Glucocorticoids exacerbate hypoxia-induced expression of the pro-apoptotic gene Bnip3 in the developing cortex.

Glucocorticoids exacerbate hypoxia-induced expression of the pro-apoptotic gene Bnip3 in the developing cortex. Research Abstract Details 

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Glucocorticoids exacerbate hypoxia-induced expression of the pro-apoptotic gene Bnip3 in the developing cortex. Abstract Text:

U S Sandau,R J Handa,

Neonatal administration of the synthetic glucocorticoid, dexamethasone (DEX) retards brain growth, alters adult behaviors and induces cell death in the rat brain, thereby implicating glucocorticoids as developmentally neuroendangering compounds. Glucocorticoids also increase expression of pro-apoptotic Bcl-2 family members and exacerbate expression of hypoxic responsive genes. Bnip3 is a pro-apoptotic Bcl-2 family member that is upregulated in response to hypoxia. In these studies, we investigated the interactions of glucocorticoid receptor and hypoxia in the regulation of Bnip3 mRNA in cortical neurons. Using quantitative real time reverse transcription-polymerase chain reaction, we found that DEX treatment of postnatal days 4-6 rat pups caused a significant increase in Bnip3 mRNA expression compared with vehicle controls. A significant increase in Bnip3 mRNA was also measured in primary cortical neurons 72 h after treatment with RU28362, a glucocorticoid receptor selective agonist. In primary cortical neurons, hypoxia increased Bnip3 mRNA expression and this was exacerbated with RU28362 treatment. To elucidate the mechanism of glucocorticoid- and hypoxia-mediated regulation of Bnip3 transcription, a Bnip3 promoter-luciferase reporter construct was utilized in primary cortical neurons. Upregulation of the Bnip3 promoter was mediated by a single glucocorticoid response element and a hypoxic response element. Bnip3 overexpression in primary cortical neurons significantly increased cell death, which is dependent on the Bnip3 transmembrane domain. However, despite the increased expression of Bnip3 following glucocorticoid and hypoxia treatment, corresponding decreases in cell survival were minimal. These studies identify a novel pathway in the developing cortex through which glucocorticoids may enhance a metabolic insult, such as hypoxia.

Glucocorticoids exacerbate hypoxia-induced expression of the pro-apoptotic gene Bnip3 in the developing cortex. Publishing Authors By Initials

US Sandau,RJ Handa,

For similar investigative techniques: genetic techniques: gene transfer techniques: transfection research abstracts see: investigative techniques: genetic techniques: gene transfer techniques: transfection research

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Glucocorticoids exacerbate hypoxia-induced expression of the pro-apoptotic gene Bnip3 in the developing cortex. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Neuroscience

VOLUME: 144

Page Numbers: 482-94

Journal Abbreviation: Neuroscience

ISSN: 0306-4522

DAY: 15

MONTH: 11

YEAR: 2006

Glucocorticoids exacerbate hypoxia-induced expression of the pro-apoptotic gene Bnip3 in the developing cortex. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 7605074

Glucocorticoids exacerbate hypoxia-induced expression of the pro-apoptotic gene Bnip3 in the developing cortex. Keywords Mesh Terms:

KEYWORDS: Transfection

MESH TERMS: methods

Chemical & Substance for Abstract: Glucocorticoids exacerbate hypoxia-induced expression of the pro-apoptotic gene Bnip3 in the developing cortex. Information

Substance Name: lactate dehydratase

Registry Number: EC 4.2.1.54

Grant and Affiliation Information for Glucocorticoids exacerbate hypoxia-induced expression of the pro-apoptotic gene Bnip3 in the developing cortex.

AFFILIATION: Department of Biomedical Sciences, Colorado State University, Fort Collins, CO 80523-1617, USA.

Country: United States

AGENCY: United States NINDS

GRANT: R01-NS039951

ACRONYM: NS

MEDLINETA: Neuroscience

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