Albumin domain II mutant with high bilirubin binding affinity has a great potential as serum bilirubin excretion enhancer for hyperbilirubinemia treatment

Background: 4Z,15Z-bilirubin-IXα (BR), an endogenous toxic compound that is sparingly soluble in water, binds human serum albumin (HSA) with high affinity in a flexible manner. Our previous findings suggest that both Lys195 and Lys199 in subdomain IIA are important for the high-affinity binding of B...

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Main Authors: Minomo, Ai, Ishima, Yu, Chuang, Victor, Suwa, Yoshiaki, Kragh-Hansen, Ulrich, Narisoko, Toru, Morioka, Hiroshi, Maruyama, Toru, Otagiri, Masaki
Format: Journal Article
Published: Elsevier BV 2013
Online Access:http://hdl.handle.net/20.500.11937/18060
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author Minomo, Ai
Ishima, Yu
Chuang, Victor
Suwa, Yoshiaki
Kragh-Hansen, Ulrich
Narisoko, Toru
Morioka, Hiroshi
Maruyama, Toru
Otagiri, Masaki
author_facet Minomo, Ai
Ishima, Yu
Chuang, Victor
Suwa, Yoshiaki
Kragh-Hansen, Ulrich
Narisoko, Toru
Morioka, Hiroshi
Maruyama, Toru
Otagiri, Masaki
author_sort Minomo, Ai
building Curtin Institutional Repository
collection Online Access
description Background: 4Z,15Z-bilirubin-IXα (BR), an endogenous toxic compound that is sparingly soluble in water, binds human serum albumin (HSA) with high affinity in a flexible manner. Our previous findings suggest that both Lys195 and Lys199 in subdomain IIA are important for the high-affinity binding of BR, and especially Lys199 in stand-alone domain II plays a prominent role in the renal elimination of BR. Our hypothesis is that HSA-domain II with high BR binding would be a useful therapeutic agent to treat hyperbilirubinemia in patients with impaired liver function. Methods: Unbound BR concentrations were determined using a modified HRP assay. To evaluate the effect of pan3_3-13 domain II mutant in promoting urinary BR excretion, the serum concentration and urinary excretion amount of BR were determined using bile duct ligation mice. Results: After three or six rounds of panning, pan3_3-13 and pan6_4 were found to have a significantly higher affinity for BR than wild-type domain II. Administration of pan3_3-13 significantly reduced serum BR level and increased its urinary excretion in the disease model mice as compared to wild-type domain II treatment. Conclusions: These results suggest that pan3_3-13 has great potential as a therapeutic agent that promotes urinary BR excretion in hyperbilirubinemia.
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publishDate 2013
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spelling curtin-20.500.11937-180602017-09-13T15:44:33Z Albumin domain II mutant with high bilirubin binding affinity has a great potential as serum bilirubin excretion enhancer for hyperbilirubinemia treatment Minomo, Ai Ishima, Yu Chuang, Victor Suwa, Yoshiaki Kragh-Hansen, Ulrich Narisoko, Toru Morioka, Hiroshi Maruyama, Toru Otagiri, Masaki Background: 4Z,15Z-bilirubin-IXα (BR), an endogenous toxic compound that is sparingly soluble in water, binds human serum albumin (HSA) with high affinity in a flexible manner. Our previous findings suggest that both Lys195 and Lys199 in subdomain IIA are important for the high-affinity binding of BR, and especially Lys199 in stand-alone domain II plays a prominent role in the renal elimination of BR. Our hypothesis is that HSA-domain II with high BR binding would be a useful therapeutic agent to treat hyperbilirubinemia in patients with impaired liver function. Methods: Unbound BR concentrations were determined using a modified HRP assay. To evaluate the effect of pan3_3-13 domain II mutant in promoting urinary BR excretion, the serum concentration and urinary excretion amount of BR were determined using bile duct ligation mice. Results: After three or six rounds of panning, pan3_3-13 and pan6_4 were found to have a significantly higher affinity for BR than wild-type domain II. Administration of pan3_3-13 significantly reduced serum BR level and increased its urinary excretion in the disease model mice as compared to wild-type domain II treatment. Conclusions: These results suggest that pan3_3-13 has great potential as a therapeutic agent that promotes urinary BR excretion in hyperbilirubinemia. 2013 Journal Article http://hdl.handle.net/20.500.11937/18060 10.1016/j.bbagen.2013.01.006 Elsevier BV restricted
spellingShingle Minomo, Ai
Ishima, Yu
Chuang, Victor
Suwa, Yoshiaki
Kragh-Hansen, Ulrich
Narisoko, Toru
Morioka, Hiroshi
Maruyama, Toru
Otagiri, Masaki
Albumin domain II mutant with high bilirubin binding affinity has a great potential as serum bilirubin excretion enhancer for hyperbilirubinemia treatment
title Albumin domain II mutant with high bilirubin binding affinity has a great potential as serum bilirubin excretion enhancer for hyperbilirubinemia treatment
title_full Albumin domain II mutant with high bilirubin binding affinity has a great potential as serum bilirubin excretion enhancer for hyperbilirubinemia treatment
title_fullStr Albumin domain II mutant with high bilirubin binding affinity has a great potential as serum bilirubin excretion enhancer for hyperbilirubinemia treatment
title_full_unstemmed Albumin domain II mutant with high bilirubin binding affinity has a great potential as serum bilirubin excretion enhancer for hyperbilirubinemia treatment
title_short Albumin domain II mutant with high bilirubin binding affinity has a great potential as serum bilirubin excretion enhancer for hyperbilirubinemia treatment
title_sort albumin domain ii mutant with high bilirubin binding affinity has a great potential as serum bilirubin excretion enhancer for hyperbilirubinemia treatment
url http://hdl.handle.net/20.500.11937/18060