Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 17, Issue 9, Pages -Publisher
MDPI AG
DOI: 10.3390/ijms17091404
Keywords
podocytes; UCH-L1; Wnt/beta-catenin; DN
Funding
- National Nature Science Foundation of China (NFSC) [81274049, 81472365]
- Foundation of Shandong Educational Committee [J15LK11]
- Science and Technology Development Plan of medicine and health care in Shandong province [2014WS0182]
- Science and Technology Development Plan in Weifang City of Shandong province [2014WS047]
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Increasing studies identified podocyte injury as a key early risk factor resulting in diabetic nephropathy (DN). The ubiquitin carboxy-terminal hydrolase 1 (UCH-L1) participates in podocyte differentiation and injury, which is elevated in the podocytes of a variety of nephritis. Whether UCH-L1 expression is positively related to podocyte injury of DN remains unclear. In this study, elevated expression of UCH-L1 and its intrinsic mechanism in high glucose (HG)-stimulated murine podocytes were investigated using western blot and real-time quantitative PCR. Kidney biopsies of DN patients and health individuals were stained by immunofluorescence (IF) method. The morphological and functional changes of podocytes were tested by F-actin staining and cell migration assay. Results demonstrated that HG induced upregulation of UCH-L1 and activation of the Wnt/-catenin signaling pathway in podocytes. However, blocking of the Wnt pathway by dickkopf related protein 1 (DKK1) eliminated the above changes. Furthermore, IF staining confirmed that, compared with healthy individuals, the expression of UCH-L1 and -catenin were obviously increased in kidney biopsy of DN patients. Overexpression of UCH-L1 remodeled its actin cytoskeleton, increased its cell migration and impacted its important proteins. All the findings manifested that Wnt/-catenin/UCH-L1 may be a new potential therapy method in the treatment of DN in future.
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