| First Author | Qing H | Year | 2017 |
| Journal | BMC Cardiovasc Disord | Volume | 17 |
| Issue | 1 | Pages | 271 |
| PubMed ID | 29047330 | Mgi Jnum | J:271770 |
| Mgi Id | MGI:6282164 | Doi | 10.1186/s12872-017-0701-4 |
| Citation | Qing H, et al. (2017) Deletion of the NR4A nuclear receptor NOR1 in hematopoietic stem cells reduces inflammation but not abdominal aortic aneurysm formation. BMC Cardiovasc Disord 17(1):271 |
| abstractText | 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. |
