Autophagy regulates chlorpyrifos-induced apoptosis in SH-SY5Y cells

Park, Jae Hyeon; Lee, Jeong Eun; Shin, In Chul; Koh, Hyun Chul

doi:10.1016/j.taap.2013.01.013

Cited by 82 publications

(61 citation statements)

References 63 publications

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“…Our finding is supported by the decreased expression of caspase-3 due to rapamycin pretreatment (Fig. 3G); this is consistent with the literature reporting its inhibition of caspase-3 activation, a hallmark of apoptosis (23,57,61). It is very likely that rapamycin has a neuroprotective effect against colistin-induced apoptosis, in which autophagy and apoptosis interplay with each other.…”

Section: Discussionsupporting

confidence: 92%

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Autophagy Regulates Colistin-Induced Apoptosis in PC-12 Cells

Zhang

Zhao

Ding

et al. 2015

Antimicrob Agents Chemother

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Section: Discussionsupporting

confidence: 92%

“…In contrast to apoptosis, autophagy is protective against acute neural injury induced by chlorpyrifos and in Parkinson's disease (23,34). Although autophagy and apoptosis have different impacts on cell fate, their functions are not completely independent (17,35).…”

Section: Discussionmentioning

confidence: 99%

Autophagy Regulates Colistin-Induced Apoptosis in PC-12 Cells

Zhang

Zhao

Ding

et al. 2015

Antimicrob Agents Chemother

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“…Autophagy is a compensatory mechanism to address the toxic effects of many pesticides. For example, Park et al (2013) found that autophagy could regulate chlorpyrifos-induced apoptosis by monitoring the expression of LC3-II and p62 in SH-SY5Y cells. Both rotenone and paraquat could up-regulate autophagy by up-regulating LC3-II expression and the number of lysosomes in SH-SY5Y cells (Xiong et al 2011).…”

Section: Abbreviationsmentioning

confidence: 99%

Autophagy response in the liver of pigeon exposed to avermectin

Wang

Liu

Khoso

et al. 2016

Environ Sci Pollut Res

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Pesticide residues are an important aspect of environmental pollution. Environmental avermectin residues have produced adverse effects in organisms. Many pesticides exert their toxic effects via the mechanism of autophagy. The purpose of this study was to examine the changes in autophagy levels and in autophagy-related genes, including LC3, Beclin 1, Dynein, ATG5, TORC1, and TORC2, resulting from exposure to subchronic levels of AVM in liver tissue in the king pigeon model. We observed abundant autophagic vacuoles with extensively degraded organelles, autophagosomal vacuoles, secondary lysosomes, and double-membrane structures in the liver. The expression levels of the autophagy-related genes LC3-I, LC3-II, Beclin 1, ATG5, and Dynein were up-regulated; however, TORC1 and TORC2 expression levels were down-regulated. These changes occurred in a concentration-dependent manner after AVM exposure for 30, 60, and 90 days in pigeons. Taken together, these results suggested that AVM increased the autophagic flux and that upregulation of autophagy might be closely related to the hepatotoxicity of AVM in birds.

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“…Whether CPF exposure also 62 induces mitophagy remains unclear. Although Park et al (2013) were broken down and fragmented into short rods or spheres. 216 Cell counting revealed that >75% cells that were exposed to CPF 217 contained fragmented mitochondria (Fig.…”

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confidence: 99%

PINK1/Parkin-mediated mitophagy alleviates chlorpyrifos-induced apoptosis in SH-SY5Y cells

et al. 2015

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Chlorpyrifos (CPF) is one of the most widely used organophosphorous insecticides. There are links between CPF exposure and neurological disorders. Mitochondrial damage has been implicated to play a key role in CPF-induced neurotoxicity. Mitophagy, the selective autophagic elimination of mitochondria, is an important mitochondrial quality control mechanism. However, the role of mitophagy in CPF-induced neurotoxicity remains unclear. In this study, CPF-caused mitochondrial damage, role and mechanism of mitophagy on CPF-induced neuroapoptosis were extensively studied by using SH-SY5Y cells. We showed that CPF treatment caused mitochondrial fragmentation, excessive ROS generation and mitochondrial depolarization, thus led to cell apoptosis. Moreover, CPF treatment also resulted in increased colocalizaton of mitochondria with LC3, decreased levels of mitochondrial proteins, PINK1 stabilization and mitochondrial accumulation of Parkin. These data suggested that CPF treatment induced PINK1/Parkin-mediated mitophagy in SH-SY5Y cells. Furthermore, knockdown of Parkin dramatically increased CPF-induced neuroapoptosis. On the other hand, overexpression of Parkin markedly alleviated CPF-induced SH-SY5Y cell apoptosis. Together, these findings implicate a protective role of PINK1/Parkin-mediated mitophagy against neuroapoptosis and that enhancing mitophagy provides a potential therapeutic strategy for CPF-induced neurological disorders.

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Autophagy regulates chlorpyrifos-induced apoptosis in SH-SY5Y cells

Cited by 82 publications

References 63 publications

Autophagy Regulates Colistin-Induced Apoptosis in PC-12 Cells

Autophagy Regulates Colistin-Induced Apoptosis in PC-12 Cells

Autophagy response in the liver of pigeon exposed to avermectin

PINK1/Parkin-mediated mitophagy alleviates chlorpyrifos-induced apoptosis in SH-SY5Y cells

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