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ILK participates in renal interstitial fibrosis by altering the phenotype of renal tubular epithelial cells via TGF-β1/smad pathway.
Eur Rev Med Pharmacol Sci. 2019 Jan; 23(1):289-296.ER

Abstract

OBJECTIVE

To explore the specific role of ILK (integrin-linked kinase) in regulating renal fibrosis and its underlying mechanism.

MATERIALS AND METHODS

NRK-52E cells were induced by transforming growth factor-β1 (TGF-β1) for observing phenotype change. Renal tubular epithelial cell marker, fibrosis marker and expression level of ILK in NRK-52E cells were also detected. After overexpression of ILK, phenotype change of NRK-52E cells was observed. For in vivo experiments, we constructed UUO (unilateral ureteral obstruction) model in CD1 mice. Renal tubular epithelial cell marker, fibrosis marker and expression level of ILK in UUO mice were detected. The regulatory effect of ILK on renal fibrosis was detected after injection of ILK overexpression plasmid. Western blot was performed to detect related genes in the TGF-β1/smad pathway.

RESULTS

Accompanied by the TGF-β1-induced phenotype change in NRK-52E cells, both mRNA and protein levels of ILK were upregulated. Overexpression of ILK remarkably stimulated the phenotype change in NRK-52E cells. Similarly, ILK was highly expressed in UUO mice. Renal fibrosis was aggravated after injection of ILK overexpression plasmid in UUO mice. Western blot results showed that expressions of p-smad3 and smad3 were upregulated during the process of renal fibrosis.

CONCLUSIONS

ILK is upregulated during the process of renal fibrosis. ILK participates in the development of renal fibrosis by altering phenotypes of renal tubular epithelial cells via a TGF-β1/smad pathway.

Authors+Show Affiliations

Department of Nephrology, The Third Affiliated Hospital of Soochow University, Changzhou, China. horizonminmin@163.com.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30657569

Citation

Li, M, et al. "ILK Participates in Renal Interstitial Fibrosis By Altering the Phenotype of Renal Tubular Epithelial Cells Via TGF-β1/smad Pathway." European Review for Medical and Pharmacological Sciences, vol. 23, no. 1, 2019, pp. 289-296.
Li M, Zhou H, Di J, et al. ILK participates in renal interstitial fibrosis by altering the phenotype of renal tubular epithelial cells via TGF-β1/smad pathway. Eur Rev Med Pharmacol Sci. 2019;23(1):289-296.
Li, M., Zhou, H., Di, J., Yang, M., & Jia, F. (2019). ILK participates in renal interstitial fibrosis by altering the phenotype of renal tubular epithelial cells via TGF-β1/smad pathway. European Review for Medical and Pharmacological Sciences, 23(1), 289-296. https://doi.org/10.26355/eurrev_201901_16775
Li M, et al. ILK Participates in Renal Interstitial Fibrosis By Altering the Phenotype of Renal Tubular Epithelial Cells Via TGF-β1/smad Pathway. Eur Rev Med Pharmacol Sci. 2019;23(1):289-296. PubMed PMID: 30657569.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - ILK participates in renal interstitial fibrosis by altering the phenotype of renal tubular epithelial cells via TGF-β1/smad pathway. AU - Li,M, AU - Zhou,H, AU - Di,J, AU - Yang,M, AU - Jia,F, PY - 2019/1/19/entrez PY - 2019/1/19/pubmed PY - 2020/6/20/medline SP - 289 EP - 296 JF - European review for medical and pharmacological sciences JO - Eur Rev Med Pharmacol Sci VL - 23 IS - 1 N2 - OBJECTIVE: To explore the specific role of ILK (integrin-linked kinase) in regulating renal fibrosis and its underlying mechanism. MATERIALS AND METHODS: NRK-52E cells were induced by transforming growth factor-β1 (TGF-β1) for observing phenotype change. Renal tubular epithelial cell marker, fibrosis marker and expression level of ILK in NRK-52E cells were also detected. After overexpression of ILK, phenotype change of NRK-52E cells was observed. For in vivo experiments, we constructed UUO (unilateral ureteral obstruction) model in CD1 mice. Renal tubular epithelial cell marker, fibrosis marker and expression level of ILK in UUO mice were detected. The regulatory effect of ILK on renal fibrosis was detected after injection of ILK overexpression plasmid. Western blot was performed to detect related genes in the TGF-β1/smad pathway. RESULTS: Accompanied by the TGF-β1-induced phenotype change in NRK-52E cells, both mRNA and protein levels of ILK were upregulated. Overexpression of ILK remarkably stimulated the phenotype change in NRK-52E cells. Similarly, ILK was highly expressed in UUO mice. Renal fibrosis was aggravated after injection of ILK overexpression plasmid in UUO mice. Western blot results showed that expressions of p-smad3 and smad3 were upregulated during the process of renal fibrosis. CONCLUSIONS: ILK is upregulated during the process of renal fibrosis. ILK participates in the development of renal fibrosis by altering phenotypes of renal tubular epithelial cells via a TGF-β1/smad pathway. SN - 2284-0729 UR - https://www.unboundmedicine.com/medline/citation/30657569/ILK_participates_in_renal_interstitial_fibrosis_by_altering_the_phenotype_of_renal_tubular_epithelial_cells_via_TGF_β1/smad_pathway_ L2 - https://www.europeanreview.org/article/16775 DB - PRIME DP - Unbound Medicine ER -