Curcumin modulates dopaminergic receptor, CREB and phospholipase c gene expression in the cerebral cortex and cerebellum of streptozotocin induced diabetic rats

Exercise can ameliorate cardiovascular dysfunctions in the diabetes condition, but its precise molecular mechanisms have not been entirely understood. The aim of the present study was to determine the impact of endurance training on expression of angiogenesis-related genes in cardiac tissue of diabetic rats. Thirty adults male Wistar rats were randomly divided into three groups (N = 10) including diabetic training (DT), sedentary diabetes (SD), and sedentary healthy (SH), in which diabetes was induced by a single dose of streptozotocin (50 mg/kg). Endurance training (ET) with moderate-intensity was performed on a motorized treadmill for six weeks. Training duration and treadmill speed were increased during five weeks, but they were kept constant at the final week, and slope was zero at all stages. Real-time polymerase chain reaction (RT-PCR) analysis was used to measure the expression of myocyte enhancer factor-2C (MEF2C), histone deacetylase-4 (HDAC4) and Calmodulin-dependent protein kinase II (CaMKII) in cardiac tissues of the rats. Our results demonstrated that six weeks of ET increased gene expression of MEF2C significantly (p < 0.05), and caused a significant reduction in HDAC4 and CaMKII gene expression in the DT rats compared to the SD rats (p < 0.05). We concluded that moderate-intensity ET could play a critical role in ameliorating cardiovascular dysfunction in a diabetes condition by regulating the expression of some angiogenesis-related genes in cardiac tissues.

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Macromolecule biosynthesis: a key function of sleep

Physiological Genomics ◽

10.1152/physiolgenomics.00275.2006 ◽

2007 ◽

Vol 31 (3) ◽

pp. 441-457 ◽

Cited By ~ 213

Author(s):

Miroslaw Mackiewicz ◽

Keith R. Shockley ◽

Micah A. Romer ◽

Raymond J. Galante ◽

John E. Zimmerman ◽

...

Keyword(s):

Gene Expression ◽

Cerebral Cortex ◽

Sleep Deprivation ◽

Expression Patterns ◽

State Level ◽

Altered Expression ◽

Mouse Cerebral Cortex ◽

Genes Encoding ◽

Function Of Sleep ◽

Cellular Components

The function(s) of sleep remains a major unanswered question in biology. We assessed changes in gene expression in the mouse cerebral cortex and hypothalamus following different durations of sleep and periods of sleep deprivation. There were significant differences in gene expression between behavioral states; we identified 3,988 genes in the cerebral cortex and 823 genes in the hypothalamus with altered expression patterns between sleep and sleep deprivation. Changes in the steady-state level of transcripts for various genes are remarkably common during sleep, as 2,090 genes in the cerebral cortex and 409 genes in the hypothalamus were defined as sleep specific and changed (increased or decreased) their expression during sleep. The largest categories of overrepresented genes increasing expression with sleep were those involved in biosynthesis and transport. In both the cerebral cortex and hypothalamus, during sleep there was upregulation of multiple genes encoding various enzymes involved in cholesterol synthesis, as well as proteins for lipid transport. There was also upregulation during sleep of genes involved in synthesis of proteins, heme, and maintenance of vesicle pools, as well as antioxidant enzymes and genes encoding proteins of energy-regulating pathways. We postulate that during sleep there is a rebuilding of multiple key cellular components in preparation for subsequent wakefulness.

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Decreased GABA Receptor Binding in the Cerebral Cortex of Insulin Induced Hypoglycemic and Streptozotocin Induced Diabetic Rats

Neurochemical Research ◽

10.1007/s11064-010-0210-7 ◽

2010 ◽

Vol 35 (10) ◽

pp. 1516-1521 ◽

Cited By ~ 16

Author(s):

Sherin Antony ◽

T. Peeyush Kumar ◽

Korah P. Kuruvilla ◽

Naijil George ◽

C. S. Paulose

Keyword(s):

Cerebral Cortex ◽

Receptor Binding ◽

Gaba Receptor ◽

Diabetic Rats

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Dihydroprogesterone Increases the Gene Expression of Myelin Basic Protein in Spinal Cord of Diabetic Rats

Journal of Molecular Neuroscience ◽

10.1007/s12031-010-9344-y ◽

2010 ◽

Vol 42 (2) ◽

pp. 135-139 ◽

Cited By ~ 26

Author(s):

Marzia Pesaresi ◽

Silvia Giatti ◽

Donato Calabrese ◽

Omar Maschi ◽

Donatella Caruso ◽

...

