Liver, Pancreas, and Biliary TractCirculating soluble vascular adhesion protein 1 accounts for the increased serum monoamine oxidase activity in chronic liver disease☆,☆☆
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Patients
Serum samples were collected and frozen at −70°C until analysis. All diagnoses were made based on standard clinical, biochemical, and histologic criteria. Patients with autoimmune hepatitis were maintained on corticosteroid and/or azathioprine treatment; posttransplant patients were stable on combination therapy (azathioprine and cyclosporine or tacrolimus) with normal or near-normal liver biochemistry. Patients with chronic liver disease were not being treated with immunosuppressive therapy.
sVAP-1 levels are increased in liver disease
VAP-1 levels in healthy controls varied from 53.5 to 127 ng/mL with a median of 87.1 ng/mL. These results are similar to the normal range we have reported for sVAP-1 (49–138 ng/mL).22 Compared with the healthy control population, sVAP-1 levels were increased in many types of chronic liver disease (Figure 1): alcoholic cirrhosis, alcoholic hepatitis, cryptogenic cirrhosis, PBC (P < 0.01 for each group vs. healthy controls), and viral hepatitis (P < 0.05 vs. controls).
Discussion
We report increased serum levels of VAP-1 in chronic liver disease but normal levels in acute fulminant hepatic failure. We also show that sVAP-1 levels correlate with serum transaminase levels in chronic disease and that it is not excreted in bile. Perhaps most interestingly, we show that sVAP-1 is responsible for the SSAO activity in the serum of patients with liver disease and provide a molecular explanation for this long-standing observation.24, 31, 32, 33
We had previously shown that sVAP-1
Acknowledgements
The authors thank Stefan Hubscher for histologic analysis, and Drs. Neil Fisher, Damian Dowling, and Simon Ollif and other colleagues in the Liver Unit for sample collection.
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KETO[<sup>18</sup>F]FDG -VAP-P1: In vivo studies of a potential PET radiotracer for diagnosis of inflammation
2023, Applied Radiation and IsotopesCitation Excerpt :It is known that VAP-1 receptor has low expression in endothelial cell surface of normal tissues. After inflammatory stimuli, VAP-1 is translocated to the luminal surface of blood vessels in the sites of inflammation, causing leukocytes migration, especially T lymphocytes CD8+ and upregulated in chronic inflammation (Kurkijärvi et al., 2000; Wu et al., 2013). Therefore, in the present study, was proved that the new potential radiopharmaceutical KETO[18F]FDG-VAP-P1 was specific for labeling the inflammatory process induced by the sponge implant once the highest uptake was observed in the region of interest.
Dual/Multi-responsive fluorogenic probes for multiple analytes in mitochondria: From design to applications
2022, TrAC - Trends in Analytical ChemistryHypoxia inhibits semicarbazide-sensitive amine oxidase activity in adipocytes
2015, Molecular and Cellular EndocrinologyCitation Excerpt :Tissue-bound SSAO is preferentially expressed in adipocytes, vascular smooth muscle cells, and in endothelia of a subset of vessels, and is a transmembrane protein with the catalytic activity located in the extra-cellular compartment. The tissue origin of soluble SSAO is not clearly understood, but it is well established that this form is increased in diabetes mellitus, congestive heart failure or liver cirrhosis (Boomsma et al., 1995, 1999; Garpenstrand et al., 1999; Kurkijarvi et al., 2000; Meszaros et al., 1999). In these chronic diseases, it has been suggested that SSAO was responsible for vascular lesions and was an independent marker of mortality in cardiac failure (Boomsma et al., 2000).
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Supported by grants from the Wellcome Trust, The European Commission, the Finnish Academy, Technology Development Center of Finland, the Sigrid Juselius Foundation, and the Finnish Cultural Foundation and Paulo Foundation.
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Address requests for reprints to: David Adams, M.D., Liver Research Laboratories, University of Birmingham, Institute for Clinical Science, Queen Elizabeth Hospital, Edgbaston, Birmingham, England. e-mail: [email protected]; fax: (44) 121-627-4297.