.-L., Wang, S., Bolshakov, S., Liu, J., Torres, K., Langley, R. R., Lazar, A. J., Hung, M. C., et al. (2010) · PLoS ONE · doi:10.1371/journal.pone.0010105 · Cited by 213
RetractedAnalysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method
Livak, K. J., & Schmittgen, T. D. (2001) · Methods · doi:10.1006/meth.2001.1262 · Cited by 180,860
Harrison's Principles of Internal Medicine.
(1988) · Annals of Internal Medicine · doi:10.7326/0003-4819-108-3-499_2 · Cited by 12,514
Generalized lacZ expression with the ROSA26 Cre reporter strain
Soriano, P. (1999) · Nature Genetics · doi:10.1038/5007 · Cited by 4,859
VEGF guides angiogenic sprouting utilizing endothelial tip cell filopodia
Gerhardt, H., Golding, M., Fruttiger, M., Ruhrberg, C., Lundkvist, A., Abramsson, A., Jeltsch, M., Mitchell, C., Alitalo, K., Shima, D., et al. (2003) · The Journal of Cell Biology · doi:10.1083/jcb.200302047 · Cited by 2,894
Biomarkers for epithelial-mesenchymal transitions
Zeisberg, M., & Neilson, E. G. (2009) · Journal of Clinical Investigation · doi:10.1172/jci36183 · Cited by 2,299 · cited 3×
“Quantitative realtime RT-PCR analysis for the expression of EndMT-related genes at different time points after MI revealed that the peak in the expression of genes such as Snail, Fsp1, Tgf1, vimentin and Col1A1 corresponds to the appearance of CD31+/SMA+ cells on day 7 post-MI (Fig.”
Endothelial-to-mesenchymal transition contributes to cardiac fibrosis
Zeisberg, E. M., Tarnavski, O., Zeisberg, M., Dorfman, A. L., McMullen, J. R., Gustafsson, E., Chandraker, A., Yuan, X., Pu, W. T., Roberts, A. B., et al. (2007) · Nature Medicine · doi:10.1038/nm1613 · Cited by 2,222
Gnecchi, M., He, H., Liang, O. D., Melo, L. G., Morello, F., Mu, H., Noiseux, N., Zhang, L., Pratt, R. E., Ingwall, J. S., et al. (2005) · Nature Medicine · doi:10.1038/nm0405-367 · Cited by 1,677
Harrison's Principles of Internal Medicine
Freeman, D. L. (2001) · JAMA: The Journal of the American Medical Association · doi:10.1001/jama.286.8.971-a · Cited by 1,624
Increased Wnt signaling during aging alters muscle stem cell fate and increases fibrosis
Brack, A. S., Conboy, M. J., Roy, S., Lee, M., Kuo, C. J., Keller, C., & Rando, T. A. (2007) · Science · doi:10.1126/science.1144090 · Cited by 1,564
Cited by
Frangogiannis, N. G. (2021) · Cardiovascular Research · doi:10.1093/cvr/cvaa324 · Cited by 1,229
Signaling pathways and targeted therapy for myocardial infarction
Zhang, Q., Wang, L., Wang, S., Cheng, H., Xu, L., Pei, G., Wang, Y., Fu, C., Jiang, Y., He, C., et al. (2022) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-022-00925-z · Cited by 831
Russo, I., & Frangogiannis, N. G. (2016) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2015.12.011 · Cited by 474
Endocardial and Epicardial Epithelial to Mesenchymal Transitions in Heart Development and Disease
von Gise, A., & Pu, W. T. (2012) · Circulation Research · doi:10.1161/circresaha.111.259960 · Cited by 419
Endothelial–mesenchymal transition in atherosclerosis
Souilhol, C., Harmsen, M. C., Evans, P. C., & Krenning, G. (2018) · Cardiovascular Research · doi:10.1093/cvr/cvx253 · Cited by 401
Metadata
- Authors
- Aisagbonhi, O., Rai, M., Ryzhov, S., Atria, N., Feoktistov, I., & Hatzopoulos, A. K.
- Venue
- Disease Models & Mechanisms
- Publisher
- The Company of Biologists
- Published
- 2011-07-01
- Volume
- 4
- Issue
- 4
- Pages
- 469-483
- ISSN
- 1754-8403 (ISSN-L)
- 1754-8411
- OpenAlex
- W2051075947
- Cited by
- 302
- References
- 60
- FWCI
- 5.17
- Type
- journal article
- Language
- en
- Open access
- gold
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