Lung autophagic response following exposure of mice to whole body irradiation, with and without amifostine

Zois, Christos E.; Giatromanolaki, Alexandra; Kainulainen, Heikki; Botaitis, Sotirios; Torvinen, Sira; Simopoulos, Constantinos; Kortsaris, Alexandros; Sivridis, Efthimios; Koukourakis, Michael I.

doi:10.1016/j.bbrc.2010.12.024

Cited by 9 publications

(9 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Also, in the lung tissue the LC3A-II in the pellet clearly increased at 24 h and 48 h after starvation. 6 We conclude that the endogenous levels of LC3A follow the pattern described in the literature, whereas we were unable to detect the same pattern for LC3B. Furthermore, it is reported that starvation conditions triggers autophagy in liver, pancreas, kidney skeletal muscle and heart in adult mice.…”

supporting

confidence: 62%

“…2B), while there was no change of the LC3A-I protein in the supernatant fraction. 6 In the kidney tissue the LC3A-II was increased after 48 h and 72 h starvation conditions, whereas in the heart, the tissue remained unchanged ( Fig. 2C and D).…”

Section: Introductionmentioning

confidence: 94%

“…Recently, we noted that following 6 Gy of γ-irradiation, normal lung cells may suffer a severe deregulation of the autophagy machinery, and this deregulation is characterized by decreased transcription of the LC3A mRNA and accumulation of LC3A and p62, either due to defective formation of autophagosomes or to an aberrant degradation processing of the formed autophagosomes. 6 The role of this phenomenon on the radiation-induced dysfunctional autophagy is under investigation.…”

mentioning

confidence: 99%

See 2 more Smart Citations

"Autophagic flux" in normal mouse tissues: Focus on endogenous LC3A processing

Zois¹,

Giatromanolaki²,

Sivridis³

et al. 2011

Autophagy

Self Cite

View full text Add to dashboard Cite

A utophagy is a major intracellular pathway for the degradation and recycling of long-lived proteins, mature ribosomes and even entire organelles. The best-studied autophagic marker is the LC3B protein and it is thought that the amount of LC3B-II correlates with the amount of autophagic membranes. Whether LC3A processing, in addition to LC3B, is a valuable endogenous "autophagic flux'' marker is far less clear. The specificity of rabbit polyclonal antibodies to LC3A and LC3B was tested against the commercial available human recombinant proteins LC3A and LC3B. In order to measure "autophagic flux'' in mouse liver, lung, kidney and heart we used: (1) a lysosomotropic reagent, chloroquine, which inhibits intralysosomal acidification and ultimately their fusion with autophagosomes, (2) nutrient starvation as an autophagic stimulus and (3) ionizing radiation, which destabilizes lysosomes. According to the immunoblotting work, the LC3A protein follows discrete patterns of LC3A-I and LC3A-II changes in liver, lung, kidney and heart tissues of mice, whereas the LC3B protein did not follow the same pattern under stressor conditions. We conclude that the endogenous LC3A processing is a major marker of autophagy flux in the mouse model. Fractionated samples (soluble vs membrane fractions) should be used in immunoblotting to allow discrimination between the soluble LC3-I and the membrane-associated LC3-II proteins and the kinetics of modification. Furthermore, "Autophagic flux" in normal mouse tissues

show abstract

supporting

confidence: 62%

Section: Introductionmentioning

confidence: 94%

mentioning

confidence: 99%

See 1 more Smart Citation

"Autophagic flux" in normal mouse tissues: Focus on endogenous LC3A processing

Zois¹,

Giatromanolaki²,

Sivridis³

et al. 2011

Autophagy

Self Cite

View full text Add to dashboard Cite

show abstract

“…15,16 Conversely, blockade of this pathway can sensitize cells to IR. In this study we demonstrate a novel cytoprotective role of autophagy as a physiological response to IR and demonstrate that deficiency in CD47 increases the expression and function of autophagy associated genes as a protective mechanism from death induced by radiation exposure in cells and in mice.…”

Section: Cd47 Deficiency Confers Cell and Tissue Radioprotection By Amentioning

confidence: 99%

“…1 Lung tissue is very sensitive to therapeutic doses of IR, and the autophagic process is regulated in this tissue after IR exposure. 14,15 To determine if protection from apoptosis by CD47 blockade correlates with increased autophagy in vivo, mice were treated IP with CD47 morpholino in saline or saline alone and exposed to total body IR (TBI). As demonstrated in Figure 9A and B, lung tissue harvested after 24 h from control mice exposed to TBI showed a 5-fold increase in apoptotic nuclei as measured by TUNEL staining.…”

Section: Cd47mentioning

confidence: 99%

CD47 deficiency confers cell and tissue radioprotection by activation of autophagy

et al. 2012

View full text Add to dashboard Cite

Oxidative stress-induced autophagy: Role in pulmonary toxicity

Malaviya

Laskin

2014

Toxicology and Applied Pharmacology

View full text Add to dashboard Cite

Autophagy is an evolutionarily conserved catabolic process important in regulating the turnover of essential proteins and in elimination of damaged organelles and protein aggregates. Autophagy is observed in the lung in response to oxidative stress generated as a consequence of exposure to environmental toxicants. Whether autophagy plays role in promoting cell survival or cytotoxicity is unclear. In this article recent findings on oxidative stress-induced autophagy in the lung are reviewed; potential mechanisms initiating autophagy are also discussed. A better understanding of autophagy and its role in pulmonary toxicity may lead to the development of new strategies to treat lung injury associated with oxidative stress.

show abstract

Lung autophagic response following exposure of mice to whole body irradiation, with and without amifostine

Cited by 9 publications

References 31 publications

"Autophagic flux" in normal mouse tissues: Focus on endogenous LC3A processing

"Autophagic flux" in normal mouse tissues: Focus on endogenous LC3A processing

CD47 deficiency confers cell and tissue radioprotection by activation of autophagy

Oxidative stress-induced autophagy: Role in pulmonary toxicity

Contact Info

Product

Resources

About