Cysteine-rich 61 (Cyr61) belongs to the CCN family and mediates cell proliferation, survival, and apoptosis. Our previous studies showed that Cyr61 protected against hyperoxia-induced lung cell death via Akt phosphorylation. Caveolin-1 (cav-1), a 22-kDa transmembrane scaffolding protein, is the principal structural component of caveolae. Emerging data show that cav-1 regulates signal transduction-associated proteins that reside in the caveolae. Numerous integrin-related pathways, including PI3K/Akt-induced cell survival are controlled by cav-1-mediated signaling. Our data showed that recombinant Cyr61 promoted cell proliferation and resistance to hyperoxia-induced cell death in vitro . Neutralizing antibodies reversed the above effects, indicating functional role of secreted Cyr61 in response to hyperoxic stress. While deletion of cav-1 protected cells from hyperoxia-induced cell death, Cyr61-neutralizing antibodies abolished this protective effect. Furthermore, Cyr61 and cav-1 colocalized and physically interacted via integrins in bronchial epithelial cells. Deletion of cav-1 increased extracellular and decreased cytosolic Cyr61, both in vitro and in vivo . Pretreatment with Brefeldin A increased intracellular Cyr61 in cav-1 −/− cells, while decreasing extracellular Cyr61. Taken together, Cav-1/Cyr61 interaction via integrins represents a novel pathway of Cyr61 signaling involving cav-1-dependent processes, which play a critical role in regulating hyperoxia-induced cell death.—Jin, Y., Kim, H. P., Cao, J., Zhang, M., Ifedigbo, E., Choi, A. M. K. Caveolin-1 regulates the secretion and cytoprotection of Cyr61 in hyperoxic cell death.
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Caveolin-1 regulates the secretion and cytoprotection of Cyr61 in hyperoxic cell death
Jin, Yang; Kim, Hong Pyo; Cao, Jiaofei; Zhang, Meng; Ifedigbo, Emeka; Choi, Augustine M. K.
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, Volume 23 (2): 341
Fed of American Socs for Experimental Biology – Feb 1, 2009
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