Fusion protein of retinol‐binding protein and albumin domain III reduces liver fibrosis

Abstract Activated hepatic stellate cells (HSCs) play a key role in liver fibrosis, and inactivating HSCs has been considered a promising therapeutic approach. We previously showed that albumin and its derivative designed for stellate cell‐targeting, retinol‐binding protein–albumin domain III fusion...

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Main Authors: Hongsik Lee, Hyeyeun Jeong, Sangeun Park, Wonbaek Yoo, Soyoung Choi, Kyungmin Choi, Min‐Goo Lee, Mihwa Lee, DaeRyong Cha, Young‐Sik Kim, Jeeyoung Han, Wonkon Kim, Sun‐Hwa Park, Junseo Oh
Format: Article
Language:English
Published: Springer Nature 2015-04-01
Series:EMBO Molecular Medicine
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Online Access:https://doi.org/10.15252/emmm.201404527
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author Hongsik Lee
Hyeyeun Jeong
Sangeun Park
Wonbaek Yoo
Soyoung Choi
Kyungmin Choi
Min‐Goo Lee
Mihwa Lee
DaeRyong Cha
Young‐Sik Kim
Jeeyoung Han
Wonkon Kim
Sun‐Hwa Park
Junseo Oh
author_facet Hongsik Lee
Hyeyeun Jeong
Sangeun Park
Wonbaek Yoo
Soyoung Choi
Kyungmin Choi
Min‐Goo Lee
Mihwa Lee
DaeRyong Cha
Young‐Sik Kim
Jeeyoung Han
Wonkon Kim
Sun‐Hwa Park
Junseo Oh
author_sort Hongsik Lee
collection DOAJ
description Abstract Activated hepatic stellate cells (HSCs) play a key role in liver fibrosis, and inactivating HSCs has been considered a promising therapeutic approach. We previously showed that albumin and its derivative designed for stellate cell‐targeting, retinol‐binding protein–albumin domain III fusion protein (referred to as R‐III), inactivate cultured HSCs. Here, we investigated the mechanism of action of albumin/R‐III in HSCs and examined the anti‐fibrotic potential of R‐III in vivo. R‐III treatment and albumin expression downregulated retinoic acid (RA) signaling which was involved in HSC activation. RA receptor agonist and retinaldehyde dehydrogenase overexpression abolished the anti‐fibrotic effect of R‐III and albumin, respectively. R‐III uptake into cultured HSCs was significantly decreased by siRNA‐STRA6, and injected R‐III was localized predominantly in HSCs in liver. Importantly, R‐III administration reduced CCl4‐ and bile duct ligation‐induced liver fibrosis. R‐III also exhibited a preventive effect against CCl4‐inducd liver fibrosis. These findings suggest that the anti‐fibrotic effect of albumin/R‐III is, at least in part, mediated by downregulation of RA signaling and that R‐III is a good candidate as a novel anti‐fibrotic drug.
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spelling doaj-art-0064c9599aaa4cbbb6dd48df0f533c342025-08-20T04:02:56ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842015-04-017681983010.15252/emmm.201404527Fusion protein of retinol‐binding protein and albumin domain III reduces liver fibrosisHongsik Lee0Hyeyeun Jeong1Sangeun Park2Wonbaek Yoo3Soyoung Choi4Kyungmin Choi5Min‐Goo Lee6Mihwa Lee7DaeRyong Cha8Young‐Sik Kim9Jeeyoung Han10Wonkon Kim11Sun‐Hwa Park12Junseo Oh13Department of Internal Medicine, College of Medicine, Korea UniversityDepartment of Anatomy, College of Medicine, Korea UniversityDepartment of Anatomy, College of Medicine, Korea UniversityDepartment of Anatomy, College of Medicine, Korea UniversityDepartment of Anatomy, College of Medicine, Korea UniversityDepartment of Physiology, College of Medicine, Korea UniversityDepartment of Physiology, College of Medicine, Korea UniversityDepartment of Nephrology, College of Medicine, Korea UniversityDepartment of Nephrology, College of Medicine, Korea UniversityDepartment of Pathology, College of Medicine, Korea UniversityDepartment of Pathology, Inha University HospitalMedical Proteomics Research Center, KRIBBDepartment of Anatomy, College of Medicine, Korea UniversityDepartment of Anatomy, College of Medicine, Korea UniversityAbstract Activated hepatic stellate cells (HSCs) play a key role in liver fibrosis, and inactivating HSCs has been considered a promising therapeutic approach. We previously showed that albumin and its derivative designed for stellate cell‐targeting, retinol‐binding protein–albumin domain III fusion protein (referred to as R‐III), inactivate cultured HSCs. Here, we investigated the mechanism of action of albumin/R‐III in HSCs and examined the anti‐fibrotic potential of R‐III in vivo. R‐III treatment and albumin expression downregulated retinoic acid (RA) signaling which was involved in HSC activation. RA receptor agonist and retinaldehyde dehydrogenase overexpression abolished the anti‐fibrotic effect of R‐III and albumin, respectively. R‐III uptake into cultured HSCs was significantly decreased by siRNA‐STRA6, and injected R‐III was localized predominantly in HSCs in liver. Importantly, R‐III administration reduced CCl4‐ and bile duct ligation‐induced liver fibrosis. R‐III also exhibited a preventive effect against CCl4‐inducd liver fibrosis. These findings suggest that the anti‐fibrotic effect of albumin/R‐III is, at least in part, mediated by downregulation of RA signaling and that R‐III is a good candidate as a novel anti‐fibrotic drug.https://doi.org/10.15252/emmm.201404527albuminanti‐fibrotic drugfibrosishepatic stellate cellretinoic acid
spellingShingle Hongsik Lee
Hyeyeun Jeong
Sangeun Park
Wonbaek Yoo
Soyoung Choi
Kyungmin Choi
Min‐Goo Lee
Mihwa Lee
DaeRyong Cha
Young‐Sik Kim
Jeeyoung Han
Wonkon Kim
Sun‐Hwa Park
Junseo Oh
Fusion protein of retinol‐binding protein and albumin domain III reduces liver fibrosis
EMBO Molecular Medicine
albumin
anti‐fibrotic drug
fibrosis
hepatic stellate cell
retinoic acid
title Fusion protein of retinol‐binding protein and albumin domain III reduces liver fibrosis
title_full Fusion protein of retinol‐binding protein and albumin domain III reduces liver fibrosis
title_fullStr Fusion protein of retinol‐binding protein and albumin domain III reduces liver fibrosis
title_full_unstemmed Fusion protein of retinol‐binding protein and albumin domain III reduces liver fibrosis
title_short Fusion protein of retinol‐binding protein and albumin domain III reduces liver fibrosis
title_sort fusion protein of retinol binding protein and albumin domain iii reduces liver fibrosis
topic albumin
anti‐fibrotic drug
fibrosis
hepatic stellate cell
retinoic acid
url https://doi.org/10.15252/emmm.201404527
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