Pathogens and autophagy: subverting to survive

Colombo, María Isabel

doi:10.1038/sj.cdd.4401767

Cited by 33 publications

(24 citation statements)

References 23 publications

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“…Autophagy may be an intracellular host defensive mechanism against viruses, or it can be used by viruses for their own benefit of efficient replication (Colombo, 2005). We examined the effect of autophagy on Ad replication.…”

Section: Resultsmentioning

confidence: 99%

Adenoviruses induce autophagy to promote virus replication and oncolysis

et al. 2011

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Adenoviruses with deletion of E1b have been used in clinical trials to treat cancers that are resistant to conventional therapies. The efficacy of viral replication within cancer cells determines the results of oncolytic therapy, which remains poorly understood and requires further improvement. In this report, we show that adenoviruses induce autophagy by increasing the conversion of LC3-I to LC3-II and the formation of the Atg12-Atg5 complex. Inhibition of autophagy with 3-methyladenine (3MA) resulted in a decreased synthesis of adenovirus structural proteins, and thereby a poor viral replication; promotion of autophagy with rapamycin increased adenovirus yield. This study indicates that adenovirus-induced autophagy correlates positively with virus replication and oncolytic cell death, and that autophagy may generate nutrients that can be used for building viral progeny particles. These results further suggest that chemotherapeutic agents that increase cancer cell autophagy may improve the efficacy of oncolytic virotherapy.

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Section: Resultsmentioning

confidence: 99%

Adenoviruses induce autophagy to promote virus replication and oncolysis

et al. 2011

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“…Autophagy also degrades damaged organelles (e.g. mitochondria), as well as intracellular bacteria and viruses [20,21], and it is implicated in longevity during situations of caloric restriction [22]. Furthermore, autophagy is also involved in eliminating protein aggregates that often appear in a variety of neurodegenerative diseases [12].…”

Section: Autophagy As a Cytoprotective Mechanismmentioning

confidence: 99%

How autophagy is related to programmed cell death during the development of the nervous system

Boya

Mellén

Rosa

2008

Biochemical Society Transactions

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Programmed cell death, together with proliferation and differentiation, is an essential process during the development of the nervous system. During neurogenesis, neurons and glia are generated in large numbers and, subsequently, they die in a process that depends on trophic signalling that refines the cytoarchitecture and connectivity of the nervous system. In addition, programmed cell death also affects proliferating neuroepithelial cells and recently differentiated neuroblasts. Autophagy is a lysosomal degradative pathway that allows the recycling of cell constituents, and seems to be able to play a dual role. It may serve to protect the cell by preventing the accumulation of deleterious products and organelles and supplying energy and amino acids. On the other hand, it has been considered a type of cell death. The role of autophagy during development is little characterized. The retina provides an excellent model system to study autophagy in the context of neural development, and to establish its relationship with proliferation, differentiation and cell death. In the present review, we summarize recent findings showing that autophagy contributes to the development of the nervous system by providing energy for cell corpse removal after physiological cell death, a process associated with retinal neurogenesis.

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“…In addition to enhanced autophagy during starvation, basal levels of autophagy are also important for intracellular quality control of superfluous and damaged proteins and organelles (Komatsu et al, 2007a). Besides these fundamental roles, autophagy is thought to be involved in the degradation of intracellular bacteria, antigen presentation, tumour suppression, cell death and differentiation (Colombo, 2005;Lunemann and Munz, 2008;Maiuri et al, 2008;Orvedahl and Levine, 2008;Scarlatti et al, 2008). Therefore, it is not surprising that alterations in autophagy have been associated with different human pathological conditions (Kundu and Thompson, 2008;Levine and Kroemer, 2008;Mizushima et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Desmethylclomipramine induces the accumulation of autophagy markers by blocking autophagic flux

Rossi

Munarriz

Bartesaghi

et al. 2009

Journal of Cell Science

112

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Alterations in the autophagic pathway are associated with the onset and progression of various diseases. However, despite the therapeutic potential for pharmacological modulators of autophagic flux, few such compounds have been characterised. Here we show that clomipramine, an FDA-approved drug long used for the treatment of psychiatric disorders, and its active metabolite desmethylclomipramine (DCMI) interfere with autophagic flux. Treating cells with DCMI caused a significant and specific increase in autophagosomal markers and a concomitant blockage of the degradation of autophagic cargo. This observation might be relevant in therapy in which malignant cells exploit autophagy to survive stress conditions, rendering them more susceptible to the action of cytotoxic agents. In accordance, DCMI-mediated obstruction of autophagic flux increased the cytotoxic effect of chemotherapeutic agents. Collectively, our studies describe a new function of DCMI that can be exploited for the treatment of pathological conditions in which manipulation of autophagic flux is thought to be beneficial.

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Pathogens and autophagy: subverting to survive

Cited by 33 publications

References 23 publications

Adenoviruses induce autophagy to promote virus replication and oncolysis

Adenoviruses induce autophagy to promote virus replication and oncolysis

How autophagy is related to programmed cell death during the development of the nervous system

Desmethylclomipramine induces the accumulation of autophagy markers by blocking autophagic flux

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