Keyword(s):

Gene Expression ◽

Spinal Cord ◽

Myelin Basic Protein ◽

Basic Protein ◽

Diabetic Rats

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Oxidative Stress-Dependent Impairment of Cardiac-Specific Transcription Factors in Experimental Diabetes

Endocrinology ◽

10.1210/en.2006-0728 ◽

2006 ◽

Vol 147 (12) ◽

pp. 5967-5974 ◽

Cited By ~ 73

Author(s):

Manuela Aragno ◽

Raffaella Mastrocola ◽

Claudio Medana ◽

Maria Graziella Catalano ◽

Ilenia Vercellinatto ◽

...

Keyword(s):

Oxidative Stress ◽

Gene Expression ◽

Left Ventricle ◽

Nuclear Factor Κb ◽

Diabetic Rats ◽

Nuclear Factor ◽

Downstream Signaling ◽

Zdf Rats ◽

Myogenic Factors ◽

Age Receptors

Oxidative stress plays a key role in the pathogenesis of diabetic cardiomyopathy, which is characterized by myocyte loss and fibrosis, finally resulting in heart failure. The study looked at the downstream signaling whereby oxidative stress leads to reduced myocardial contractility in the left ventricle of diabetic rats and the effects of dehydroepiandrosterone (DHEA), which production is suppressed in the failing heart and prevents the oxidative damage induced by hyperglycemia in several experimental models. DHEA was given orally at a dose of 4 mg/rat per day for 21 d to rats with streptozotocin (STZ)-induced diabetes and genetic diabetic-fatty (ZDF) rats. Oxidative balance, advanced glycated end products (AGEs) and AGE receptors, cardiac myogenic factors, and myosin heavy-chain gene expression were determined in the left ventricle of treated and untreated STZ-diabetic rats and ZDF rats. Oxidative stress induced by chronic hyperglycemia increased AGE and AGE receptors and led to activation of the pleoitropic transcription factor nuclear factor-κB. Nuclear factor-κB activation triggered a cascade of signaling, which finally led to the switch in the cardiac myosin heavy-chain (MHC) gene expression from the α-MHC isoform to the β-MHC isoform. DHEA treatment, by preventing the activation of the oxidative pathways induced by hyperglycemia, counteracted the enhanced AGE receptor activation in the heart of STZ-diabetic rats and ZDF rats and normalized downstream signaling, thus avoiding impairment of the cardiac myogenic factors, heart autonomic nervous system and neural crest derivatives (HAND) and myogenic enhancer factor-2, and the switch in MHC gene expression, which are the early events in diabetic cardiomyopathy.

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Microarray analysis reveals novel gene expression changes associated with erectile dysfunction in diabetic rats

Physiological Genomics ◽

10.1152/physiolgenomics.00112.2005 ◽

2005 ◽

Vol 23 (2) ◽

pp. 192-205 ◽

Cited By ~ 34

Author(s):

Chris J. Sullivan ◽

Thomas H. Teal ◽

Ian P. Luttrell ◽

Khoa B. Tran ◽

Mette A. Peters ◽

...

Keyword(s):

Gene Expression ◽

Smooth Muscle ◽

Erectile Dysfunction ◽

Splice Variants ◽

Full Range ◽

Diabetic Rats ◽

Differentially Expressed ◽

Diabetic Rat ◽

Literature Mining ◽

Mrna Levels

To investigate the full range of molecular changes associated with erectile dysfunction (ED) in Type 1 diabetes, we examined alterations in penile gene expression in streptozotocin-induced diabetic rats and littermate controls. With the use of Affymetrix GeneChip arrays and statistical filtering, 529 genes/transcripts were considered to be differentially expressed in the diabetic rat cavernosum compared with control. Gene Ontology (GO) classification indicated that there was a decrease in numerous extracellular matrix genes (e.g., collagen and elastin related) and an increase in oxidative stress-associated genes in the diabetic rat cavernosum. In addition, PubMatrix literature mining identified differentially expressed genes previously shown to mediate vascular dysfunction [e.g., ceruloplasmin ( Cp), lipoprotein lipase, and Cd36] as well as genes involved in the modulation of the smooth muscle phenotype (e.g., Kruppel-like factor 5 and chemokine C-X3-C motif ligand 1). Real-time PCR was used to confirm changes in expression for 23 relevant genes. Further validation of Cp expression in the diabetic rat cavernosum demonstrated increased mRNA levels of the secreted and anchored splice variants of Cp. CP protein levels showed a 1.9-fold increase in tissues from diabetic rats versus controls. Immunohistochemistry demonstrated localization of CP protein in cavernosal sinusoids of control and diabetic animals, including endothelial and smooth muscle layers. Overall, this study broadens the scope of candidate genes and pathways that may be relevant to the pathophysiology of diabetes-induced ED as well as highlights the potential complexity of this disorder.

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