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Calmodulin is essential for angiogenesis in response to hypoxic stress in endothelial cells
Author(s) -
Shen WeiGan,
Peng WanXin,
Dai Gu,
Xu JianFeng,
Zhang Yu,
Li ChaoJun
Publication year - 2007
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2006.09.017
Subject(s) - microbiology and biotechnology , angiogenesis , lamellipodium , endothelial stem cell , hypoxia (environmental) , biology , actin cytoskeleton , endothelium , cytoskeleton , chemistry , in vitro , cell , biochemistry , cancer research , endocrinology , organic chemistry , oxygen
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 Ca 2+ –CaM in the vascular endothelium is described. Ca 2+ –CaM activation induced by hypoxia in endothelial cells is essential for angiogenic cellular responses. Inhibition of Ca 2+ –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 Ca 2+ –CaM activation is more closely associated with the regulation of angiogenic key events, especially in response to hypoxic stress.