Abstract:
:Aortic dissection and intramural haematoma comprise an aortopathy involving separation of the aortic wall. Underlying mechanisms of the condition remain unclear. Here we show that granulocyte macrophage colony-stimulating factor (GM-CSF) is a triggering molecule for this condition. Transcription factor Krüppel-like factor 6 (KLF6)-myeloid-specific conditional deficient mice exhibit this aortic phenotype when subjected to aortic inflammation. Mechanistically, KLF6 downregulates expression and secretion of GM-CSF. Administration of neutralizing antibody against GM-CSF prevents the condition in these mice. Conversely, administration of GM-CSF in combination with aortic inflammation to wild-type mice is sufficient to induce the phenotype, suggesting the general nature of effects. Moreover, patients with this condition show highly increased circulating levels of GM-CSF, which is also locally expressed in the dissected aorta. GM-CSF is therefore a key regulatory molecule causative of this aortopathy, and modulation of this cytokine might be an exploitable treatment strategy for the condition.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Son BK,Sawaki D,Tomida S,Fujita D,Aizawa K,Aoki H,Akishita M,Manabe I,Komuro I,Friedman SL,Nagai R,Suzuki Tdoi
10.1038/ncomms7994subject
Has Abstractpub_date
2015-04-29 00:00:00pages
6994issn
2041-1723pii
ncomms7994journal_volume
6pub_type
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