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Opposite Expression of SPARC between the Liver and Pancreas in Streptozotocin-Induced Diabetic Rats.

Aseer KR, Kim SW, Choi MS, Yun JW - PLoS ONE (2015)

Bottom Line: 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.High and low cellular insulin content was found in the diabetic liver and pancreas, respectively.

View Article: PubMed Central - PubMed

Affiliation: Department of Biotechnology, Daegu University, Kyungsan, Kyungbuk, 712-714, Republic of Korea.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus

Sex-dependent changes in body weight (A), blood glucose levels (B), and plasma insulin levels (C) in healthy control and STZ-induced diabetic rats.Statistical significance between male and female rats was calculated by One-way ANOVA followed by Tukey’s post hoc tests, where p-value is *p<0.05 and **p<0.01, and significance between controls and diabetics is represented by †p<0.05 and ††p<0.01.
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pone.0131189.g001: Sex-dependent changes in body weight (A), blood glucose levels (B), and plasma insulin levels (C) in healthy control and STZ-induced diabetic rats.Statistical significance between male and female rats was calculated by One-way ANOVA followed by Tukey’s post hoc tests, where p-value is *p<0.05 and **p<0.01, and significance between controls and diabetics is represented by †p<0.05 and ††p<0.01.

Mentions: To investigate the role of SPARC in T1DM, we developed an experimental diabetic rat model using STZ (50 mg/kg body weight) as outlined in our previous study [7]. We comparatively determined total body weights, blood glucose levels, and plasma insulin levels in control and STZ-induced diabetic male and female rats. As shown in Fig 1A, both diabetic rats showed reduced body weight, and the males were more significantly reduced than the females after 2 weeks of STZ treatment. Further, blood glucose levels were higher in both genders upon STZ induction, indicating insulin insufficiency (Fig 1B). Reduction of insulin levels was also observed in both genders of diabetic rats, and females showed lower insulin levels than male counterparts (Fig 1C).


Opposite Expression of SPARC between the Liver and Pancreas in Streptozotocin-Induced Diabetic Rats.

Aseer KR, Kim SW, Choi MS, Yun JW - PLoS ONE (2015)

Sex-dependent changes in body weight (A), blood glucose levels (B), and plasma insulin levels (C) in healthy control and STZ-induced diabetic rats.Statistical significance between male and female rats was calculated by One-way ANOVA followed by Tukey’s post hoc tests, where p-value is *p<0.05 and **p<0.01, and significance between controls and diabetics is represented by †p<0.05 and ††p<0.01.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4481468&req=5

pone.0131189.g001: Sex-dependent changes in body weight (A), blood glucose levels (B), and plasma insulin levels (C) in healthy control and STZ-induced diabetic rats.Statistical significance between male and female rats was calculated by One-way ANOVA followed by Tukey’s post hoc tests, where p-value is *p<0.05 and **p<0.01, and significance between controls and diabetics is represented by †p<0.05 and ††p<0.01.
Mentions: To investigate the role of SPARC in T1DM, we developed an experimental diabetic rat model using STZ (50 mg/kg body weight) as outlined in our previous study [7]. We comparatively determined total body weights, blood glucose levels, and plasma insulin levels in control and STZ-induced diabetic male and female rats. As shown in Fig 1A, both diabetic rats showed reduced body weight, and the males were more significantly reduced than the females after 2 weeks of STZ treatment. Further, blood glucose levels were higher in both genders upon STZ induction, indicating insulin insufficiency (Fig 1B). Reduction of insulin levels was also observed in both genders of diabetic rats, and females showed lower insulin levels than male counterparts (Fig 1C).

Bottom Line: 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.High and low cellular insulin content was found in the diabetic liver and pancreas, respectively.

View Article: PubMed Central - PubMed

Affiliation: Department of Biotechnology, Daegu University, Kyungsan, Kyungbuk, 712-714, Republic of Korea.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus