HSP70-1 is required for interleukin-5-induced angiogenic responses through eNOS pathwayopen access
- Authors
- Park, Sung Lyea; Chung, Tae-Wook; Kim, Sangtae; Hwang, Byungdoo; Kim, Jung Min; Lee, Hwan Myung; Cha, Hee-Jae; Seo, Yoonhee; Choe, Soo Young; Ha, Ki-Tae; Kim, Gonhyung; Yun, Seok-Joong; Park, Sung-Soo; Choi, Yung Hyun; Kim, Bo Kyung; Kim, Won-Tae; Cha, Eun-Jong; Patterson, Cam; Kim, Wun-Jae; Moon, Sung-Kwon
- Issue Date
- Mar-2017
- Publisher
- NATURE PUBLISHING GROUP
- Citation
- SCIENTIFIC REPORTS, v.7
- Journal Title
- SCIENTIFIC REPORTS
- Volume
- 7
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/4683
- DOI
- 10.1038/srep44687
- ISSN
- 2045-2322
- Abstract
- 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-5R alpha. Our data demonstrate that binding of IL-5 to IL-5R alpha receptors enhances angiogenic responses by stimulating the expression of HSP70-1 via the eNOS signaling pathway.
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