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Knock down of caveolin‐1 affects morphological and functional hallmarks of human endothelial cells
Author(s) -
Madaro Luca,
Antonangeli Fabrizio,
Favia Annarita,
Esposito Bianca,
Biamonte Filippo,
Bouché Marina,
Ziparo Elio,
Sica Gigliola,
Filippini Antonio,
D'Alessio Alessio
Publication year - 2013
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.24526
Subject(s) - microbiology and biotechnology , biology , angiogenesis , caveolae , caveolin 1 , carcinogenesis , cell , matrix metalloproteinase , gene silencing , downregulation and upregulation , senescence , signal transduction , chemistry , cancer research , genetics , cancer , gene
Caveolin‐1 (CAV1) is the principal structural component of caveolae which functions as scaffolding protein for the integration of a variety of signaling pathways. In this study, we investigated the involvement of CAV1 in endothelial cell (EC) functions and show that siRNA‐induced CAV1 silencing in the human EC line EA.hy926 induces distinctive morphological changes, such as a marked increase in cell size and formation of stress fibers. Design‐based stereology was employed in this work to make unbiased quantification of morphometric properties such as volume, length, and surface of CAV1 silenced versus control cells. In addition, we showed that downregulation of CAV1 affects cell cycle progression at G1/S phase transition most likely by perturbation of AKT signaling. With the aim to assess the contribution of CAV1 to typical biological processes of EC, we report here that CAV1 targeting affects cell migration and matrix metalloproteinases (MMPs) activity, and reduces angiogenesis in response to VEGF, in vitro. Taken together our data suggest that the proper expression of CAV1 is important not only for maintaining the appropriate morphology and size of ECs but it might represent a prospective molecular target for studying key biological mechanisms such as senescence and tumorigenesis. J. Cell. Biochem. 114: 1843–1851, 2013. © 2013 Wiley Periodicals, Inc.