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RISS 인기검색어
- 검색키워드
- 저자 : Dadakhujaev, Shorafidinkhuja (검색결과 3 건)
- 무료
- 기관 내 무료
- 유료
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Interplay between autophagy and apoptosis in TrkA-induced cell death.
Dadakhujaev, Shorafidinkhuja,Jung, Eun Joo,Noh, Hae Sook,Hah, Young-Sool,Kim, Chang Jae,Kim, Deok Ryong Landes Bioscience 2009 Autophagy Vol.5 No.1
<P>Autophagy is a self-eating process to eradicate damaged proteins or organelles in cells. This process begins with formation of a double-membrane structure, called an autophagosome, which can sequester soluble proteins and organelles eventually degraded by lysosomal proteases after fusion with the lysosome. Autophagy was initially identified as a cell survival mechanism under stress conditions such as nutrient deprivation. More recently, it is also considered as type-II programmed cell death. In our recent report, we observed that overexpression of TrkA caused massive cell death via both apoptosis and autophagy. Overexpression of TrkA abated catalase activity and subsequently resulted in the production of a large amount of reactive oxygen species in cells. These consequences led to autophagic cell death. The autophagic cell death in TrkA-overexpressing cells was validated by GFP-LC3 dot formation, production of autophagosomes or acidic vacuoles, LC3 lipidation and depletion of autopahgy-related genes. In addition, we also observed some evidence for apoptosis in TrkA-expressing cells. Many cells expressing TrkA exhibited annexin V-positive staining, activation of caspase-7 and BAX. Moreover, TrkA activated the JNK pathway, leading to phosphorylation of H2AX. In this report, we suggest that two cell death mechanisms occur simultaneously and interlink with each other. The JNK-calpain pathway might be a central process to mediate the two processes in TrkA-overexpressing cells, although further study still remains to prove the interplay between autophagy and apoptosis.</P>
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Interplay between autophagy and apoptosis in TrkA-induced cell death.
Dadakhujaev, Shorafidinkhuja,Jung, Eun Joo,Noh, Hae Sook,Hah, Young-Sool,Kim, Chang Jae,Kim, Deok Ryong Landes Bioscience 2009 AUTOPHAGY Vol.5 No.1
<P>Autophagy is a self-eating process to eradicate damaged proteins or organelles in cells. This process begins with formation of a double-membrane structure, called an autophagosome, which can sequester soluble proteins and organelles eventually degraded by lysosomal proteases after fusion with the lysosome. Autophagy was initially identified as a cell survival mechanism under stress conditions such as nutrient deprivation. More recently, it is also considered as type-II programmed cell death. In our recent report, we observed that overexpression of TrkA caused massive cell death via both apoptosis and autophagy. Overexpression of TrkA abated catalase activity and subsequently resulted in the production of a large amount of reactive oxygen species in cells. These consequences led to autophagic cell death. The autophagic cell death in TrkA-overexpressing cells was validated by GFP-LC3 dot formation, production of autophagosomes or acidic vacuoles, LC3 lipidation, and depletion of autopahgy-related genes. In addition, we also observed some evidence for apoptosis in TrkA-expressing cells. Many cells expressing TrkA exhibited annexin V-positive staining, activation of caspase-7 and BAX. Moreover, TrkA activated the JNK pathway, leading to phosphorylation of H2AX. In this report, we suggest that two cell death mechanisms occur simultaneously and interlink with each other. The JNK-calpain pathway might be a central process to mediate the two processes in TrkA-overexpressing cells, although further study still remains to prove the interplay between autophagy and apoptosis.</P>
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Choi, Seung‐,Il,Dadakhujaev, Shorafidinkhuja,Ryu, Hyunmi,im Kim, Tae,Kim, Eung Kweon Blackwell Publishing Ltd 2011 Journal of pineal research Vol.51 No.1
<P><B>Abstract: </B> Considering that oxidative stress plays a role in corneal fibroblast degeneration during granular corneal dystrophy type 2 (GCD2) and melatonin is an effective antioxidant, we examined the ability of melatonin to protect against oxidative stress‐induced cell death of primary cultured normal and GCD2‐homozygous corneal fibroblasts. Melatonin treatment protected primary cultured normal and GCD2 corneal fibroblasts from paraquat (PQ)‐induced oxidative stress and caused increased expression levels of Cu/Zn‐superoxide dismutase (SOD1) and glutathione reductase (GR) in both types of cells. Interestingly, catalase expression increased in normal corneal fibroblasts, but decreased in GCD2 corneal fibroblasts after melatonin treatment. Melatonin also reduced the levels of intracellular reactive oxygen species and H<SUB>2</SUB>O<SUB>2</SUB> in both cell types. In addition, the selective melatonin receptor antagonist luzindole blocked melatonin‐induced expression of SOD1 and GR. The expression levels of melatonin receptors 1A (MT1) and 1B (MT2) were significantly higher in GCD2 corneal fibroblasts than in normal cells. These results suggest that increased expression of melatonin receptors may be involved in the defense mechanisms against oxidative stress in GCD2 corneal fibroblasts, and melatonin may have potential therapeutic implications for GCD2 treatment.</P>
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