L’autophagie et le dernier soupir de la cellule

Pattingre, Sophie; Codogno, Patrice

doi:10.1051/medsci/20072389696

Cited by 2 publications

(1 citation statement)

References 16 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…L'induction permet la mise en place d'une structure membranaire dite pré-autophagosomale. Elle est sous la dépendance de la GTPase IRGM (immunity-related GTPase family, M) et de deux complexes protéiques, un premier qui fait intervenir la protéine mTor (mammalian target of rapamycin) et un second associant la protéine adaptatrice Beclin 1 [14] avec une PI3-kinase de classe III. L'élon-gation de cette structure conduit à la formation d'une membrane d'isolement, appelée phagophore, qui piège une portion de cytoplasme et capture les élé-ments à ingérer.…”

unclassified

Altération de l’autophagie chez les patients atteints de maladie de Crohn

Glasser¹,

Lapaquette²,

Darfeuille‐Michaud³

2009

Med Sci (Paris)

View full text Add to dashboard Cite

unclassified

Altération de l’autophagie chez les patients atteints de maladie de Crohn

Glasser¹,

Lapaquette²,

Darfeuille‐Michaud³

2009

Med Sci (Paris)

View full text Add to dashboard Cite

1-Methyl-4-Phenylpyridinium-Induced Cell Death via Autophagy Through a Bcl-2/Beclin 1 Complex-Dependent Pathway

et al. 2013

View full text Add to dashboard Cite

Several lines of evidence suggest that the mechanism underlying drug-induced neuronal apoptosis is initiated by the increased production of reactive oxygen species (ROS). 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a neurotoxin, has been shown to initiate an apoptotic cascade by increasing ROS in the dopaminergic neurons of the substantia nigra, leading to the morphological and physiological features associated with Parkinson's disease. Recently, it has been reported that autophagy, a type of programmed cell death independent of the apoptotic cascade, also plays a role in neuronal damage. Although autophagy is negatively regulated by the mammalian target of rapamycin receptor (mTOR), there is some evidence showing a novel function for the anti-apoptotic protein Bcl-2. Bcl-2 is proposed to play a role in negatively regulating autophagy by blocking an essential protein in the signaling pathway, Beclin 1. Nevertheless, it is unclear whether autophagy is also correlated with apoptotic signaling in 1-methyl-4-phenylpyridinium (MPP(+)) toxicity. Therefore, we hypothesized that the MPP(+) toxicity generally associated with initiating the apoptotic signaling cascade also increases an autophagic phenotype in neuronal cells. Using the SK-N-SH dopaminergic cell lines, we demonstrate that MPP(+) increases the expression of microtubule-associated protein light chain 3 (LC3-II), an autophagosome membrane marker and the mTOR signaling pathway, and Beclin 1 while decreasing the Bcl-2 levels. Moreover, these expressions correlate with a decreased binding ratio between Bcl-2 and Beclin 1, in effect limiting the regulation of the downstream autophagic markers, such as LC3-II. Our results indicate that MPP(+) can induce autophagy in SK-N-SH cells by decreasing the Bcl-2/Beclin 1 complex.

show abstract

L’autophagie et le dernier soupir de la cellule

Cited by 2 publications

References 16 publications

Altération de l’autophagie chez les patients atteints de maladie de Crohn

Altération de l’autophagie chez les patients atteints de maladie de Crohn

1-Methyl-4-Phenylpyridinium-Induced Cell Death via Autophagy Through a Bcl-2/Beclin 1 Complex-Dependent Pathway

Contact Info

Product

Resources

About