Opposite Expression of SPARC between the Liver and Pancreas in Streptozotocin-Induced Diabetic Rats.
Secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein that regulates several cellular events, including inflammation and tissue remodelling. In this study, we investigated the tissue-specific expression of SPARC in streptozotocin (STZ)-induced diabetes, and found that SPARC...
Main Authors: | , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Public Library of Science (PLoS)
2015-01-01
|
Series: | PLoS ONE |
Online Access: | http://europepmc.org/articles/PMC4481468?pdf=render |
id |
doaj-5a5d32bb891f4ddb91333d503e57d756 |
---|---|
record_format |
Article |
spelling |
doaj-5a5d32bb891f4ddb91333d503e57d7562020-11-25T01:45:18ZengPublic Library of Science (PLoS)PLoS ONE1932-62032015-01-01106e013118910.1371/journal.pone.0131189Opposite Expression of SPARC between the Liver and Pancreas in Streptozotocin-Induced Diabetic Rats.Kanikkai Raja AseerSang Woo KimMyung-Sook ChoiJong Won YunSecreted protein acidic and rich in cysteine (SPARC) is a matricellular protein that regulates several cellular events, including inflammation and tissue remodelling. In this study, we investigated the tissue-specific expression of SPARC in streptozotocin (STZ)-induced diabetes, and found that SPARC was significantly up-regulated in the liver while down-regulated in the pancreas of STZ-induced diabetic rats. Chronic inflammation occurred in the diabetic pancreas accompanied by up-regulation of CCAAT/enhancer-binding protein beta (C/EBPβ) and its targets (TNFα, Il6, CRP, and Fn1) as well as myeloperoxidase (Mpo) and C-X-C chemokine receptor type 2 (Cxcr2). Diabetic liver showed significant up-regulation of Tgfb1 as well as moderately less up-regulated TNFα and reduced Fn1, resulting in elevated fibrogenesis. PARP-1 was not up-regulated during CD95-mediated apoptosis, resulting in restoration of high ATP levels in the diabetic liver. On the contrary, CD95-dependent apoptosis was not observed in the diabetic pancreas due to up-regulation of PARP-1 and ATP depletion, resulting in necrosis. The cytoprotective machinery was damaged by pancreatic inflammation, whereas adequate antioxidant capacity indicates low oxidative stress in the diabetic liver. High and low cellular insulin content was found in the diabetic liver and pancreas, respectively. Furthermore, we identified six novel interacting partner proteins of SPARC by co-immunoprecipitation in the diabetic liver and pancreas, and their interactions with SPARC were predicted by bioinformatics tools. Taken together, opposite expression of SPARC in the diabetic liver and pancreas may be related to inflammation and immune cell infiltration, degrees of apoptosis and fibrosis, cytoprotective machinery, and cellular insulin levels.http://europepmc.org/articles/PMC4481468?pdf=render |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Kanikkai Raja Aseer Sang Woo Kim Myung-Sook Choi Jong Won Yun |
spellingShingle |
Kanikkai Raja Aseer Sang Woo Kim Myung-Sook Choi Jong Won Yun Opposite Expression of SPARC between the Liver and Pancreas in Streptozotocin-Induced Diabetic Rats. PLoS ONE |
author_facet |
Kanikkai Raja Aseer Sang Woo Kim Myung-Sook Choi Jong Won Yun |
author_sort |
Kanikkai Raja Aseer |
title |
Opposite Expression of SPARC between the Liver and Pancreas in Streptozotocin-Induced Diabetic Rats. |
title_short |
Opposite Expression of SPARC between the Liver and Pancreas in Streptozotocin-Induced Diabetic Rats. |
title_full |
Opposite Expression of SPARC between the Liver and Pancreas in Streptozotocin-Induced Diabetic Rats. |
title_fullStr |
Opposite Expression of SPARC between the Liver and Pancreas in Streptozotocin-Induced Diabetic Rats. |
title_full_unstemmed |
Opposite Expression of SPARC between the Liver and Pancreas in Streptozotocin-Induced Diabetic Rats. |
title_sort |
opposite expression of sparc between the liver and pancreas in streptozotocin-induced diabetic rats. |
publisher |
Public Library of Science (PLoS) |
series |
PLoS ONE |
issn |
1932-6203 |
publishDate |
2015-01-01 |
description |
Secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein that regulates several cellular events, including inflammation and tissue remodelling. In this study, we investigated the tissue-specific expression of SPARC in streptozotocin (STZ)-induced diabetes, and found that SPARC was significantly up-regulated in the liver while down-regulated in the pancreas of STZ-induced diabetic rats. Chronic inflammation occurred in the diabetic pancreas accompanied by up-regulation of CCAAT/enhancer-binding protein beta (C/EBPβ) and its targets (TNFα, Il6, CRP, and Fn1) as well as myeloperoxidase (Mpo) and C-X-C chemokine receptor type 2 (Cxcr2). Diabetic liver showed significant up-regulation of Tgfb1 as well as moderately less up-regulated TNFα and reduced Fn1, resulting in elevated fibrogenesis. PARP-1 was not up-regulated during CD95-mediated apoptosis, resulting in restoration of high ATP levels in the diabetic liver. On the contrary, CD95-dependent apoptosis was not observed in the diabetic pancreas due to up-regulation of PARP-1 and ATP depletion, resulting in necrosis. The cytoprotective machinery was damaged by pancreatic inflammation, whereas adequate antioxidant capacity indicates low oxidative stress in the diabetic liver. High and low cellular insulin content was found in the diabetic liver and pancreas, respectively. Furthermore, we identified six novel interacting partner proteins of SPARC by co-immunoprecipitation in the diabetic liver and pancreas, and their interactions with SPARC were predicted by bioinformatics tools. Taken together, opposite expression of SPARC in the diabetic liver and pancreas may be related to inflammation and immune cell infiltration, degrees of apoptosis and fibrosis, cytoprotective machinery, and cellular insulin levels. |
url |
http://europepmc.org/articles/PMC4481468?pdf=render |
work_keys_str_mv |
AT kanikkairajaaseer oppositeexpressionofsparcbetweentheliverandpancreasinstreptozotocininduceddiabeticrats AT sangwookim oppositeexpressionofsparcbetweentheliverandpancreasinstreptozotocininduceddiabeticrats AT myungsookchoi oppositeexpressionofsparcbetweentheliverandpancreasinstreptozotocininduceddiabeticrats AT jongwonyun oppositeexpressionofsparcbetweentheliverandpancreasinstreptozotocininduceddiabeticrats |
_version_ |
1725023723628527616 |