Evidence for the involvement of GD3 ganglioside in autophagosome formation and maturation

Matarrese, Paola; Garofalo, Tina; Manganelli, Valeria; Gambardella, Lucrezia; Marconi, Matteo; Grasso, Maria Grazia; Tinari, Antonella; Misasi, Roberta; Malorni, Walter; Sorice, Maurizio

doi:10.4161/auto.27959

Cited by 88 publications

(102 citation statements)

References 55 publications

(64 reference statements)

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“…For instance, a paradigmatic component of lipid rafts, GD3 ganglioside, plays a positive role in autophagosome formation. 25 In addition, another component of lipid rafts, ceramides, has also been implicated in autophagy induction via blockage of AKT activation, upregulation of BECN1 or suppression of nutrient transporter expression. 24,26,44 Notably, these studies do not provide the direct evidence to show whether the function of those lipids in autophagy regulation is lipid rafts dependent and whether CAV1 is involved in the regulation of these lipids.…”

Section: Discussionmentioning

confidence: 99%

“…23 In contrast, there is conflicting evidence indicating that some components of lipid rafts, such as ceramides and GD3 ganglioside, play a positive role in autophagy regulation. [24][25][26] In this study, we aimed to evaluate the involvement of CAV1 in autophagy. Our data clearly A c c e p t e d M a n u s c r i p t 6 demonstrate that deficiency of CAV1 promotes autophagy and lysosomal function via the disruption of lipid rafts, independent of caveolae.…”

Section: Introductionmentioning

confidence: 99%

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Critical role of CAV1/caveolin-1 in cell stress responses in human breast cancer cells via modulation of lysosomal function and autophagy

et al. 2015

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CAV1 (caveolin 1, caveolae protein, 22kDa) is well known as a principal scaffolding protein of caveolae, a specialized plasma membrane structure. Relatively, the caveolae-independent function of CAV1 is less studied. Autophagy is a process known to involve various membrane structures, including autophagosomes, lysosomes, and autolysosomes for degradation of intracellular proteins and organelles. Currently, the function of CAV1 in autophagy remains largely elusive. In this study, we demonstrate for the first time that CAV1 deficiency promotes both basal and inducible autophagy. Interestingly, the promoting effect was found mainly in the late stage of autophagy via enhancing lysosomal function and autophagosome-lysosome fusion. Notably, the regulatory function of CAV1 in lysosome and autophagy was found to be caveolae-independent, and acts through lipid rafts. Furthermore, the elevated autophagy level induced by CAV1 deficiency serves as a cell survival mechanism under starvation. Importantly, downregulation of CAV1 and enhanced autophagy level were observed in human breast cancer cells and tissues. Taken together, our data reveal a novel function of CAV1 and lipid rafts in breast cancer development via modulation of lysosomal function and autophagy.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Critical role of CAV1/caveolin-1 in cell stress responses in human breast cancer cells via modulation of lysosomal function and autophagy

et al. 2015

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“…DFs, untreated or treated with Hank's solution (HBSS) for 4 hours, were stained for detection of autophagy. Cell staining was performed both in living and fixed cells by using the Cyto-ID Autophagy Detection Kit (Enzo Life Sciences, Lausanne, Switzerland) according to Matarrese et al [61]. …”

Section: Methodsmentioning

confidence: 99%

Mitochondria hyperfusion and elevated autophagic activity are key mechanisms for cellular bioenergetic preservation in centenarians

Sgarbi

Matarrese²,

Lanzarini

et al. 2014

Aging

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Mitochondria have been considered for long time as important determinants of cell aging because of their role in the production of reactive oxygen species. In this study we investigated the impact of mitochondrial metabolism and biology as determinants of successful aging in primary cultures of fibroblasts isolated from the skin of long living individuals (LLI) (about 100 years old) compared with those from young (about 27 years old) and old (about 75 years old) subjects. We observed that fibroblasts from LLI displayed significantly lower complex I-driven ATP synthesis and higher production of H2O2 in comparison with old subjects. Despite these changes, bioenergetics of these cells appeared to operate normally. This lack of functional consequences was likely due to a compensatory phenomenon at the level of mitochondria, which displayed a maintained supercomplexes organization and an increased mass. This appears to be due to a decreased mitophagy, induced by hyperfused, elongated mitochondria. The overall data indicate that longevity is characterized by a preserved bioenergetic function likely attained by a successful mitochondria remodeling that can compensate for functional defects through an increase in mass, i.e. a sort of mitochondrial “hypertrophy”.

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“…In assessing the role of lipid rafts in autophagic flux, Matarrese et al . (2014; [61]) demonstrated that the ganglioside GD3 colocalizes with LC3 in response to classic autophagic stimuli. GD3 also colocalizes with PI3P, which recruits ATG18 and other components of the core machinery [61] during the nucleation stage.…”

Section: Glycoconjugates Regulate Autophagosome Membrane Dynamicsmentioning

confidence: 99%

Molecular Functions of Glycoconjugates in Autophagy

Fahie

Zachara

2016

Journal of Molecular Biology

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Glycoconjugates, glycans, carbohydrates, and sugars: these terms encompass a class of biomolecules that are diverse in both form and function ranging from free oligosaccharides, glycoproteins and proteoglycans, to glycolipids that make up a complex glycan-code that impacts normal physiology and disease. Recent data suggests that one mechanism by which glycoconjugates impact physiology is through the regulation of the process of autophagy. Autophagy is a degradative pathway necessary for differentiation, organism development, and the maintenance of cell and tissue homeostasis. In this review, we will highlight what is known about the regulation of autophagy by glycoconjugates focusing on signaling mechanisms from the extracellular surface and the regulatory roles of intracellular glycans. Glycan signaling from the extracellular matrix converges on “master” regulators of autophagy including AMPK and mTORC1, thus impacting their localization, activity and/or expression. Within the intracellular milieu, gangliosides are constituents of the autophagosome membrane, a subset of proteins composing the autophagic machinery are regulated by glycosylation, and oligosaccharide exposure in the cytosol triggers an autophagic response. The examples discussed provide some mechanistic insights into glycan regulation of autophagy and reveals areas for future investigation.

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Evidence for the involvement of GD3 ganglioside in autophagosome formation and maturation

Cited by 88 publications

References 55 publications

Critical role of CAV1/caveolin-1 in cell stress responses in human breast cancer cells via modulation of lysosomal function and autophagy

Critical role of CAV1/caveolin-1 in cell stress responses in human breast cancer cells via modulation of lysosomal function and autophagy

Mitochondria hyperfusion and elevated autophagic activity are key mechanisms for cellular bioenergetic preservation in centenarians

Molecular Functions of Glycoconjugates in Autophagy

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