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Sp1 mediates microRNA-29c-regulated type I collagen production in renal tubular epithelial cells.
Exp Cell Res. 2013 Aug 15; 319(14):2254-65.EC

Abstract

Specificity protein 1 (Sp1), a ubiquitously expressed transcription factor, plays a potential pathogenic role for fibrotic disease in many organs by regulating the expression of several fibrosis-related genes, however, its role in kidney fibrosis and the mechanisms regulating its expression remain incompletely clarified. Here, we found that Sp1 was markedly induced and closely correlated with interstitial type I collagen accumulation in kidney tubular epithelia from obstructive nephropathy. In vitro, both Sp1 and type I collagen expression were up-regulated in TGF-β1-treated kidney tubular epithelial cells (NRK-52E), whereas knockdown of Sp1 largely abolished TGF-β1-induced type I collagen production, suggesting that Sp1 induction is partially responsible for type I collagen expression. In addition, we found that miR-29c expression was remarkably reduced in either the tubular epithelial cells from kidney with UUO nephropathy or TGF-β1-treated NRK-52E cells. Knockdown of miR-29c could sufficiently induce Sp1 and type I collagen expression, whereas ectopic expression of miR-29c largely abolished their expression stimulated by TGF-β1 in NRK-52E cells. Furthermore, knockdown of Sp1 effectively hindered type I collagen induction stimulated by miR-29c down-regulation. Collectively, this study demonstrates that Sp1 acts as an essential mediator for miR-29c in regulating type I collagen production in tubular epithelial cells, which may provide a novel mechanistic insight about miR-29c in renal fibrosis.

Authors+Show Affiliations

Center for Kidney Disease, Second Affiliated Hospital, Nanjing Medical University, Nanjing 210003, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23806282

Citation

Jiang, Lei, et al. "Sp1 Mediates microRNA-29c-regulated Type I Collagen Production in Renal Tubular Epithelial Cells." Experimental Cell Research, vol. 319, no. 14, 2013, pp. 2254-65.
Jiang L, Zhou Y, Xiong M, et al. Sp1 mediates microRNA-29c-regulated type I collagen production in renal tubular epithelial cells. Exp Cell Res. 2013;319(14):2254-65.
Jiang, L., Zhou, Y., Xiong, M., Fang, L., Wen, P., Cao, H., Yang, J., Dai, C., & He, W. (2013). Sp1 mediates microRNA-29c-regulated type I collagen production in renal tubular epithelial cells. Experimental Cell Research, 319(14), 2254-65. https://doi.org/10.1016/j.yexcr.2013.06.007
Jiang L, et al. Sp1 Mediates microRNA-29c-regulated Type I Collagen Production in Renal Tubular Epithelial Cells. Exp Cell Res. 2013 Aug 15;319(14):2254-65. PubMed PMID: 23806282.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Sp1 mediates microRNA-29c-regulated type I collagen production in renal tubular epithelial cells. AU - Jiang,Lei, AU - Zhou,Yang, AU - Xiong,Mingxia, AU - Fang,Li, AU - Wen,Ping, AU - Cao,Hongdi, AU - Yang,Junwei, AU - Dai,Chunsun, AU - He,Weichun, Y1 - 2013/06/24/ PY - 2013/05/13/received PY - 2013/06/12/revised PY - 2013/06/14/accepted PY - 2013/6/29/entrez PY - 2013/6/29/pubmed PY - 2013/10/19/medline KW - ECM KW - MicroRNA-29c KW - Renal fibrosis KW - Sp1 KW - Specificity protein 1 KW - TGF KW - Tubular epithelial cell KW - Type I collagen KW - UTR KW - UUO KW - excessive extracellular matrix KW - miR KW - microRNA KW - siRNA KW - small interfering RNA KW - specificity protein 1 KW - transforming growth factor KW - unilateral ureteral obstruction KW - untranslated region SP - 2254 EP - 65 JF - Experimental cell research JO - Exp Cell Res VL - 319 IS - 14 N2 - Specificity protein 1 (Sp1), a ubiquitously expressed transcription factor, plays a potential pathogenic role for fibrotic disease in many organs by regulating the expression of several fibrosis-related genes, however, its role in kidney fibrosis and the mechanisms regulating its expression remain incompletely clarified. Here, we found that Sp1 was markedly induced and closely correlated with interstitial type I collagen accumulation in kidney tubular epithelia from obstructive nephropathy. In vitro, both Sp1 and type I collagen expression were up-regulated in TGF-β1-treated kidney tubular epithelial cells (NRK-52E), whereas knockdown of Sp1 largely abolished TGF-β1-induced type I collagen production, suggesting that Sp1 induction is partially responsible for type I collagen expression. In addition, we found that miR-29c expression was remarkably reduced in either the tubular epithelial cells from kidney with UUO nephropathy or TGF-β1-treated NRK-52E cells. Knockdown of miR-29c could sufficiently induce Sp1 and type I collagen expression, whereas ectopic expression of miR-29c largely abolished their expression stimulated by TGF-β1 in NRK-52E cells. Furthermore, knockdown of Sp1 effectively hindered type I collagen induction stimulated by miR-29c down-regulation. Collectively, this study demonstrates that Sp1 acts as an essential mediator for miR-29c in regulating type I collagen production in tubular epithelial cells, which may provide a novel mechanistic insight about miR-29c in renal fibrosis. SN - 1090-2422 UR - https://www.unboundmedicine.com/medline/citation/23806282/Sp1_mediates_microRNA_29c_regulated_type_I_collagen_production_in_renal_tubular_epithelial_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4827(13)00268-1 DB - PRIME DP - Unbound Medicine ER -