Abstract:
:Diabetic nephropathy (DN) is the leading cause of end-stage renal disease worldwide with high morbidity and mortality. Glomerular mesangial cell (MC) proliferation, inflammatory cell infiltration and extracellular matrix (ECM) accumulation are the main pathological characteristics of DN. A previous study revealed that polycystin-1 N-terminal fragment (PC-1 NF) fusion protein could inhibit ECM accumulation in a mesangial proliferative glomerulonephritis model. However, the role of PC-1 NF fusion protein in DN remains unknown. The results of the present study indicated that PC-1 NF fusion protein significantly abolished high glucose (HG)-induced glomerular MC viability over three time points measured (24, 48 and 72 h). In addition, PC-1 NF suppressed the levels of monocyte chemotactic peptide-1 and tumor necrosis factor α, as well as the expression of fibronectin and collagen IV, in HG-stimulated MCs. Furthermore, PC-1 NF fusion protein efficiently inhibited the activation of Wnt/β-catenin signaling pathway in HG-stimulated MCs. Taken together, these data indicated that PC-1 NF fusion protein inhibited HG-induced MC proliferation, inflammation, and ECM expression via the modulation of the Wnt signaling pathway. The present study indicated that PC-1 NF fusion protein may be a potential agent in treating DN.
journal_name
Exp Ther Medjournal_title
Experimental and therapeutic medicineauthors
Xiao L,Chen Y,Yuan Y,Xu B,Gao Q,Chen P,Zhang T,Guan Tdoi
10.3892/etm.2019.7793subject
Has Abstractpub_date
2019-09-01 00:00:00pages
2029-2036issue
3eissn
1792-0981issn
1792-1015pii
ETM-0-0-7793journal_volume
18pub_type
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