Cellular expression of CD26/dipeptidyl peptidase IV

Iwanaga, Toshihiko; Nio‐Kobayashi, Junko

doi:10.2220/biomedres.42.229

Cited by 4 publications

(5 citation statements)

References 59 publications

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“…DPP4 and ACE1 gene expression increased WT and Nln -/female animals fed HD, considering both RPL19 and cyclophilin A as housekeeping genes. Both DPP4 and ACE1 metabolize peptides on the extracellular milieu [107,108], suggesting that in females, conversely to males, the extracellular peptide metabolism plays a major role in diet-induced obesity. Interestingly, DPP4 preferentially degrades peptides containing an alanine or proline at the penultimate position (P1 position), which includes the glucagon-like peptide-1 (GLP-1) [109,110].…”

Section: Discussionmentioning

confidence: 99%

Neurolysin Knockout Mice in a Diet-Induced Obesity Model

Caprioli,

Eichler,

Silva

et al. 2023

IJMS

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Neurolysin oligopeptidase (E.C.3.4.24.16; Nln), a member of the zinc metallopeptidase M3 family, was first identified in rat brain synaptic membranes hydrolyzing neurotensin at the Pro-Tyr peptide bond. The previous development of C57BL6/N mice with suppression of Nln gene expression (Nln-/-), demonstrated the biological relevance of this oligopeptidase for insulin signaling and glucose uptake. Here, several metabolic parameters were investigated in Nln-/- and wild-type C57BL6/N animals (WT; n = 5–8), male and female, fed either a standard (SD) or a hypercaloric diet (HD), for seven weeks. Higher food intake and body mass gain was observed for Nln-/- animals fed HD, compared to both male and female WT control animals fed HD. Leptin gene expression was higher in Nln-/- male and female animals fed HD, compared to WT controls. Both WT and Nln-/- females fed HD showed similar gene expression increase of dipeptidyl peptidase 4 (DPP4), a peptidase related to glucagon-like peptide-1 (GLP-1) metabolism. The present data suggest that Nln participates in the physiological mechanisms related to diet-induced obesity. Further studies will be necessary to better understand the molecular mechanism responsible for the higher body mass gain observed in Nln-/- animals fed HD.

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Section: Discussionmentioning

confidence: 99%

Neurolysin Knockout Mice in a Diet-Induced Obesity Model

Caprioli,

Eichler,

Silva

et al. 2023

IJMS

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“…In the liver, CD26/DPP4 expression was demonstrated along the entire biliary tree. In addition, sinusoidal endothelial cells in murine hepatic tissue also stain positive for CD26/DPP4 (Iwanaga & Nio‐Kobayashi, 2021). In human cirrhotic liver specimens, only a mild alteration of the zonal distribution of CD26/DPP4 expression was observed (Matsumoto et al, 1992).…”

Section: Evidence To Repurpose Pharmacological Cd26/dpp4 Inhibition I...mentioning

confidence: 99%

“…CD26/DPP4 in cardiac tissue is mainly expressed on the surface of vascular endothelial cells of the coronary capillaries as well as in infiltrating immune cells (Cuijpers et al, 2021; Iwanaga & Nio‐Kobayashi, 2021). Cytosolic expression of CD26/DPP4 was further observed in some cardiomyocytes (Cuijpers et al, 2021).…”

Section: Evidence To Repurpose Pharmacological Cd26/dpp4 Inhibition I...mentioning

confidence: 99%

“…Additional myofibroblast progenitors can be recruited from the periphery, as bone marrow-derived fibrocytes contribute to scar formation after myocardial infarction (van Amerongen et al, 2008). CD26/DPP4 in cardiac tissue is mainly expressed on the surface of vascular endothelial cells of the coronary capillaries as well as in infiltrating immune cells (Cuijpers et al, 2021;Iwanaga & Nio-Kobayashi, 2021). Cytosolic expression of CD26/DPP4 was further observed in some cardiomyocytes (Cuijpers et al, 2021).…”

