Suppression of Proinflammatory Cytokines Interleukin-1β and Tumor Necrosis Factor-α in Astrocytes by a V<sub>1</sub>Vasopressin Receptor Agonist: A cAMP Response Element-Binding Protein-Dependent Mechanism

Zhao, Lingjuan; Brinton, Roberta Dı́az

doi:10.1523/jneurosci.4922-03.2004

Cited by 61 publications

(42 citation statements)

References 66 publications

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“…Members of the CREB family of proteins have also been shown to bind activator protein (AP-1) target DNA sequences, thus inhibiting AP-1-mediated transcription in differentiating keratinocytes (18,37). We (49,51) and others (56) have found evidence to support a role for diminished CREB repressor activity in hypoxia-induced expression of proinflammatory genes such as TNF-␣ in intestinal epithelial cells. We have demonstrated (51) that CREB is targeted to degradation in a phosphorylation-dependent manner, leading to the induction of gene transcription.…”

Section: Discussionmentioning

confidence: 69%

“…CREB was initially described as a signal-dependent activator of genes such as somatostatin, via PKA-dependent phosphorylation of Ser133 (1,31,32). However, we (6,49,51) and others (56) have also reported that CREB may act as a repressor for genes including TNF-␣. Thus CREB plays an ambiguous role in the regulation of transcription that appears to be gene specific.…”

mentioning

confidence: 83%

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Hypoxia induces epithelial amphiregulin gene expression in a CREB-dependent manner

O’Reilly

Leonard²,

Kieran³

et al. 2006

American Journal of Physiology-Cell Physiology

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Hypoxia occurs during a number of conditions in which altered epithelial proliferation is critical, including tumor development. Microarray analysis of colon-derived epithelial cells revealed a hypoxia-dependent increase in the expression of amphiregulin, an EGF receptor (EGFR) ligand that activates epithelial proliferation and has been associated with the development of colonic tumors. Amphiregulin expression was also induced in tissues from mice exposed to whole animal hypoxia. The hypoxic upregulation of amphiregulin was independent of the classic transcriptional response mediated via hypoxia-inducible factor (HIF)-1α. Transfection of HeLa cells with truncated amphiregulin promoter reporter constructs revealed that a 37-bp segment upstream from the TATA box retained hypoxic sensitivity. This sequence contains an evolutionarily conserved cAMP response element (CRE) that constitutively binds the CRE binding protein (CREB). Deletion of the CRE abolished sensitivity to hypoxia. Thus hypoxia promotes intestinal epithelial amphiregulin expression in a CRE-dependent manner, an event that may contribute to increased proliferation. These data also further support a role for CREB as an HIF-independent hypoxia-responsive transcription factor in the regulation of intestinal epithelial gene expression.

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Section: Discussionmentioning

confidence: 69%

mentioning

confidence: 83%

Hypoxia induces epithelial amphiregulin gene expression in a CREB-dependent manner

O’Reilly

Leonard²,

Kieran³

et al. 2006

American Journal of Physiology-Cell Physiology

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“…Studies in progress reveal that VP can partially prevent nutrient deprivation-induced cell death and caspase-3 activation in rat hippocampal cell cultures containing about 95% neurons (Chen and Aguilera, unpublished). It has been shown that VP inhibits the secretion of the proinflammatory cytokines, interleukin 1β and TNF from cultured astroglia (23). Although the latter effect could contribute to protection in some conditions, the present demonstration that VP has antiapoptotic actions in a neuronal cell line, suggest that VP can excert neuroprotection directly in neuron expressing V1 receptors (24)(25)(26)(27).…”

Section: Discussionmentioning

confidence: 73%

Anti-apoptotic actions of vasopressin in H32 neurons involve map kinase transactivation and bad phosphorylation

Volpi¹,

Aguilera²

2008

Experimental Neurology

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Vasopressin (VP) secreted within the brain modulates neuronal function acting as a neurotransmitter. Based on the observation that VP prevented serum deprivation-induced cell death in the neuronal cell line, H32, which expresses endogenous V1 receptors, we tested the hypothesis that VP has antiapoptotic properties. Flow cytometry experiments showed that 10nM VP prevented serum deprivation-induced cell death and annexin V binding. Serum deprivation increased caspase-3 activity in a time and serum concentration dependent manner, and VP prevented these effects through interaction with receptors of V1 subtype. The signaling pathways mediating the anti-apoptotic effect of VP involve mitogen activated protein (MAP) kinase and extracellular signal-regulated kinases (ERK), Ca 2+ /calmodulin dependent kinase (CaMK) and protein kinase C (PKC). Western blot analyses revealed time-dependent decreases of Bad phosphorylation and increases in cytosolic levels of cytochrome c following serum deprivation, effects which were prevented by 10nM VP. These data demonstrate that activation of endogenous V1 VP receptors prevents serum deprivation-induced apoptosis, through phosphorylation-inactivation of the pro-apoptotic protein, Bad, and consequent decreases in cytosolic cytochome c and caspase-3 activation. The data suggest that VP has antiapoptotic activity in neurons and that VP may act as a neuroprotective agent in the brain.

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“…We have also shown the effects of IL-1 and HIV-1 gp120, leading to CD38 upregulation in primary astrocyte cultures (Banerjee et al, 2008) and increased CD38 mRNA and protein expression in HIVE brain (Kou et al, 2009). IL-1-activated astrocytes are known to release cytokines like IL-6 and chemokines like CCL2, CXCL8 and RANTES (Lee and Aarhus, 1993;Zhao and Brinton, 2004;Sharma et al, 2007). Our work showed that CD38 is a partial regulator of chemokine and cytokine signaling by IL-1-activated astrocytes, thus affecting the inflammatory milieu during HIVE (Kou et al, 2009).…”

Section: Neuroinflammation During Hive and Astrocytesmentioning

confidence: 65%

Astrocyte CD38: Links to Neuroinflammation in HAND

Banerjee¹,

Ghorpade²

2011

Pathogenesis of Encephalitis

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Suppression of Proinflammatory Cytokines Interleukin-1β and Tumor Necrosis Factor-α in Astrocytes by a V₁Vasopressin Receptor Agonist: A cAMP Response Element-Binding Protein-Dependent Mechanism

Cited by 61 publications

References 66 publications

Hypoxia induces epithelial amphiregulin gene expression in a CREB-dependent manner

Hypoxia induces epithelial amphiregulin gene expression in a CREB-dependent manner

Anti-apoptotic actions of vasopressin in H32 neurons involve map kinase transactivation and bad phosphorylation

Astrocyte CD38: Links to Neuroinflammation in HAND

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Suppression of Proinflammatory Cytokines Interleukin-1β and Tumor Necrosis Factor-α in Astrocytes by a V1Vasopressin Receptor Agonist: A cAMP Response Element-Binding Protein-Dependent Mechanism

Cited by 61 publications

References 66 publications

Hypoxia induces epithelial amphiregulin gene expression in a CREB-dependent manner

Hypoxia induces epithelial amphiregulin gene expression in a CREB-dependent manner

Anti-apoptotic actions of vasopressin in H32 neurons involve map kinase transactivation and bad phosphorylation

Astrocyte CD38: Links to Neuroinflammation in HAND

Contact Info

Product

Resources

About

Suppression of Proinflammatory Cytokines Interleukin-1β and Tumor Necrosis Factor-α in Astrocytes by a V₁Vasopressin Receptor Agonist: A cAMP Response Element-Binding Protein-Dependent Mechanism