| First Author | Park SL | Year | 2017 |
| Journal | Sci Rep | Volume | 7 |
| Pages | 44687 | PubMed ID | 28317868 |
| Mgi Jnum | J:275325 | Mgi Id | MGI:6296546 |
| Doi | 10.1038/srep44687 | Citation | Park SL, et al. (2017) HSP70-1 is required for interleukin-5-induced angiogenic responses through eNOS pathway. Sci Rep 7:44687 |
| abstractText | We report a pivotal role for IL-5 as an angiogenic activator. IL-5 increased proliferation, migration and colony tube formation in HUVECs associated with the phosphorylation of ERK and AKT/eNOS, and promoted microvessel sprouting from an angiogenesis animal model. The angiogenic effects were confirmed in IL-5-deficient mice and addition of IL-5 antibody. HSP70-1 was identified via expression profiling following IL-5 stimulation. A siRNA knockdown of HSP70-1 suppressed angiogenic responses and eNOS phosphorylation induced by IL-5. HSP70-1 overexpression enhanced IL-5-induced angiogenic responses. In addition, IL-5-induced neo-vascular formation was verified in both HSP70-1 knockout and HSP70-1 transgenic mice. Furthermore, transcription factor AP-1 was a main factor in IL-5-induced HSP70-1 in response to ERK and AKT signaling pathway. Angiogenic responses induced by VEGF had no effect in either HSP70-1 siRNA in vitro or HSP70-1 knockout mice. IL-5-induced angiogenic responses depended on the binding of IL-5Ralpha. Our data demonstrate that binding of IL-5 to IL-5Ralpha receptors enhances angiogenic responses by stimulating the expression of HSP70-1 via the eNOS signaling pathway. |
