Nitric Oxide-Induced Autophagy in MC3T3-E1 Cells is Associated with Cytoprotection via AMPK Activation

Yang, Jung Yoon; Park, Min Young; Park, Sam Young; Yoo, H.I.; Kim, Min Seok; Kim, Jae Hyung; Kim, Won Jae; Jung, Ji Yeon

doi:10.4196/kjpp.2015.19.6.507

Cited by 14 publications

(25 citation statements)

References 57 publications

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“…45 In the present study, treatment with rapamycin or 3-MA alone had no significant influence on cell viability, which was consistent with previous studies revealing that pretreatment with rapamycin (no more than 2 μM) or 3-MA (no more than 10 mM) had no significant influence on cell viability, differentiation, mineralization, apoptosis of osteoblasts, or the expression of autophagy and osteogenesis-related factors. 23,37,46,47 The cell viability further increased when the cells were pretreated with rapamycin but obviously decreased when they were pretreated with 3-MA, revealing that autophagy was involved in the Ta-NP-induced cell proliferation and had a promoting effect. This statement is consistent with the finding that nano-TiO 2 -induced autophagy played a protective role against oxidative stress and promoted cell proliferation.…”

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confidence: 99%

Involvement of autophagy in tantalum nanoparticle-induced osteoblast proliferation

Kang¹,

Wei²,

Song³

et al. 2017

IJN

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Porous tantalum (Ta) implants are highly corrosion resistant and biocompatible, and they possess significantly better initial stability than that of conventional titanium (Ti) implants. During loading wear, Ta nanoparticles (Ta-NPs) that were deposited on the surface of a porous Ta implant are inevitably released and come into direct contact with peri-implant osteoblasts. The wear debris may influence cell behavior and implant stabilization. However, the interaction of Ta-NPs with osteoblasts has not been clearly investigated. This study aimed to investigate the effect of Ta-NPs on cell proliferation and their underlying mechanism. The Cell Counting Kit-8 (CCK-8) assay was used to measure the cell viability of MC3T3-E1 mouse osteoblasts and showed that Ta-NP treatment could increase cell viability. Then, confocal microscopy, Western blotting, and transmission electron microscopy were used to confirm the autophagy induced by Ta-NPs, and evidence of autophagy induction was observed as positive LC3 puncta, high-LC3-II expression, and autophagic vesicle ultrastructures. The CCK-8 assay revealed that the cell viability was further increased and decreased by the application of an autophagy inducer and inhibitor, respectively. In addition, pre-treatment with autophagy inhibitor 3-methyladenine (3-MA) inhibited the Ta-NP-induced autophagy. These results indicate that the Ta-NPs can promote cell proliferation, that an autophagy inducer can further strengthen this effect and that an autophagy inhibitor can weaken this effect. In conclusion, autophagy was involved in Ta-NP-induced cell proliferation and had a promoting effect.

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confidence: 99%

Involvement of autophagy in tantalum nanoparticle-induced osteoblast proliferation

Kang¹,

Wei²,

Song³

et al. 2017

IJN

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“…The unconjugated form of Atg8/LC3 (LC3-I) is found in the cytosol, while the conjugated form (LC3-II) targets the autophagosomal membrane [3328]. LC3-II remains in the membrane until it is degraded by lysosomes.…”

Section: Resultsmentioning

confidence: 99%

“…Notably, autophagy regulates several survival and cell death signaling pathways in cancer [3031]. To date, some key autophagic mediators, including p53, autophagy-related genes (ATGs), mTOR, and Beclin-1, are known to modulate autophagic activity in cancer initiation and progression [293031]. Because autophagy-modulating agents such as rapamycin and chloroquine have already been used clinically to treat cancer, it is conceivable that understanding and targeting autophagic pathways can provide new insights for the discovery of cancer therapeutics.…”

Section: Discussionmentioning

confidence: 99%

“…Apoptosis, the major form of controlled cell death, is involved in various diseases such as neurodegenerative diseases, autoimmune diseases, cardiovascular diseases, and cancer [29323334]. Therefore, investigations into the molecular mechanisms of apoptosis regulation have revealed a number of promising therapeutic targets and have been utilized in drug discovery and medical research.…”

