Hydrolysis and transport of proline-containing peptides in renal brush-border membrane vesicles from dipeptidyl peptidase IV-positive and dipeptidyl peptidase IV-negative rat strains.

Tiruppathì, Chinnaswamy; Miyamoto, Yusei; Ganapathy, Vadivel; Roesel, Raffaello; Whitford, Gary M.; Leibach, Frederick H.

doi:10.1016/s0021-9258(19)40041-0

Cited by 96 publications

(15 citation statements)

References 36 publications

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“…Apart from the glucose-lowering effect, this drug has a renoprotective effect through antioxidant and anti-inflammatory mechanisms, and it is antifibrotic through suppression of TGF-β-mediated signaling [149][150][151]. DPP-4 is expressed in most of the specific organs and cells, with relatively high concentrations and activities found in the kidney, especially in the brush borders of proximal tubular cells [152,153].…”

Section: Approaches To Management Of Diabetic Nephropathymentioning

confidence: 99%

Diabetic Nephropathy: Challenges in Pathogenesis, Diagnosis, and Treatment

Samsu

2021

BioMed Research International

363

292

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Diabetic nephropathy (DN) is the leading cause of end-stage renal disease worldwide. Chronic hyperglycemia and high blood pressure are the main risk factors for the development of DN. In general, screening for microalbuminuria should be performed annually, starting 5 years after diagnosis in type 1 diabetes and at diagnosis and annually thereafter in type 2 diabetes. Standard therapy is blood glucose and blood pressure control using the renin-angiotensin system blockade, targeting A 1 c < 7 % , and <130/80 mmHg. Regression of albuminuria remains an important therapeutic goal. However, there are problems in diagnosis and treatment of nonproteinuric DN (NP-DN), which does not follow the classic pattern of DN. In fact, the prevalence of DN continues to increase, and additional therapy is needed to prevent or ameliorate the condition. In addition to conventional therapies, vitamin D receptor activators, incretin-related drugs, and therapies that target inflammation may also be promising for the prevention of DN progression. This review focuses on the role of inflammation and oxidative stress in the pathogenesis of DN, approaches to diagnosis in classic and NP-DN, and current and emerging therapeutic interventions.

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Section: Approaches To Management Of Diabetic Nephropathymentioning

confidence: 99%

Diabetic Nephropathy: Challenges in Pathogenesis, Diagnosis, and Treatment

Samsu

2021

BioMed Research International

363

292

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“…Previous studies from our laboratory have shown that dipeptidyl peptidase IV (DPPIV ; EC 3.4.14.5) is of vital importance for the digestion and assimilation of prolyl peptides in the mammalian small intestine [1,2]. This enzyme has also been suggested to have important roles in a number of biological processes such as the activation of T lymphocytes [3], cell-substratum interactions [4,5], hormone regulation [6] and reclamation of urinary peptides in the kidney proximal tubule [7]. In the small intestine, DPPIV exhibits a characteristic pattern of distribution along the proximal-distal axis, with somewhat higher expression in the distal region [8,9].…”

Section: Introductionmentioning

confidence: 99%

Regulation of the gene for human dipeptidyl peptidase IV by hepatocyte nuclear factor 1α

et al. 1999

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Hepatocyte nuclear factor 1 was identified as the transcription factor binding to a 20 bp (-150 to -131) region of the gene for human dipeptidyl peptidase IV, which has been shown to be important for the expression of dipeptidyl peptidase IV in the human intestinal and hepatic epithelial cell lines Caco-2 and HepG2. Functional analysis of the hepatocyte nuclear factor 1 site was performed with two minimal dipeptidyl peptidase IV promoter constructs (-250 to -41, and -150 to -41) with and without a 3 bp mutation in the hepatocyte nuclear factor 1 sequence, and used in transient transfection experiments with Caco-2 cells. The results show that the mutated constructs were able to drive transcription at only 5-10% of the activity of the non-mutated controls. Co-transfection of 3T3 cells with hepatocyte nuclear factor 1 (alpha or beta) and dipeptidyl peptidase IV promoter constructs (-250 to -41 or -150 to -41) resulted in a 2.5-6-fold increase in transcription over controls with hepatocyte nuclear factor 1 alpha but not with hepatocyte nuclear factor 1 beta. The results of this study show that hepatocyte nuclear factor 1 binds to the -150 to -131 region of the human dipeptidyl peptidase IV promoter and is necessary for transcriptional activation of the gene for dipeptidyl peptidase IV.

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“…The role of DPP4 in CRP-driven kidney injury is still largely unknown. By our human CRP transgenic db/db mice model, 31,32 we found that the renal expression level of DPP4 was largely enhanced in glomerulus and tubules of the 20-week-old CRP tg db/db mice compared with the db/db mice, as well as non-diabetic db/m and CRP tg db/m littermates, as shown by immunohistochemistry (IHC) (Figure 1A). The induction of DPP4 in the diabetic kidney of CRP tg db/db mice was highly associated with the human CRP-driven CD32b activation, as shown by IHC, western blot, and real-time polymerase chain reaction (PCR) (Figure 1).…”

Section: Resultsmentioning

confidence: 86%