Cargando…

Involvement of heparan sulfate 3‐O‐sulfotransferase isoform‐1 in the insulin secretion pathway

Aims/Introduction:  Heparan sulfate (HS) mediates a variety of molecular recognition events that are essential for differentiation, morphogenesis and homeostasis through various HS forms that result from differential sulfate modification. Recently, we found that HS is localized exclusively around βß...

Descripción completa

Detalles Bibliográficos
Autores principales: Takahashi, Iwao, Ohashi, Kazuaki, Nata, Koji
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4019256/
https://www.ncbi.nlm.nih.gov/pubmed/24843591
http://dx.doi.org/10.1111/j.2040-1124.2012.00205.x
_version_ 1782480146404474880
author Takahashi, Iwao
Ohashi, Kazuaki
Nata, Koji
author_facet Takahashi, Iwao
Ohashi, Kazuaki
Nata, Koji
author_sort Takahashi, Iwao
collection PubMed
description Aims/Introduction:  Heparan sulfate (HS) mediates a variety of molecular recognition events that are essential for differentiation, morphogenesis and homeostasis through various HS forms that result from differential sulfate modification. Recently, we found that HS is localized exclusively around βß‐cells in islets of adult mice and is required for insulin secretion. The aim of this study was to examine the contribution of HS sulfate groups to insulin secretion. Materials and Methods:  Glucose‐induced insulin secretion (GIIS) was examined in mouse pancreatic islets, the mouse pancreatic β‐cell line MIN6 cells and its derivative MIN6T3 cells after removal of sulfate groups by sodium chlorate, a competitive inhibitor of glycosaminoglycan sulfation. Quantitative reverse transcription polymerase chain reaction was used for analyzing messenger ribonucleic acid (mRNA) expression of HS modification enzymes. Expression of HS 3‐O‐sulfotransferase isoform‐1 (Hs3st1) was silenced and GIIS was examined. Results:  Impaired insulin secretion by islets, MIN6 cells and MIN6T3 cells was observed after treatment with sodium chlorate. Sodium chlorate‐treatment upregulated the mRNA expression of sulfotransferases expressed in MIN6T3 cells. Expression of the Hs3st1 was strongly upregulated by sodium chlorate‐treatment, and its silencing by RNA interference reduced GIIS in MIN6T3 cells. Conclusions:  Our data suggest that the 3‐O‐sulfate group of HS that is modified by Hs3st1 plays a significant role(s) in the insulin secretory pathway, selectively through an interaction with factor(s) upstream of membrane depolarization in β‐cells. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2012.00205.x, 2012)
format Online
Article
Text
id pubmed-4019256
institution National Center for Biotechnology Information
language English
publishDate 2012
publisher Blackwell Publishing Ltd
record_format MEDLINE/PubMed
spelling pubmed-40192562014-05-19 Involvement of heparan sulfate 3‐O‐sulfotransferase isoform‐1 in the insulin secretion pathway Takahashi, Iwao Ohashi, Kazuaki Nata, Koji J Diabetes Investig Articles Aims/Introduction:  Heparan sulfate (HS) mediates a variety of molecular recognition events that are essential for differentiation, morphogenesis and homeostasis through various HS forms that result from differential sulfate modification. Recently, we found that HS is localized exclusively around βß‐cells in islets of adult mice and is required for insulin secretion. The aim of this study was to examine the contribution of HS sulfate groups to insulin secretion. Materials and Methods:  Glucose‐induced insulin secretion (GIIS) was examined in mouse pancreatic islets, the mouse pancreatic β‐cell line MIN6 cells and its derivative MIN6T3 cells after removal of sulfate groups by sodium chlorate, a competitive inhibitor of glycosaminoglycan sulfation. Quantitative reverse transcription polymerase chain reaction was used for analyzing messenger ribonucleic acid (mRNA) expression of HS modification enzymes. Expression of HS 3‐O‐sulfotransferase isoform‐1 (Hs3st1) was silenced and GIIS was examined. Results:  Impaired insulin secretion by islets, MIN6 cells and MIN6T3 cells was observed after treatment with sodium chlorate. Sodium chlorate‐treatment upregulated the mRNA expression of sulfotransferases expressed in MIN6T3 cells. Expression of the Hs3st1 was strongly upregulated by sodium chlorate‐treatment, and its silencing by RNA interference reduced GIIS in MIN6T3 cells. Conclusions:  Our data suggest that the 3‐O‐sulfate group of HS that is modified by Hs3st1 plays a significant role(s) in the insulin secretory pathway, selectively through an interaction with factor(s) upstream of membrane depolarization in β‐cells. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2012.00205.x, 2012) Blackwell Publishing Ltd 2012-03-06 2012-08-20 /pmc/articles/PMC4019256/ /pubmed/24843591 http://dx.doi.org/10.1111/j.2040-1124.2012.00205.x Text en © 2012 Asian Association for the Study of Diabetes and Blackwell Publishing Asia Pty Ltd
spellingShingle Articles
Takahashi, Iwao
Ohashi, Kazuaki
Nata, Koji
Involvement of heparan sulfate 3‐O‐sulfotransferase isoform‐1 in the insulin secretion pathway
title Involvement of heparan sulfate 3‐O‐sulfotransferase isoform‐1 in the insulin secretion pathway
title_full Involvement of heparan sulfate 3‐O‐sulfotransferase isoform‐1 in the insulin secretion pathway
title_fullStr Involvement of heparan sulfate 3‐O‐sulfotransferase isoform‐1 in the insulin secretion pathway
title_full_unstemmed Involvement of heparan sulfate 3‐O‐sulfotransferase isoform‐1 in the insulin secretion pathway
title_short Involvement of heparan sulfate 3‐O‐sulfotransferase isoform‐1 in the insulin secretion pathway
title_sort involvement of heparan sulfate 3‐o‐sulfotransferase isoform‐1 in the insulin secretion pathway
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4019256/
https://www.ncbi.nlm.nih.gov/pubmed/24843591
http://dx.doi.org/10.1111/j.2040-1124.2012.00205.x
work_keys_str_mv AT takahashiiwao involvementofheparansulfate3osulfotransferaseisoform1intheinsulinsecretionpathway
AT ohashikazuaki involvementofheparansulfate3osulfotransferaseisoform1intheinsulinsecretionpathway
AT natakoji involvementofheparansulfate3osulfotransferaseisoform1intheinsulinsecretionpathway