Repeated Immobilization Stress Increases Nur77 Expression in the Bed Nucleus of the Stria Terminalis

Campos-Melo, Danae; Quiroz, Gabriel; Noches, Verónica; Gysling, Katia; Forray, María Inés; Andrés, Marı́a Estela

doi:10.1007/s12640-011-9243-1

Cited by 10 publications

(9 citation statements)

References 84 publications

(103 reference statements)

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“…In the PVN, it has been shown that Nur77 is no longer induced after chronic stress stimuli (Umemoto et al, 1994, 1997). In contrast, in the ventral region of the BNST, we observed a higher number of cells expressing Nur77 after repeated immobilization stress compared with acute stress (Campos-Melo et al, 2011). Interestingly, the data of the group of Marta Antonelli (Katunar et al, 2010) suggest that Nurr1 may be the transcription factor setting up the new parameters of the dopamine system after prenatal stress.…”

Section: Functional Role Of Nur Transcription Factors In the Addictiocontrasting

confidence: 55%

“…We reported that cells expressing CRF in the BNST also express Nur77 (Campos-Melo et al, 2011), even though the expression of Nur77 is wider than CRF in this nucleus. Nur77 expression increases significantly in the dorso-lateral and ventro-medial subdivisions of the BNST after acute and repeated immobilization stress (Campos-Melo et al, 2011), same areas where CRF expression increases after repeated immobilization stress (Santibanez et al, 2006). Several years ago, it was shown that the intracerebroventricular injection of CRF increases CRF expression in the PVN (Parkes et al, 1993).…”

Section: Nur Transcription Factors During the Stress Responsementioning

confidence: 93%

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Nur transcription factors in stress and addiction

Campos-Melo

Galleguillos

Sánchez

et al. 2013

Front. Mol. Neurosci.

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The Nur transcription factors Nur77 (NGFI-B, NR4A1), Nurr1 (NR4A2), and Nor-1 (NR4A3) are a sub-family of orphan members of the nuclear receptor superfamily. These transcription factors are products of immediate early genes, whose expression is rapidly and transiently induced in the central nervous system by several types of stimuli. Nur factors are present throughout the hypothalamus-pituitary-adrenal (HPA) axis where are prominently induced in response to stress. Drugs of abuse and stress also induce the expression of Nur factors in nuclei of the motivation/reward circuit of the brain, indicating their participation in the process of drug addiction and in non-hypothalamic responses to stress. Repeated use of addictive drugs and chronic stress induce long-lasting dysregulation of the brain motivation/reward circuit due to reprogramming of gene expression and enduring alterations in neuronal function. Here, we review the data supporting that Nur transcription factors are key players in the molecular basis of the dysregulation of neuronal circuits involved in chronic stress and addiction.

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Section: Functional Role Of Nur Transcription Factors In the Addictiocontrasting

confidence: 55%

Section: Nur Transcription Factors During the Stress Responsementioning

confidence: 93%

Nur transcription factors in stress and addiction

Campos-Melo

Galleguillos

Sánchez

et al. 2013

Front. Mol. Neurosci.

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“…Immunofluorescence assays were performed essentially as described previously (32). Brain slices were incubated with anti-CoREST1 (612146 from BD Transduction Laboratories) for 48 h at 4°C, and then anti-CoREST2 (HPA021638 from Sigma) was added, followed by incubation for 12 h. Subsequently, slices were mounted on glass slides and incubated with secondary anti-rabbit IgG coupled to Alexa Fluor 594 and anti-mouse IgG coupled to Alexa Fluor 488.…”

Section: Animalsmentioning

confidence: 99%

Differential Properties of Transcriptional Complexes Formed by the CoREST Family

Barrios

Gómez

Sáez

et al. 2014

Molecular and Cellular Biology

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dMammalian genomes harbor three CoREST genes. rcor1 encodes CoREST (CoREST1), and the paralogues rcor2 and rcor3 encode CoREST2 and CoREST3, respectively. Here, we describe specific properties of transcriptional complexes formed by CoREST proteins with the histone demethylase LSD1/KDM1A and histone deacetylases 1 and 2 (HDAC1/2) and the finding that all three CoRESTs are expressed in the adult rat brain. CoRESTs interact equally strongly with LSD1/KDM1A. Structural analysis shows that the overall conformation of CoREST3 is similar to that of CoREST1 complexed with LSD1/KDM1A. Nonetheless, transcriptional repressive capacity of CoREST3 is lower than that of CoREST1, which correlates with the observation that CoREST3 leads to a reduced LSD1/KDM1A catalytic efficiency. Also, CoREST2 shows a lower transcriptional repression than CoREST1, which is resistant to HDAC inhibitors. CoREST2 displays lower interaction with HDAC1/2, which is barely present in LSD1/KDM1A-CoREST2 complexes. A nonconserved leucine in the first SANT domain of CoREST2 severely weakens its association with HDAC1/2. Furthermore, CoREST2 mutants with increased HDAC1/2 interaction and those without HDAC1/2 interaction exhibit equivalent transcriptional repression capacities, indicating that CoREST2 represses in an HDAC-independent manner. In conclusion, differences among CoREST proteins are instrumental in the modulation of protein-protein interactions and catalytic activities of LSD1/KDM1A-CoREST-HDAC complexes, fine-tuning gene expression regulation.

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“…Nr4a1, like other Nr4a members, is involved in early sympathetic stress response in the neuroendocrine system 8–11 . At the same time, Nr4a1 plays an important role in leukocytes, where it is a central regulator of innate and adaptive immune responses.…”

Section: Introductionmentioning

confidence: 99%

Transcription factor Nr4a1 couples sympathetic and inflammatory cues in CNS-recruited macrophages to limit neuroinflammation

et al. 2015

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Molecular mechanisms linking the sympathetic stress response and inflammation remain enigmatic. Here we demonstrate that the transcription factor Nr4a1 regulates production of norepinephrine (NE) in macrophages, thereby limiting experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. Lack of Nr4a1 in myeloid cells led to enhanced NE production, accelerated leukocyte infiltration to the central nervous system (CNS) and disease exacerbation in vivo. In contrast, myeloid-specific deletion of tyrosine hydroxylase (TH), the rate-limiting enzyme in catecholamine biosynthesis, protected against EAE. Further, we found that Nr4a1 repressed autocrine NE production in macrophages by recruiting the corepressor CoREST to the Th promoter. Our data reveal a new role for macrophages in neuroinflammation and identify Nr4a1 as a key regulator of macrophage catecholamine production.

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Repeated Immobilization Stress Increases Nur77 Expression in the Bed Nucleus of the Stria Terminalis

Cited by 10 publications

References 84 publications

Nur transcription factors in stress and addiction

Nur transcription factors in stress and addiction

Differential Properties of Transcriptional Complexes Formed by the CoREST Family

Transcription factor Nr4a1 couples sympathetic and inflammatory cues in CNS-recruited macrophages to limit neuroinflammation

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