The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
E-Cadherin Expression Is Regulated by miR-192/215 by a Mechanism That Is Independent of the Profibrotic Effects of Transforming Growth Factor-β
Open accessAbstract
OBJECTIVE: Increased deposition of extracellular matrix (ECM) within the kidney is driven by profibrotic mediators including transforming growth factor-β (TGF-β) and connective tissue growth factor (CTGF). We investigated whether some of their effects may be mediated through changes in expression of certain microRNAs (miRNAs). RESEARCH DESIGN AND METHODS: Proximal tubular cells, primary rat mesangial cells, and human podocytes were analyzed for changes in the expression of key genes, ECM proteins, and miRNA after exposure to TGF-β (1–10 ng/μl). Tubular cells were also infected with CTGF-adenovirus. Kidneys from diabetic apoE mice were also analyzed for changes in gene expression and miRNA levels. RESULTS: TGF-β treatment was associated with morphologic and phenotypic changes typical of epithelial-mesenchymal transition (EMT) including increased fibrogenesis in all renal cell types and decreased E-cadherin expression in tubular cells. TGF-β treatment also modulated the expression of certain miRNAs, including decreased expression of miR-192/215 in tubular cells, mesangial cells, which are also decreased in diabetic kidney. Ectopic expression of miR-192/215 increased E-cadherin levels via repressed translation of ZEB2 mRNA, in the presence and absence of TGF-β, as demonstrated by a ZEB2 3′-untranslated region luciferase reporter assay. However, ectopic expression of miR-192/215 did not affect the expression of matrix proteins or their induction by TGF-β. In contrast, CTGF increased miR-192/215 levels, causing a decrease in ZEB2, and consequently increased E-cadherin mRNA. CONCLUSIONS: These data demonstrate the linking role of miRNA-192/215 and ZEB2 in TGF-β/CTGF–mediated changes in E-cadherin expression. These changes appear to occur independently of augmentation of matrix protein synthesis, suggesting that a multistep EMT program is not necessary for fibrogenesis to occur.
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Snail, Zeb and bHLH factors in tumour progression: An alliance against the epithelial phenotype?
Peinado, H., Olmeda, D., & Cano, A. (2007) · Nature reviews. Cancer · doi:10.1038/nrc2131 · Cited by 3,121
The snail superfamily of zinc-finger transcription factors
Nieto, M. A. (2002) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm757 · Cited by 1,719
Concordant Regulation of Translation and mRNA Abundance for Hundreds of Targets of a Human microRNA
Hendrickson, D. G., Hogan, D. J., McCullough, H. L., Myers, J. W., Herschlag, D., Ferrell, J. E., & Brown, P. O. (2009) · PLoS Biology · doi:10.1371/journal.pbio.1000238 · Cited by 418
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MicroRNA therapeutics: towards a new era for the management of cancer and other diseases
Rupaimoole, R., & Slack, F. J. (2017) · Nature Reviews Drug Discovery · doi:10.1038/nrd.2016.246 · Cited by 4,741
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
Interplay between miRNAs and human diseases
Paul, P., Chakraborty, A., Sarkar, D., Langthasa, M., Rahman, M., Bari, M., Singha, R. S., Malakar, A. K., & Chakraborty, S. (2018) · Journal of Cellular Physiology · doi:10.1002/jcp.25854 · Cited by 420
Smad3-Mediated Upregulation of miR-21 Promotes Renal Fibrosis
Zhong, X., Chung, A. C. K., Chen, H.-Y., Meng, X.-M., & Lan, H. Y. (2011) · Journal of the American Society of Nephrology · doi:10.1681/asn.2010111168 · Cited by 409
MicroRNAs in kidney physiology and disease
Trionfini, P., Benigni, A., & Remuzzi, G. (2015) · Nature Reviews Nephrology · doi:10.1038/nrneph.2014.202 · Cited by 353
Metadata
- Authors
- Wang, B., Herman-Edelstein, M., Koh, P., Burns, W., Jandeleit-Dahm, K., Watson, A., Saleem, M., Goodall, G. J., Twigg, S. M., Cooper, M. E., & Kantharidis, P.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2010-04-14
- Volume
- 59
- Issue
- 7
- Pages
- 1794-1802
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2148362020
- Cited by
- 244
- References
- 3
- FWCI
- 19.87
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Wang, B., Herman-Edelstein, M., Koh, P., Burns, W., Jandeleit-Dahm, K., Watson, A., Saleem, M., Goodall, G. J., Twigg, S. M., Cooper, M. E., & Kantharidis, P. (2010). E-Cadherin Expression Is Regulated by miR-192/215 by a Mechanism That Is Independent of the Profibrotic Effects of Transforming Growth Factor-β. Diabetes. https://doi.org/10.2337/db09-1736
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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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