Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2067934 | Cell Biology International | 2007 | 9 Pages |
Abstract
Angiogenesis, the formation of new blood vessels that is regulated by hypoxia, is a critical process for the growth and spread of tumors. Multiple phases of this process, including migration, adhesion, and formation of new capillary tubes, are needed for optimal tumor growth. Here, a new regulatory function for Ca2+-CaM in the vascular endothelium is described. Ca2+-CaM activation induced by hypoxia in endothelial cells is essential for angiogenic cellular responses. Inhibition of Ca2+-CaM activity suppressed endothelial cell migration, adhesion on collagen I substrate, invasion and impaired in vitro endothelial cell differentiation into tube-like structures. We also reported that CaM is co-distributed with the actin structures in the lamellipodia in migrating cells, whereas the actin cytoskeleton rearrangement induced by hypoxia was disrupted and HIF-1 transcriptional activity was decreased when treated with CaM antagonists into cultures. These data indicate that Ca2+-CaM activation is more closely associated with the regulation of angiogenic key events, especially in response to hypoxic stress.
Keywords
PBSDMEMTFPLamellipodiaHREHIFBSADulbecco's modified Eagle's mediumbovine serum albuminAngiogenesisactinTrifluoperazineCAMhypoxia inducible factor-1hypoxia response elementVascular endothelial growth factorVascular Endothelial Growth Factor (VEGF)Hypoxia Inducible Factorphosphate buffer salineHypoxiaCalmodulin
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Authors
Wei-Gan Shen, Wan-Xin Peng, Gu Dai, Jian-Feng Xu, Yu Zhang, Chao-Jun Li,