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Corticosteroid resistance in sepsis is influenced by microRNA-124-induced downregulation of glucocorticoid receptor-α*

Acquired glucocorticoid resistance frequently complicates the therapy of sepsis. It leads to an exaggerated proinflammatory response and has been related to altered expression profiles of glucocorticoid receptor isoforms glucocorticoid receptor-α (mediating anti-inflammatory effects) and glucocortic...

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Bibliographic Details
Main Author: Ledderose, Carola (Author)
Format: Article (Journal)
Language:English
Published: 2012/10/01
In: Critical care medicine
Year: 2012, Volume: 40, Issue: 10, Pages: 2745-2753
ISSN:1530-0293
DOI:10.1097/CCM.0b013e31825b8ebc
Online Access:Verlag, Volltext: http://dx.doi.org/10.1097/CCM.0b013e31825b8ebc
Verlag, Volltext: https://journals.lww.com/ccmjournal/Abstract/2012/10000/Corticosteroid_resistance_in_sepsis_is_influenced.1.aspx
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Author Notes:Carola Ledderose, Patrick Möhnle, Elisabeth Limbeck, Stefanie Schütz, Florian Weis, Jessica Rink, Josef Briegel, Simone Kreth
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Summary:Acquired glucocorticoid resistance frequently complicates the therapy of sepsis. It leads to an exaggerated proinflammatory response and has been related to altered expression profiles of glucocorticoid receptor isoforms glucocorticoid receptor-α (mediating anti-inflammatory effects) and glucocorticoid receptor-β (acting as a dominant negative inhibitor). We investigated the impact of glucocorticoid receptor isoforms on glucocorticoid effects in human T-cells. We hypothesized that 1) changes of the ratio of glucocorticoid receptor isoforms impact glucocorticoid resistance and 2) glucocorticoid receptor-α expression is controlled by microRNA-mediated gene silencing.
Item Description:Gesehen am 04.06.2018
Physical Description:Online Resource
ISSN:1530-0293
DOI:10.1097/CCM.0b013e31825b8ebc

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