Abstract:
BACKGROUND:The NR4A3 orphan nuclear hormone receptor, NOR1, functions as a constitutively active transcription factor to regulate inflammation, proliferation, and cell survival during pathological vascular remodeling. Inflammatory processes represent key mechanisms leading to abdominal aortic aneurysm (AAA) formation. However, a role of NOR1 in AAA formation has not been investigated previously. METHODS:Inflammatory gene expression was analyzed in bone marrow-derived macrophages isolated from NOR1-deficient mice. Low-density lipoprotein receptor-deficient (LDLr-/-) mice were irradiated and reconstituted with hematopoietic stem cells obtained from NOR1-/- or wild-type littermate mice. Animals were infused with angiotensin II and fed a diet enriched in saturated fat to induce AAA formation. Quantification of AAA formation was performed by ultrasound and ex vivo measurements. RESULTS:Among 184 inflammatory genes that were analyzed, 36 genes were differentially regulated in LPS-treated NOR1-deficient macrophages. Albeit this difference in gene regulation, NOR1-deficiency in hematopoietic stem cells did not affect development of AAA formation in bone marrow-derived stem cell transplanted LDLr-deficient mice. CONCLUSION:NOR1 deletion induced differential inflammatory gene transcription in macrophages but did not influence AAA formation in mice.
journal_name
BMC Cardiovasc Disordjournal_title
BMC cardiovascular disordersauthors
Qing H,Jones KL,Heywood EB,Lu H,Daugherty A,Bruemmer Ddoi
10.1186/s12872-017-0701-4subject
Has Abstractpub_date
2017-10-18 00:00:00pages
271issue
1issn
1471-2261pii
10.1186/s12872-017-0701-4journal_volume
17pub_type
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pub_type: 杂志文章,meta分析
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pub_type: 杂志文章,meta分析
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pub_type: 杂志文章,多中心研究
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更新日期:2013-07-05 00:00:00
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pub_type: 杂志文章
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