Journal
SCIENTIFIC REPORTS
Volume 9, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-019-43730-5
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Funding
- Mitsubishi Tanabe Pharma Corporation
- Japan Society for the Promotion of Science [23790381, 25282028, 25670414]
- Kanazawa Medical University [C2011-4, C2012-1, S2016-3, S2017-1, K2017-16]
- Lilly-Incretin Basic Research Grant from the Japan Diabetes Foundation
- Japanese Government MEXT (Ministry of Education, Culture, Sports, Science, and Technology) Fellowship Program
- Kanazawa Medical University
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Diabetic kidney disease (DKD) is appeared to be higher risk of declining kidney function compared to non-diabetic kidney disease with same magnitude of albuminuria. Epithelial-mesenchymal transition (EMT) program of tubular epithelial cells (TECs) could be important for the production of the extracellular matrix in the kidney. Caveolin-1 (CAV1), dipeptidyl peptidase-4 (DPP-4) and integrin beta 1 have shown to be involved in EMT program. Here, we found diabetic kidney is prone for albuminuria induced TECs damage and DPP-4 plays a vital role in such parenchymal damages in diabetic mice. The bovine serum albumin (BSA) injection induced severe TECs damage and altered expression levels of DPP-4, integrin beta 1, CAV1, and EMT programs including relevant microRNAs in type 1 diabetic CD-1 mice when compared to non-diabetic mice; teneligliptin (TENE) ameliorated these alterations. TENE suppressed the close proximity among DPP-4, integrin beta 1 and CAV1 in a culture of HK-2 cells. These findings suggest that DPP-4 inhibition can be relevant for combating proteinuric DKD by targeting the EMT program induced by the crosstalk among DPP-4, integrin beta 1 and CAV1.
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