TY - JOUR
T1 - NEU3 sialidase is activated under hypoxia and protects skeletal muscle cells from apoptosis through the activation of the epidermal growth factor receptor signaling pathway and the hypoxia-inducible factor (HIF)-1α
AU - Scaringi, Raffaella
AU - Piccoli, Marco
AU - Papini, Nadia
AU - Cirillo, Federica
AU - Conforti, Erika
AU - Bergante, Sonia
AU - Tringali, Cristina
AU - Garatti, Andrea
AU - Gelfi, Cecilia
AU - Venerando, Bruno
AU - Menicanti, Lorenzo
AU - Tettamanti, Guido
AU - Anastasia, Luigi
PY - 2013/2/1
Y1 - 2013/2/1
N2 - NEU3 sialidase, a key enzyme in ganglioside metabolism, is activated under hypoxic conditions in cultured skeletal muscle cells (C2C12). NEU3 up-regulation stimulates the EGF receptor signaling pathway, which in turn activates the hypoxia-inducible factor (HIF-1α), resulting in a final increase of cell survival and proliferation. In the same cells, stable overexpression of sialidase NEU3 significantly enhances cell resistance to hypoxia, whereas stable silencing of the enzyme renders cells more susceptible to apoptosis. These data support the working hypothesis of a physiological role played by NEU3 sialidase in protecting cells from hypoxic stress and may suggest new directions in the development of therapeutic strategies against ischemic diseases, particularly of the cerebro-cardiovascular system.
AB - NEU3 sialidase, a key enzyme in ganglioside metabolism, is activated under hypoxic conditions in cultured skeletal muscle cells (C2C12). NEU3 up-regulation stimulates the EGF receptor signaling pathway, which in turn activates the hypoxia-inducible factor (HIF-1α), resulting in a final increase of cell survival and proliferation. In the same cells, stable overexpression of sialidase NEU3 significantly enhances cell resistance to hypoxia, whereas stable silencing of the enzyme renders cells more susceptible to apoptosis. These data support the working hypothesis of a physiological role played by NEU3 sialidase in protecting cells from hypoxic stress and may suggest new directions in the development of therapeutic strategies against ischemic diseases, particularly of the cerebro-cardiovascular system.
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U2 - 10.1074/jbc.M112.404327
DO - 10.1074/jbc.M112.404327
M3 - Article
C2 - 23209287
AN - SCOPUS:84873305472
VL - 288
SP - 3153
EP - 3162
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
SN - 0021-9258
IS - 5
ER -