NEU3 Sialidase Strictly Modulates GM3 Levels in Skeletal Myoblasts C2C12 Thus Favoring Their Differentiation and Protecting Them from Apoptosis

被引：43

作者：

Anastasia, Luigi ^{[1
,2
]}

Papini, Nadia ^{[1
,2
]}

Colazzo, Francesca ^{[1
,2
]}

Palazzolo, Giacomo ^{[1
,2
]}

Tringali, Cristina ^{[1
]}

Dileo, Loredana ^{[1
,2
]}

Piccoli, Marco ^{[1
,2
]}

Conforti, Erika ^{[1
,2
]}

Sitzia, Clementina ^{[1
,2
]}

Monti, Eugenio ^{[3
]}

Sampaolesi, Maurilio ^{[4
,5
]}

Tettamanti, Guido ^{[2
]}

Venerando, Bruno ^{[1
,2
]}

机构：

[1] Univ Milan, Dept Med Chem Biochem & Biotechnol, I-20090 Milan, Italy

[2] IRCCS, Policlin San Donato, Lab Stem Cells Tissue Engn, I-20097 San Donato Milanese, Italy

[3] Univ Brescia, Dept Biomed & Biotechnol Sci, I-25123 Brescia, Italy

[4] Univ Hosp Gasthuisberg, Stem Cell Res Inst, B-3000 Louvain, Belgium

[5] Univ Pavia, Dept Expt Med, I-27100 Pavia, Italy

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 2008年 / 283卷 / 52期

关键词：

D O I：

10.1074/jbc.M805755200

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Membrane-bound sialidase NEU3, often referred to as the "ganglioside sialidase," has a critical regulatory function on the sialoglycosphingolipid pattern of the cell membrane, with an anti-apoptotic function, especially in cancer cells. Although other sialidases have been shown to be involved in skeletal muscle differentiation, the role of NEU3 had yet to be disclosed. Herein we report that NEU3 plays a key role in skeletal muscle differentiation by strictly modulating the ganglioside content of adjacent cells, with special regard to GM3. Induced down-regulation of NEU3 in murine C2C12 myoblasts, even when partial, totally inhibits their capability to differentiate by increasing the GM3 level above a critical point, which causes epidermal growth factor receptor inhibition (and ultimately its down-regulation) and an higher responsiveness of myoblasts to the apoptotic stimuli.

引用

页码：36265 / 36271

页数：7

共 42 条

[1]

BARONDES SH, 1994, J BIOL CHEM, V269, P20807

[2] MyoD and the transcriptional control of myogenesis [J].