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Glucagon-Like Peptide-1 Mediates the Protective Effect of the Dipeptidyl Peptidase IV Inhibitor on Renal Fibrosis via Reducing the Phenotypic Conversion of Renal Microvascular Cells in Monocrotaline-Treated Rats
Joint Authors
Wang, Hong
Xu, Jian
Wang, Jingjing
Cheng, Yusheng
Li, Xiang
He, Mengyu
Zhu, Jiali
Han, Honghao
Wei, Guihong
Kong, Hui
Xie, Weiping
Zuo, Xiangrong
Source
Issue
Vol. 2018, Issue 2018 (31 Dec. 2018), pp.1-14, 14 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2018-01-23
Country of Publication
Egypt
No. of Pages
14
Main Subjects
Abstract EN
Chronic kidney diseases are characterized by renal fibrosis with excessive matrix deposition, leading to a progressive loss of functional renal parenchyma and, eventually, renal failure.
Renal microcirculation lesions, including the phenotypic conversion of vascular cells, contribute to renal fibrosis.
Here, renal microcirculation lesions were established with monocrotaline (MCT, 60 mg/kg).
Sitagliptin (40 mg/kg/d), a classical dipeptidyl peptidase-4 (DPP-4) inhibitor, attenuated the renal microcirculation lesions by inhibiting glomerular tuft hypertrophy, glomerular mesangial expansion, and microvascular thrombosis.
These effects of sitagliptin were mediated by glucagon-like peptide-1 receptor (GLP-1R), since they were blocked by the GLP-1R antagonist exendin-3 (Ex-3, 40 ug/kg/d).
The GLP-1R agonist liraglutide showed a similar renal protective effect in a dose-independent manner.
In addition, sitagliptin, as well as liraglutide, alleviated the MCT-induced apoptosis of renal cells by increasing the expression of survival factor glucose-regulated protein 78 (GRP78), which was abolished by the GLP-1R antagonist Ex-3.
Sitagliptin and liraglutide also effectively ameliorated the conversion of vascular smooth muscle cells (SMCs) from a synthetic phenotype to contractile phenotype.
Moreover, sitagliptin and liraglutide inhibited endothelial-mesenchymal transition (EndMT) via downregulating transforming growth factor-β1 (TGF-β1).
Collectively, these findings suggest that DPP-4 inhibition can reduce microcirculation lesion-induced renal fibrosis in a GLP-1-dependent manner.
American Psychological Association (APA)
Xu, Jian& Wang, Jingjing& Cheng, Yusheng& Li, Xiang& He, Mengyu& Zhu, Jiali…[et al.]. 2018. Glucagon-Like Peptide-1 Mediates the Protective Effect of the Dipeptidyl Peptidase IV Inhibitor on Renal Fibrosis via Reducing the Phenotypic Conversion of Renal Microvascular Cells in Monocrotaline-Treated Rats. BioMed Research International،Vol. 2018, no. 2018, pp.1-14.
https://search.emarefa.net/detail/BIM-1124700
Modern Language Association (MLA)
Xu, Jian…[et al.]. Glucagon-Like Peptide-1 Mediates the Protective Effect of the Dipeptidyl Peptidase IV Inhibitor on Renal Fibrosis via Reducing the Phenotypic Conversion of Renal Microvascular Cells in Monocrotaline-Treated Rats. BioMed Research International No. 2018 (2018), pp.1-14.
https://search.emarefa.net/detail/BIM-1124700
American Medical Association (AMA)
Xu, Jian& Wang, Jingjing& Cheng, Yusheng& Li, Xiang& He, Mengyu& Zhu, Jiali…[et al.]. Glucagon-Like Peptide-1 Mediates the Protective Effect of the Dipeptidyl Peptidase IV Inhibitor on Renal Fibrosis via Reducing the Phenotypic Conversion of Renal Microvascular Cells in Monocrotaline-Treated Rats. BioMed Research International. 2018. Vol. 2018, no. 2018, pp.1-14.
https://search.emarefa.net/detail/BIM-1124700
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1124700