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| Content Provider | PubMed Central |
|---|---|
| Author | Chen, Yiliang Kennedy, David J. Ramakrishnan, Devi Prasadh Yang, Moua Huang, Wenxin Li, Zhichuan Xie, Zijian Chadwick, Alexandra C. Sahoo, Daisy Silverstein, Roy L. |
| Abstract | One characteristic of atherosclerosis is the accumulation of lipid-laden macrophage foam cells in the arterial wall. We have previously shown that the binding of oxidized LDL (oxLDL) to the scavenger receptor CD36 activates the kinase Lyn, initiating a cascade that inhibits macrophage migration and is necessary for foam cell generation. Here, we identified the plasma membrane ion transporter Na/K-ATPase as a key component in the macrophage oxLDL-CD36 signaling axis. Using peritoneal macrophages isolated from Atp1a1 heterozygous or Cd36 null mice, we demonstrated that CD36 recruited a Na/K-ATPase-Lyn complex for Lyn activation in response to oxLDL. Macrophages deficient in the α1 Na/K-ATPase catalytic subunit did not respond to activation of CD36, showing attenuated oxLDL uptake and foam cell formation, and oxLDL failed to inhibit migration of these macrophages. Furthermore, Apoe-null mice, which are a model of atherosclerosis, were protected from diet-induced atherosclerosis by global deletion of a single allele encoding the α1 Na+/K+-ATPase subunit or reconstitution with macrophages that lacked an allele encoding the α1 Na+/K+-ATPase subunit.. These findings identify Na/K-ATPase as a potential target for preventing or treating anti-atherosclerotic therapy. |
| Related Links | http://dx.doi.org/10.1126/scisignal.aaa9623 |
| Starting Page | 91 |
| File Format | |
| ISSN | 19450877 |
| e-ISSN | 19379145 |
| Journal | Science signaling |
| Issue Number | 393 |
| Volume Number | 8 |
| Language | English |
| Publisher Date | 2015-09-08 |
| Access Restriction | Open |
| Subject Keyword | Medicine(all) Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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