We are analyzing https://link.springer.com/article/10.1007/s10753-010-9281-5.

Title:
Elevated Expression of Liver X Receptor Alpha (LXRα) in Myocardium of Streptozotocin-Induced Diabetic Rats | Inflammation
Description:
The present study was designed to investigate the myocardial expression of liver X receptor alpha (LXRα) in a streptozotocin (STZ)-induced diabetic rat model. Immunohistochemical staining, quantitative real-time RT-PCR, and Western blot analysis were used to determine the expression of LXRα in the myocardium of STZ-induced diabetic rats. The myocardial expression of LXRα target genes, long-chain acyl-CoA synthetase 3 (ACSL3), fatty acid transporter protein (FAT/CD36), ATP-binding cassette transporter A1 (ABCA1), and ABCG1 were also detected. Bisulfite sequencing analysis was employed to examine the methylation status of the CpG island at the LXRα promoter region in the myocardium of STZ-induced diabetic rats. We found that LXRα mRNA and protein expression in the left ventricles, right ventricles, and atria of diabetic rats were gradually increased during the progression of diabetic cardiomyopathy (DCM). The mRNA expression levels of ACSL3 and FAT/CD36 and the protein expression levels of ABCA1 and ABCG1 were also markedly increased in different heart chambers of diabetic rats. Moreover, there was a significant difference in the methylation status of LXRα gene between the ventricles of control and diabetic rats (P < 0.05). Our findings suggest that elevated expression of LXRα may be involved in the progression of DCM, and demethylation of LXRα is likely to be responsible for its increased expression in myocardial tissues.
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Topics {✒️}

quantitative real-time rt-pcr month download article/chapter modulates gene activation diabetes-induced myocardial structural streptozotocin-induced diabetes mellitus thyroid hormone-responsive elements receptor-mediated gene regulation streptozotocin-induced diabetic rats stz-induced diabetic rats thyroid hormone receptors pancreatic beta-cells streptozotocin-induced diabetes article inflammation aims full article pdf reduces cardiac hypertrophy related subjects privacy choices/manage cookies cell cycle arrest article cheng check access instant access xianghong yang china medical university methylation status diabetic cardiomyopathy revisited receptor-mediated lipotoxicity lxrα promoter region protein expression levels prenatal protein restriction prostate cancer cells european economic area endocrine reviews 25 orphan receptor specific shengjing hospital affiliated conditions privacy policy receptor alpha western blot analysis bisulfite sequencing analysis lxrα gene mrna expression levels myocyte-specific overexpression putative metabolic effects chronic lymphocytic leukemia angiotensin ii-dependent article log accepting optional cookies heart chambers traditional chinese medicine myocardial expression lxrα target genes

Schema {🗺️}

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         description:The present study was designed to investigate the myocardial expression of liver X receptor alpha (LXRα) in a streptozotocin (STZ)-induced diabetic rat model. Immunohistochemical staining, quantitative real-time RT-PCR, and Western blot analysis were used to determine the expression of LXRα in the myocardium of STZ-induced diabetic rats. The myocardial expression of LXRα target genes, long-chain acyl-CoA synthetase 3 (ACSL3), fatty acid transporter protein (FAT/CD36), ATP-binding cassette transporter A1 (ABCA1), and ABCG1 were also detected. Bisulfite sequencing analysis was employed to examine the methylation status of the CpG island at the LXRα promoter region in the myocardium of STZ-induced diabetic rats. We found that LXRα mRNA and protein expression in the left ventricles, right ventricles, and atria of diabetic rats were gradually increased during the progression of diabetic cardiomyopathy (DCM). The mRNA expression levels of ACSL3 and FAT/CD36 and the protein expression levels of ABCA1 and ABCG1 were also markedly increased in different heart chambers of diabetic rats. Moreover, there was a significant difference in the methylation status of LXRα gene between the ventricles of control and diabetic rats (P < 0.05). Our findings suggest that elevated expression of LXRα may be involved in the progression of DCM, and demethylation of LXRα is likely to be responsible for its increased expression in myocardial tissues.
         datePublished:2010-12-07T00:00:00Z
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      headline:Elevated Expression of Liver X Receptor Alpha (LXRα) in Myocardium of Streptozotocin-Induced Diabetic Rats
      description:The present study was designed to investigate the myocardial expression of liver X receptor alpha (LXRα) in a streptozotocin (STZ)-induced diabetic rat model. Immunohistochemical staining, quantitative real-time RT-PCR, and Western blot analysis were used to determine the expression of LXRα in the myocardium of STZ-induced diabetic rats. The myocardial expression of LXRα target genes, long-chain acyl-CoA synthetase 3 (ACSL3), fatty acid transporter protein (FAT/CD36), ATP-binding cassette transporter A1 (ABCA1), and ABCG1 were also detected. Bisulfite sequencing analysis was employed to examine the methylation status of the CpG island at the LXRα promoter region in the myocardium of STZ-induced diabetic rats. We found that LXRα mRNA and protein expression in the left ventricles, right ventricles, and atria of diabetic rats were gradually increased during the progression of diabetic cardiomyopathy (DCM). The mRNA expression levels of ACSL3 and FAT/CD36 and the protein expression levels of ABCA1 and ABCG1 were also markedly increased in different heart chambers of diabetic rats. Moreover, there was a significant difference in the methylation status of LXRα gene between the ventricles of control and diabetic rats (P < 0.05). Our findings suggest that elevated expression of LXRα may be involved in the progression of DCM, and demethylation of LXRα is likely to be responsible for its increased expression in myocardial tissues.
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         diabetic cardiomyopathy
         myocardial expression
         DNA methylation
         Immunology
         Rheumatology
         Pharmacology/Toxicology
         Pathology
         Internal Medicine
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