Section: Cardiomyopathy Myocardial Infarction and Heart Failurementioning

confidence: 99%

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Targeting cluster of differentiation 26 / dipeptidyl peptidase 4 (CD26/DPP4) in organ fibrosis

Ohm

Moneke

Jungraithmayr

2022

British J Pharmacology

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Cluster of differentiation 26 (CD26)/dipeptidyl peptidase 4 (DPP4) is an exopeptidase that is expressed as a transmembrane protein in many organs but also present in a circulating soluble form. Beyond its enzymatic and costimulatory activity, CD26/DPP4 is involved in the pathogenesis of chronic fibrotic diseases across many organ types, such as liver cirrhosis, kidney fibrosis and lung fibrosis. Organ fibrosis is associated with a high morbidity and mortality, and there are no causative therapies that can effectively attenuate the progress of the disease. Growing evidence suggests that inhibiting CD26/DPP4 can modulate the profibrotic tissue microenvironment and thus reduce fibrotic changes within affected organs. This review summarizes the role of CD26/DPP4 in fibroproliferative disorders and highlights new opportunities for an antifibrotic treatment by CD26/DPP4 inhibition. As a major advantage, CD26/DPP4 inhibitors have been in safe and routine clinical use in type 2 diabetes for many years and thus qualify for repurposing to repurpose as a promising therapeutic against fibrosis.

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“… 4 , 5 Lymphocytes, fibroblasts, endothelial cells, and apical portions of acinar and epithelial cells express DPP-4, which is also found in plasma as in soluble circulating form. 6 , 7 …”

Section: Introduction To Dpp-4 Enzymementioning

confidence: 99%

Potential Effect of DPP-4 Inhibitors Towards Hepatic Diseases and Associated Glucose Intolerance

Sharma¹,

Virmani²,

Sharma³

et al. 2022

DMSO

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Dipeptidyl-peptidase-4 (DPP-4) is an enzyme having various properties and physiological roles in lipid accumulation, resistance to anticancer agents, and immune stimulation. DPP-4 includes membrane-bound peptidases and is a kind of enzyme that cleaves alanine or proline-containing peptides such as incretins, chemokines, and appetite-suppressing hormones (neuropeptide) at their N-terminal dipeptides. DPP-4 plays a role in the final breakdown of peptides produced by other endo and exo-peptidases from nutritious proteins and their absorption in these tissues. DPP-4 enzyme activity has different modes of action on glucose metabolism, hunger regulation, gastrointestinal motility, immune system function, inflammation, and pain regulation. According to the literature survey, as DPP-4 levels increase in individuals with liver conditions, up-regulation of hepatic DPP-4 expression is likely to be the cause of glucose intolerance or insulin resistance. This review majorly focuses on the cleavage of alanine or proline-containing peptides such as incretins by the DPP-4 and its resulting conditions like glucose intolerance and cause of DPP-4 level elevation due to some liver conditions. Thus, we have discussed the various effects of DPP-4 on the liver diseases like hepatitis C, non-alcoholic fatty liver, hepatic regeneration and stem cell, hepatocellular carcinoma, and the impact of elevated DPP-4 levels in association with liver diseases as a cause of glucose intolerance and their treatment drug of choices. In addition, the effect of DPP-4 inhibitors on obesity and their negative aspects are also discussed in brief.

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Cellular expression of CD26/dipeptidyl peptidase IV

Cited by 4 publications

References 59 publications

Neurolysin Knockout Mice in a Diet-Induced Obesity Model

Neurolysin Knockout Mice in a Diet-Induced Obesity Model

Targeting cluster of differentiation 26 / dipeptidyl peptidase 4 (CD26/DPP4) in organ fibrosis

Potential Effect of DPP-4 Inhibitors Towards Hepatic Diseases and Associated Glucose Intolerance

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