Downregulation of the CCAAT-Enhancer Binding Protein β in ΔFosB Transgenic Mice and by Electroconvulsive Seizures

Chen, Jingshan; Newton, Samuel S.; Zeng, Le; Adams, David H.; Dow, Anthoni L; Madsén, Torsten; Nestler, Eric J.; Duman, Ronald S.

doi:10.1038/sj.npp.1300289

Cited by 14 publications

(8 citation statements)

References 35 publications

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“…However, FosB is a unique transcription factor that plays a role in long-term adaptive changes in the brain. A number of genes are regulated by FosB expression in vitro and in vivo including genes encoding the AMPA GluR2 receptor and other transcription factors (Chen et al, 2004;McClung et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Differential Regulation of c-Fos and FosB in the Rat Brain After Amygdala Kindling

2006

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Members of the inducible transcription factor Fos family, that are part of the AP-1 complex that binds to the corresponding promoter site, are implicated in the regulation of gene transcription after acute and chronic seizures. However, little is known about the temporal expression of the AP-1 transcription factors and if individual proteins composing this complex have distinct roles in development and maintenance of permanent epilepsy. In this study, the AP-1 binding capacity, its content of different Fos proteins, and the anatomical specificity, were analyzed 2 or 18 h after achieving full kindling in rats. The same analysis was performed in fully kindled animal receiving a new stimulus after a 3-week pause to determine the extent of stability of the AP-1 transcription factors. While both c-Fos and FosB were induced in all cortical areas after a single stimulus, only FosB-immunoreactivity remained after 18 h. A single stimulation to kindled animals left undisturbed for 3 weeks induced a long-lasting upregulation of AP-1 binding in the frontal cortex, but not in the hippocampus suggesting a permanent exposure of AP-1 heterocomplexes in the frontal cortex. Supershift assays showed that FosB is the dominant component of the long-term AP-1 complex. It is concluded that the AP-1 binding complex in fully kindled rats is composed of different proteins, and that FosB-containing AP-1 complexes mediate long-term effects in the frontal cortex.

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Section: Discussionmentioning

confidence: 99%

Differential Regulation of c-Fos and FosB in the Rat Brain After Amygdala Kindling

2006

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“…Thus, C/EBPβ levels are increased in rat cerebellum by hypothyroidism (Alvarez et al 2005), in the hippocampus by experimental diabetes (Kazkayasi et al 2013), in rat frontal cortex and midbrain by systemic lysergic acid diethylamide injection (Nichols and Sanders-Bush 2004) and in rat hypothalamic neurons by dehydrationinduced remodeling (Qiu et al 2007). Down-regulation of C/EBPβ in the CNS is rarer and it has been reported in mouse in prefrontal cortex after inflammatory pain by facial carrageenan injection (Poh et al 2011) and in hippocampus after chronic electroconvulsive seizures (Chen et al 2004b). Hypoxic preconditioning in rats and mice (Bernaudin et al 2002;Tang et al 2006b) and exposure to hyperbaric oxygen in rats (Hirata et al 2007) upregulate CNS C/EBPδ levels in unidentified cells.…”

Section: Other Modelsmentioning

confidence: 95%

C/EBPβ and C/EBPδ transcription factors: Basic biology and roles in the CNS

Pulido-Salgado

Vidal-Taboada

Saura

2015

Progress in Neurobiology

141

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“…Because C/EBP␤ deletion mainly affected lipogenic genes in Lepr db/db mice rather than in C/EBP␤ Ϫ/Ϫ mice, it suggests that C/EBP␤ likely controls the inducible expression of these genes under lipogenic conditions in different tissues. C/EBP␤ is expressed at relatively high levels in the hippocampus where it regulates stress behavior in response to adrenal-glucocorticoids (81,82). In pituitary cells, C/EBP␤ overexpression stimulates expression of both pro-opiomelanocortin-␣ (an anorectic peptide) and suppressor of cytokine signaling-3 (SOC-3) (83), a feedback inhibitor of leptin receptor signaling (84).…”

