The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
A microRNA circuit mediates transforming growth factor-β1 autoregulation in renal glomerular mesangial cells
Open accessAbstract
Enhanced transforming growth factor-β1 (TGF-β1) expression in renal cells promotes fibrosis and hypertrophy during the progression of diabetic nephropathy. The TGF-β1 promoter is positively controlled by the E-box regulators, Upstream Stimulatory Factors (USFs), in response to diabetic (high glucose) conditions; however, it is not clear whether TGF-β1 is autoregulated by itself. Since changes in microRNAs (miRNAs) have been implicated in kidney disease, we tested their involvement in this process. TGF-β1 levels were found to be upregulated by microRNA-192 (miR-192) or miR-200b/c in mouse mesangial cells. Amounts of miR-200b/c were increased in glomeruli from type 1 (streptozotocin) and type 2 (db/db) diabetic mice, and in mouse mesangial cells treated with TGF-β1 in vitro. Levels of miR-200b/c were also upregulated by miR-192 in the mesangial cells, suggesting that miR-200b/c are downstream of miR-192. Activity of the TGF-β1 promoter was upregulated by TGF-β1 or miR-192, demonstrating that the miR-192-miR-200 cascade induces TGF-β1 expression. TGF-β1 increased the occupancy of activators USF1 and Tfe3, and decreased that of the repressor Zeb1 on the TGF-β1 promoter E-box binding sites. Inhibitors of miR-192 decreased the expression of miR-200b/c, Col1a2, Col4a1 and TGF-β1 in mouse mesangial cells, and in mouse kidney cortex. Thus, miRNA-regulated circuits may amplify TGF-β1 signaling accelerating chronic fibrotic diseases such as diabetic nephropathy.
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Cites
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“Their widespread and distinct expression patterns under normal and disease states make miRNAs attractive molecular therapeutic targets for human diseases, especially because of the recent advances in the development of chemically modified inhibitors of miRNAs like antagomirs(20) and locked nucleic acid (LNA) antimiRs.…”
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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
Cellular and molecular mechanisms of renal fibrosis
Liu, Y. (2011) · Nature Reviews Nephrology · doi:10.1038/nrneph.2011.149 · Cited by 1,446
Recent Developments in Myofibroblast Biology
Hinz, B., Phan, S. H., Thannickal, V. J., Prunotto, M., Desmoulière, A., Varga, J., De Wever, O., Mareel, M., & Gabbiani, G. (2012) · The American Journal of Pathology · doi:10.1016/j.ajpath.2012.02.004 · Cited by 1,193
TGF-β/Smad signaling in renal fibrosis
Meng, X.-M., Tang, P. M.-K., Li, J., & Lan, H. Y. (2015) · Frontiers in Physiology · doi:10.3389/fphys.2015.00082 · Cited by 666
Epigenetics and epigenomics in diabetic kidney disease and metabolic memory
Kato, M., & Natarajan, R. (2019) · Nature Reviews Nephrology · doi:10.1038/s41581-019-0135-6 · Cited by 600
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Metadata
- Authors
- Kato, M., Arce, L., Wang, M., Putta, S., Lanting, L., & Natarajan, R.
- Venue
- Kidney International
- Publisher
- Elsevier BV
- Published
- 2011-08
- Volume
- 80
- Issue
- 4
- Pages
- 358-368
- ISSN
- 0085-2538 (ISSN-L)
- OpenAlex
- W2045991006
- Cited by
- 238
- References
- 5
- FWCI
- 16.88
- Type
- journal article
- Language
- en
- Open access
- bronze
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