Section: Discussionmentioning

confidence: 99%

“…These responses have been implicated in suppression of tumor formation and responses to many types of cancer therapy [34]. Apoptosis and autophagy usually function to eliminate damaged cells and damaged proteins, respectively [3334]. Dysfunction of these events is associated with oncogenesis and cancer progression.…”

Section: Discussionmentioning

confidence: 99%

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Novel functional roles of caspase-related genes in the regulation of apoptosis and autophagy

Shin

Min

2016

Korean J Physiol Pharmacol

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Caspases, a family of cysteine proteases, cleave substrates and play significant roles in apoptosis, autophagy, and development. Recently, our group identified 72 genes that interact with Death Caspase-1 (DCP-1) proteins in Drosophila by genetic screening of 15,000 EP lines. However, the cellular functions and molecular mechanisms of the screened genes, such as their involvement in apoptosis and autophagy, are poorly understood in mammalian cells. In order to study the functional characterizations of the genes in human cells, we investigated 16 full-length human genes in mammalian expression vectors and tested their effects on apoptosis and autophagy in human cell lines. Our studies revealed that ALFY, BIRC4, and TAK1 induced autophagy, while SEC61A2, N-PAC, BIRC4, WIPI1, and FALZ increased apoptotic cell death. BIRC4 was involved in both autophagy and apoptosis. Western blot analysis and luciferase reporter activity indicated that ALFY, BIRC4, PDGFA, and TAK1 act in a p53-dependent manner, whereas CPSF1, SEC61A2, N-PAC, and WIPI1 appear to be p53-independent. Overexpression of BIRC4 and TAK1 caused upregulation of p53 and accumulation of its target proteins as well as an increase in p53 mRNA levels, suggesting that these genes are involved in p53 transcription and expression of its target genes followed by p53 protein accumulation. In conclusion, apoptosis and/or autophagy mediated by BIRC4 and TAK1 may be regulated by p53 and caspase activity. These novel findings may provide valuable information that will aid in a better understanding of the roles of caspase-related genes in human cell lines and be useful for the process of drug discovery.

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Acteoside inhibits autophagic apoptosis of retinal ganglion cells to rescue glaucoma‐induced optic atrophy

Chen

Zeng

et al. 2019

J of Cellular Biochemistry

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Background Glaucoma is the world's second biggest cause of blindness, and patients progressively lose their eyesight. The current clinical treatment for glaucoma involves controlling intraocular pressure with drugs or surgery; however, some patients still progressively lose their eyesight. This treatment is also similar to the treatment of traumatic optic neuropathy. Thus, saving retinal ganglion cells (RGCs) from apoptosis is essential. Methods The role of Acteoside on autophagy modulation in the 661 W cell line. Results In this study, we first find that Acteoside inhibits autophagy, Rapamycin alleviates this inhibition and the PI3K inhibitor, 3‐MA or LY294002, synergistically promotes it. In a mechanistic study, we find that Optineurin (OPTN) mediates Acteoside regulation of autophagy. OPTN overexpression or knockdown activates or inhibits autophagy, respectively. OPTN is inhibited by autophagy inhibitors, such as Acteoside and 3‐MA and is promoted by the autophagy activator, Rapamycin. Meanwhile, PI3K and AKT are elevated by Acteoside and 3‐MA and inhibited by Rapamycin. Finally, we find that Acteoside inhibits apoptosis in parallel to autophagy and that this inhibition is also mediated by OPTN. Conclusion In summary, we conclude that Acteoside inhibits autophagy‐induced apoptosis in RGCs through the OPTN and PI3K/AKT/mTOR pathway, and glaucoma patients may benefit from Acteoside treatment alone or in combination with other autophagy inhibitors.

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Nitric Oxide-Induced Autophagy in MC3T3-E1 Cells is Associated with Cytoprotection via AMPK Activation

Cited by 14 publications

References 57 publications

Involvement of autophagy in tantalum nanoparticle-induced osteoblast proliferation

Involvement of autophagy in tantalum nanoparticle-induced osteoblast proliferation

Novel functional roles of caspase-related genes in the regulation of apoptosis and autophagy

Acteoside inhibits autophagic apoptosis of retinal ganglion cells to rescue glaucoma‐induced optic atrophy

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