Section: Discussionmentioning

confidence: 99%

CCAAT/Enhancer-binding Protein β Deletion Reduces Adiposity, Hepatic Steatosis, and Diabetes in Lepr Mice

Schroeder-Gloeckler¹,

Rahman²,

Janssen³

et al. 2007

Journal of Biological Chemistry

119

101

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CCAAT/enhancer-binding protein ␤ (C/EBP␤) plays a key role in initiation of adipogenesis in adipose tissue and gluconeogenesis in liver; however, the role of C/EBP␤ in hepatic lipogenesis remains undefined. Here we show that C/EBP␤ inactivation in Lepr db/db mice attenuates obesity, fatty liver, and diabetes. In addition to impaired adipogenesis, livers from C/EBP␤ ؊/؊ x Lepr db/db mice had dramatically decreased triglyceride content and reduced lipogenic enzyme activity. C/EBP␤ deletion in Lepr db/db mice down-regulated peroxisome proliferator-activated receptor ␥2 (PPAR␥2) and stearoyl-CoA desaturase-1 and up-regulated PPAR␣ independent of SREBP1c. Conversely, C/EBP␤ overexpression in wild-type mice increased PPAR␥2 and stearoyl-CoA desaturase-1 mRNA and hepatic triglyceride content. In FAO cells, overexpression of the liver inhibiting form of C/EBP␤ or C/EBP␤ RNA interference attenuated palmitate-induced triglyceride accumulation and reduced PPAR␥2 and triglyceride levels in the liver in vivo. Leptin and the anti-diabetic drug metformin acutely down-regulated C/EBP␤ expression in hepatocytes, whereas fatty acids up-regulate C/EBP␤ expression. These data provide novel evidence linking C/EBP␤ expression to lipogenesis and energy balance with important implications for the treatment of obesity and fatty liver disease.Obesity is the most common nutritional disorder in Western societies. Today in the United States, more than 60% of people are either overweight (body mass index (BMI) Ͼ 25) or obese (BMI Ͼ 30) (1). Obesity is frequently associated with type II diabetes, hypertension, and hyperlipidemia, all known risk factors for cardiovascular disease (2). Obesity is also a major risk factor for non-alcoholic fatty liver disease, one of the most common emerging liver diseases in Western countries coinciding with the worldwide obesity epidemic (3, 4). The underlying transcriptional events that contribute to obesity and its associated disorders are not well understood. Some of the genes that regulate body weight have been identified as well as additional neuropeptides, hormones, and nutritional factors that play a role in body weight regulation, particularly through the ␤-adrenergic system (5, 6). Discovery of the hormone leptin and its receptors, which suppress appetite and reduce fat mass, has dramatically increased our understanding of the regulation of energy balance (7,8). More recently, the study of specific transcription factor genes and their metabolism has provided powerful new tools for understanding the integrated mechanisms underlying obesity and diabetes (9 -11). This is most elegantly illustrated using tissue-specific gene knockouts and overexpression models to elucidate the mechanism of action of the PPAR 5 family of nuclear hormone receptors (12). The CCAAT/enhancer-binding protein (C/EBP) family includes five nuclear transcription factors, C/EBP ␣, ␤, ␥, ␦, and ⑀, encoded by separate genes located on different chromosomes (13,14). Collectively, C/EBPs are expressed across a variety of cell types, and...

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Downregulation of the CCAAT-Enhancer Binding Protein β in ΔFosB Transgenic Mice and by Electroconvulsive Seizures

Cited by 14 publications

References 35 publications

Differential Regulation of c-Fos and FosB in the Rat Brain After Amygdala Kindling

Differential Regulation of c-Fos and FosB in the Rat Brain After Amygdala Kindling

C/EBPβ and C/EBPδ transcription factors: Basic biology and roles in the CNS

CCAAT/Enhancer-binding Protein β Deletion Reduces Adiposity, Hepatic Steatosis, and Diabetes in Lepr Mice

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