Liver transplantation: New treatment for mucopolysaccharidosis type VI in rats.

arylsulfatase B glycosaminoglycan liver transplantation lysosomal storage disorder mucopolysaccharidosis VI

Journal

Pediatrics international : official journal of the Japan Pediatric Society
ISSN: 1442-200X
Titre abrégé: Pediatr Int
Pays: Australia
ID NLM: 100886002

Informations de publication

Date de publication:
Feb 2019
Historique:
received: 13 04 2018
revised: 22 08 2018
accepted: 26 10 2018
pubmed: 15 12 2018
medline: 12 3 2019
entrez: 15 12 2018
Statut: ppublish

Résumé

Mucopolysaccharidosis (MPS) VI is a rare, autosomal recessive congenital metabolic disorder caused by deficient activity of the lysosomal metabolic enzyme, N-acetylgalactosamine 4-sulfatase. Enzyme replacement therapy (ERT) is the current treatment for MPS VI, although it involves limited compliance to the therapy and high cost. The aim of this study was to develop a new method of treatment by conducting an orthotopic liver transplantation (LTx) using an animal model of human MPS VI, and to evaluate and examine its effectiveness for treating MPS VI. LTx was carried out from normal unaffected to affected MPS VI rats (MPR), which were then killed after LTx, and tissues from the heart, spleen, and knee joint, as well as serum, collected for biological and morphologic evaluation. Liver-transplanted (LTx) MPR had the same level of N-acetylgalactosamine 4-sulfatase activity in the liver and lungs as normal unaffected MPR, and the urinary secretion of mucopolysaccharides/glycosaminoglycan (GAG) in LTx MPR was significantly decreased. Furthermore, on histopathology, the spleens of LTx MPR showed elimination of vacuole cells. In the knee joints, growth plates became thinner, and on radiography the facial and cranial bones of LTx MPR were morphologically normal. LTx from normal to affected MPR was effective for symptoms of MPS and accumulation of GAG, suggesting that LTx could be a promising alternative approach for MPS VI.

Sections du résumé

BACKGROUND BACKGROUND
Mucopolysaccharidosis (MPS) VI is a rare, autosomal recessive congenital metabolic disorder caused by deficient activity of the lysosomal metabolic enzyme, N-acetylgalactosamine 4-sulfatase. Enzyme replacement therapy (ERT) is the current treatment for MPS VI, although it involves limited compliance to the therapy and high cost. The aim of this study was to develop a new method of treatment by conducting an orthotopic liver transplantation (LTx) using an animal model of human MPS VI, and to evaluate and examine its effectiveness for treating MPS VI.
METHODS METHODS
LTx was carried out from normal unaffected to affected MPS VI rats (MPR), which were then killed after LTx, and tissues from the heart, spleen, and knee joint, as well as serum, collected for biological and morphologic evaluation.
RESULTS RESULTS
Liver-transplanted (LTx) MPR had the same level of N-acetylgalactosamine 4-sulfatase activity in the liver and lungs as normal unaffected MPR, and the urinary secretion of mucopolysaccharides/glycosaminoglycan (GAG) in LTx MPR was significantly decreased. Furthermore, on histopathology, the spleens of LTx MPR showed elimination of vacuole cells. In the knee joints, growth plates became thinner, and on radiography the facial and cranial bones of LTx MPR were morphologically normal.
CONCLUSIONS CONCLUSIONS
LTx from normal to affected MPR was effective for symptoms of MPS and accumulation of GAG, suggesting that LTx could be a promising alternative approach for MPS VI.

Identifiants

pubmed: 30548979
doi: 10.1111/ped.13751
doi:

Types de publication

Evaluation Study Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

180-189

Subventions

Organisme : Ministry of Education, Culture, Sports, Science and Technology of Japan
Organisme : National Center for Child Health and Development

Informations de copyright

© 2018 Japan Pediatric Society.

Auteurs

Sumika Toyama (S)

Division of Transplantation Immunology, National Center for Child Health and Development, Tokyo, Japan.
Division of Life Science and Engineering, Tokyo Denki University, Saitama, Japan.

Ohsuke Migita (O)

Department of Clinical Diagnosis, National Center for Child Health and Development, Tokyo, Japan.

Masayuki Fujino (M)

Division of Transplantation Immunology, National Center for Child Health and Development, Tokyo, Japan.
AIDS Research Center, National Institute of Infectious Diseases, Tokyo, Japan.

Tetsuo Kunieda (T)

Graduate School of Natural Science and Technology, Okayama University, Okayama, Japan.

Motomichi Kosuga (M)

Department of Clinical Diagnosis, National Center for Child Health and Development, Tokyo, Japan.

Yasuyuki Fukuhara (Y)

Department of Clinical Diagnosis, National Center for Child Health and Development, Tokyo, Japan.

Yukitoshi Nagahara (Y)

Division of Life Science and Engineering, Tokyo Denki University, Saitama, Japan.

Xiao-Kang Li (XK)

Division of Transplantation Immunology, National Center for Child Health and Development, Tokyo, Japan.

Torayuki Okuyama (T)

Department of Clinical Diagnosis, National Center for Child Health and Development, Tokyo, Japan.

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Classifications MeSH