Primary Graft Dysfunction in Lung Transplantation: The Role of CD26/Dipeptidylpeptidase IV and Vasoactive Intestinal Peptide

Zhai, Wei; Jungraithmayr, Wolfgang; Meester, Ingrid De; İnci, İlhan; Augustyns, Koen; Arni, Stephan; Hillinger, Sven; Weder, W.; Korom, Stephan

doi:10.1097/tp.0b013e31819e04c3

Cited by 19 publications

(14 citation statements)

References 30 publications

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“…However, there was no difference in B2R expression between the CON and Sham groups (p>0.05) (Figure 4). inhibitor on PGD after LTx, corroborating data reported by Zhai et al 14 . Secondly, research has shown that many inflammatory cells express B1R, including macrophages, epithelial cells, smooth muscle cells, endothelial cells and others 16 .…”

Section: Western Blottingsupporting

confidence: 82%

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The role of bradykinin in lung ischemia-reperfusion injury in a rat lung transplantation model

Tan

Wang

et al. 2016

Acta Cir. Bras.

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PURPOSE:To investigate the role of bradykinin in a rat lung transplantation (LTx) model and preliminarily discuss the relationship between bradykinin and CD26/DPP-4. METHODS:Rats were randomly divided into four groups: Control (CON), Sham, low potassium dextranglucose (LPD), and AB192 (n=15/group). Orthotopic single LTx was performed in the LPD and AB192 groups. The donor lungs were flush-perfused and preserved with low potassium dextranglucose (LPD) or LPD+CD26/DPP-4 catalytic inhibitor (AB192). LTx was performed after 18 h cold ischemia time and harvested two days post-LTx. Blood gas analysis (PO 2 ), wet/dry weight ratio (W/D), myeloperoxidase activity (MPO), and lipid peroxidation (MDA) were analyzed at 48 hr after transplantation. Immunohistochemical (IHC) analysis was performed in the same sample and validated by Western-Blot. RESULTS:Compared to the LPD group, the AB192 group showed higher PO 2 , lower W/D ratio, and decreased MPO and MDA. IHC studies showed strong bradykinin β2 receptor (B2R) staining in the LPD group, especially in inflammatory cells, alveolar macrophages, and respiratory epithelial cells. Expression of B2R by Western-Blot was significantly different between the AB192 and LPD groups. CONCLUSION:Bradykinin may be a competitive substrate of DPP-4, and decreased bradykinin levels may enhance protective effects against ischemia/reperfusion injury during LTx.

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Section: Western Blottingsupporting

confidence: 82%

“…In addition, the severity of PGD was shown to be related to the time of cold ischemia 14,15 . Extended cold ischemia time better reflects the role of the target protein, further broadening the scope of CD26/DPP -4 inhibitors for potential therapeutic use.…”

Section: Introductionmentioning

confidence: 99%

The role of bradykinin in lung ischemia-reperfusion injury in a rat lung transplantation model

Tan

Wang

et al. 2016

Acta Cir. Bras.

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“…also showed that mice administrated a DPP‐IV inhibitor substantially decreased the synthesis of several pro‐inflammatory and profibrotic molecules in a unilateral ureteral obstruction model . Inhibition of DPP‐IV attenuated development I/R injury in the lung during transplantation . Other reports demonstrated that DPP‐IV inhibitor reduced renal damage induced by renal I/R and also protects the heart in models of myocardial infarction .…”

Section: Discussionmentioning

confidence: 91%

Prolonged survival by combined treatment with granulocyte colony‐stimulating factor and dipeptidyl peptidase IV inhibitor in a rat small‐for‐size liver transplantation model

Hsu¹,

Nakano

Huang³

et al. 2014

Hepatology Research

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“…In addition to diabetic nephropathy, DPP IV inhibition protected the kidney against ischemia-reperfusion injury (IRI) [8]. Tissue protective effects of GLP-1 activation or DPP IV inhibition have also been demonstrated in other organs, including IRI of the lung during transplantation [9-11] and the outcome of myocardial infarction [12,13]. …”

Section: Introductionmentioning

confidence: 99%

Dipeptidyl peptidase IV inhibitor attenuates kidney injury in rat remnant kidney

et al. 2013

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BackgroundThe inhibition of dipeptidyl peptidase (DPP) IV shows protective effects on tissue injury of the heart, lung, and kidney. Forkhead box O (FoxO) transcriptional factors regulate cellular differentiation, growth, survival, the cell cycle, metabolism, and oxidative stress. The aims of this study were to investigate whether the DPP IV inhibitor sitagliptin could attenuate kidney injury and to evaluate the status of FoxO3a signaling in the rat remnant kidney model.MethodsRats were received two-step surgery of 5/6 renal mass reduction and fed on an oral dose of 200 mg/kg/day sitagliptin for 8 weeks. Before and after the administration of sitagliptin, physiologic parameters were measured. After 8 weeks of treatment, the kidneys were harvested.ResultsThe sitagliptin treatment attenuated renal dysfunction. A histological evaluation revealed that glomerulosclerosis and tubulointerstitial injury were significantly decreased by sitagliptin. Sitagliptin decreased DPP IV activity and increased the renal expression of glucagon-like peptide-1 receptor (GLP-1R). The subtotal nephrectomy led to the activation of phosphatidylinositol 3-kinase (PI3K)-Akt and FoxO3a phosphorylation, whereas sitagliptin treatment reversed these changes, resulting in PI3K-Akt pathway inactivation and FoxO3a dephosphorylation. The renal expression of catalase was increased and the phosphorylation of c-Jun N-terminal kinase (JNK) was decreased by sitagliptin. Sitagliptin treatment reduced apoptosis by decreasing cleaved caspase-3 and −9 and Bax levels and decreased macrophage infiltration.ConclusionsIn rat remnant kidneys, DPP IV inhibitor attenuated renal dysfunction and structural damage. A reduction of apoptosis, inflammation and an increase of antioxidant could be suggested as a renoprotective mechanism together with the activation of FoxO3a signaling. Therefore, DPP IV inhibitors might provide a promising approach for treating CKD, but their application in clinical practice remains to be investigated.

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Primary Graft Dysfunction in Lung Transplantation: The Role of CD26/Dipeptidylpeptidase IV and Vasoactive Intestinal Peptide

Cited by 19 publications

References 30 publications

The role of bradykinin in lung ischemia-reperfusion injury in a rat lung transplantation model

The role of bradykinin in lung ischemia-reperfusion injury in a rat lung transplantation model

Prolonged survival by combined treatment with granulocyte colony‐stimulating factor and dipeptidyl peptidase IV inhibitor in a rat small‐for‐size liver transplantation model

Dipeptidyl peptidase IV inhibitor attenuates kidney injury in rat remnant kidney

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