Quantification of autophagy flux using LC3 ELISA

Oh, Sung-hee; Choi, Yong bok; Kim, June Hyun; Weihl, Conrad C.; Ju, Jeong-Sun

doi:10.1016/j.ab.2017.05.003

Cited by 45 publications

(22 citation statements)

References 19 publications

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“…Global analysis of autophagy revealed no modification of P62, while the lipidated form of LC3 appeared to be decreased in controls. This could be explained by the fact that mitophagy is not only specific but also a relatively minute part of global autophagy signalling, thus mitophagic adaptations may not be evidenced by markers of global autophagy.…”

Section: Discussionmentioning

confidence: 99%

Distinct patterns of skeletal muscle mitochondria fusion, fission and mitophagy upon duration of exercise training

et al. 2018

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This study describes distinct patterns of molecular adaptations in human skeletal muscle under chronic exercise training. After 16 weeks of exercise, the pattern was dominated by fusion to increase mitochondrial content to the metabolic demands of exercise. In lifelong exercise, the pattern was dominated by mitophagy synchronized with increased fusion and decreased fission, indicating an increased mitochondrial turnover. In addition to these temporally distinct adaptive mechanisms, this study suggests for the first time a specific role of BCL2L13 in chronic exercise that requires constant maintenance of mitochondrial quality.

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Section: Discussionmentioning

confidence: 99%

Distinct patterns of skeletal muscle mitochondria fusion, fission and mitophagy upon duration of exercise training

et al. 2018

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“…The information obtained by using the fluorescence experimental techniques were supported and confirmed by a high sensitive, immuno-enzymatic investigation based on ELISA method [ 24 ]. The obtained data clearly indicate that the percentage of autophagic related proteins was positively correlated with incubation time.…”

Section: Resultsmentioning

confidence: 90%

Novel oxazolinoanthracyclines as tumor cell growth inhibitors—Contribution of autophagy and apoptosis in solid tumor cells death

et al. 2018

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Chemical modification of known, effective drugs are one method to improve the chemotherapy of tumors. We reported ability of oxazoline analogs of doxorubicin (O-DOX) and daunorubicin (O-DAU) to induce apoptosis and autophagy in ovarian and liver cancer cells. Reactive oxygen and nitrogen species (ROS and RNS, respectively), together with intracellular calcium-mediated downstream signaling, are essential for the anticancer effect of these new anthracycline analogs. The changes of mitochondrial membrane potential and induction of the ceramide pathway suggests that these compounds induce cell death by apoptosis. In addition, a significant increase of autophagosome formation was observed by fluorescence assay and acridine orange staining, indicating that the new analogs also induce autophagic cell death. Compared to free DOX- and DAU-treated cells, we observed inhibition of colony formation and migration, a time-dependency between ROS/RNS levels and a greater fall in mitochondrial membrane potential. Altogether, our research broadens the base of molecular oxazolinoanthracyclines targets and reveals that derivatives mediated oxidative stress, ceramide production and increase in intracellular calcium level by mitochondria. Furthermore, our data highlight the importance of mitochondria that simultaneously assume the role of activator of autophagy and apoptosis signals.

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“…As mitophagy is tightly controlled by a number of proteins, some proteins are used to assess mitophagy. LC3-II, a widely used marker of autophagy, is localized at autophagosomes and its expression level correlates with the number of autophagosomes [17] [18]. Another widely used autophagy marker is p62, also called sequestosome 1 (SQSTM1), which directly binds to LC3 and is selectively degraded by autophagy [19] [20].…”

Section: Discussionmentioning

confidence: 99%

Mitophagy in the Skeletal Muscle Is Suppressed in Spleen Qi Deficiency

Ma¹,

Liu²,

Wang³

et al. 2019

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Objective: Mitochondrial impairment in the skeletal muscle contributes to useless of limbs in spleen qi deficiency; however the genesis of such impairment is not clear. Herein, PTEN-induced putative kinase 1 (PINK1)-Parkin pathway and mitophagy were studied to explore the machinery of mitochondrial impairment. Methods: 16 male SD rats were randomly divided in the control group and spleen qi deficiency group (model group); transmission electron microscope was used to observe mitochondrial morphology; mitochondrial oxidative phosphorylation was assessed by testing mitochondrial membrane potential (MMP) and levels of ATP and ROS; western blot was used to analyze expressions of PINK1, Parkin, microtubule-associated protein 1 light chain 3-II (LC3-II) and p62. Results: Compared with those in the control group, mitochondria became small, less and scattered, MMP and the ATP level were reduced, the ROS level was elevated, PINK1 expression was decreased, p62 expression was increased, but Parkin and LC3-II expressions were not altered, in the model group. Conclusions: Suppression of mitophagy might be related to the mitochondrial damage in the skeletal muscle when spleen qi deficiency develops.

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Quantification of autophagy flux using LC3 ELISA

Cited by 45 publications

References 19 publications

Distinct patterns of skeletal muscle mitochondria fusion, fission and mitophagy upon duration of exercise training

Distinct patterns of skeletal muscle mitochondria fusion, fission and mitophagy upon duration of exercise training

Novel oxazolinoanthracyclines as tumor cell growth inhibitors—Contribution of autophagy and apoptosis in solid tumor cells death

Mitophagy in the Skeletal Muscle Is Suppressed in Spleen Qi Deficiency

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