BROWSE

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Author

Kwon, H. Moo
Inflammation and Kidney Disorder Lab
Research Interests
  • TonEBP, Obesity, Cancer, Chronic inflammatory diseases, Brain disorder, Kidney disorders, Genomic instability

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NFAT5 expression in bone marrow-derived cells enhances atherosclerosis and drives macrophage migration

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Title
NFAT5 expression in bone marrow-derived cells enhances atherosclerosis and drives macrophage migration
Author
Halterman, Julia A.Kwon, H. MooLeitinger, NorbertWamhoff, Brian R.
Keywords
Atherosclerosis; Bone marrow; Macrophage; Migration; Tonebp
Issue Date
201208
Publisher
FRONTIERS
Citation
FRONTIERS IN PHYSIOLOGY, v.3, no., pp. -
Abstract
Objective: We have previously shown that the transcription factor, nuclear factor of activated T-cells 5 (NFAT5), regulates vascular smooth muscle cell phenotypic modulation, but the role of NFAT5 in atherosclerosis is unknown. Our main objective was to determine if NFAT5 expression in bone marrow (BM)-derived cells altered atherosclerotic development and macrophage function. Methods and Results: NFAT5+/-ApoE-/- mice were generated for in vivo atherosclerosis studies. Following high fat diet feeding, en face analysis of the thoracic aorta established that genome-wide NFAT5 haploinsufficiency reduced atherosclerotic lesion formation by 73%. BM transplant studies revealed that transplantation of NFAT5+/-ApoE-/- marrow into NFAT5+/+ApoE-/- mice resulted in a similar 86% reduction in lesion formation. In vitro functional analysis of BM-derived macrophages demonstrated that NFAT5 is required for macrophage migration, which is a key event in the propagation of atherosclerosis. Conclusion: We have identified NFAT5 in BM-derived cells as a positive regulator of atherosclerotic lesion formation and macrophage function in the vasculature.
URI
http://scholarworks.unist.ac.kr/handle/201301/2545
DOI
http://dx.doi.org/10.3389/fphys.2012.00313
ISSN
1664-042X
Appears in Collections:
SLS_Journal Papers
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