Involvement of autophagy in tri-ortho-cresyl phosphate- induced delayed neuropathy in hens

Song, Fuyong; Kou, Ruirui; Zou, Chaoshuang; Gao, Yuan; Zeng, Tao; Xie, Keqin

doi:10.1016/j.neuint.2013.10.017

Cited by 21 publications

(15 citation statements)

References 46 publications

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“…Hens in delayed neuropathy model group were administered by gavage with a single dose of 750 mg/kg TOCP. This dosage of TOCP was commonly used to develop an experimental animal model of delayed neuropathy in hens [20,32]. Firstly, the hens in Apelin-13 treatment group were administered by gavage with a single dose of 750 mg/kg TOCP, and then the hens were treated with intraperitoneal injection with 10 nmol/kg Apelin-13 one time per day for 21 days.…”

Section: Animal Treatment and Groupmentioning

confidence: 99%

“…The researches revealed that OPIDN was associated with a significant autophagic dysfunction in hen nervous tissue. The suppression of basal autophagy might disrupt the turnover of proteins and organelles in neurons, eventually leading to accumulation of membrane structures, cytoskeletal protein and organelles in distal axons, which might be involved in the development of TOCPinduced delayed neuropathy [20,21].…”

Section: Introductionmentioning

confidence: 99%

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RETRACTED ARTICLE: Apelin-13 Prevents the Delayed Neuropathy Induced by Tri-ortho-cresyl Phosphate Through Regulation the Autophagy Flux in Hens

et al. 2015

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Organophosphate-induced delayed neuropathy (OPIDN) is pathologically characterized by the swollen axon containing aggregations of microtubules, neurofilaments, smooth endoplasmic reticulum and multivesicular vesicles. At present, the exact mechanism of OPIDN is unclear and the effective therapeutic methods is not available to counter this syndrome. Recent studies had shown that the autophagy was involved in OPIDN. The adipocytokine Apelin is a peptide, Apelin and its receptor are abundantly expressed in the nervous system. Recent researches illuminated that Apelin was neuroprotective factor and Apelin could regulate the autophagy in vivo and vitro model. So we investigated the effect of Apelin-13 on the OPIDN induced by Tri-ortho-cresyl phosphate (TOCP) in hens and explored the role of autophagy in Apelin-13 preventing OPIDN. Adult Roman hens were given a single dose of 750 mg/kg TOCP by gavage for 21 days to induce OPIDN, and neural dysfunction were detected, and the formation of autophagosomes in spinal cord neurons was observed by transmission electron microscopy, and the molecular markers of autophagy microtubule-associated protein light chain-3 (LC3) and the autophagy substrates p62/SQSTM1 were determined by Western blot analysis. The results demonstrated that the obvious neurological dysfunction such as hindlimb paralysis and paralysis of gait was present, the number of autophagosomes in the neurons of spinal cords was significantly increased, the level of LC3-II and p62 expressions and the ratio of LC3-II/LC3-I in spinal cords and sciatic nerve were significantly increased in the OPIDN model group compared with the control group. Compared with the OPIDN model group, the neurological dysfunction of tens was obviously reduced, the clinical signs scores was significantly decreased, the number of autophagosomes in the neurons of hen spinal cords was significantly decreased, the level of LC3-II and p62 expressions and the ratio of LC3-II/LC3-I in spinal cords and sciatic nerve were significantly decreased in Apelin-13 treatment group. Our results suggested that Apelin-13 prevented against the OPIDN induced by TOCP in hens, which the mechanism might be associated with regulation autophagy flux by Apelin-13.

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Section: Animal Treatment and Groupmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Apelin-13 Prevents the Delayed Neuropathy Induced by Tri-ortho-cresyl Phosphate Through Regulation the Autophagy Flux in Hens

et al. 2015

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“…The present data indicated that autophagy was activated by Aβ1-40 treatment via promoting the conversion of LC3-I to LC3-II and increasing the level of beclin-1, which was enhanced by overexpression of let-7a. Atg-5 and Atg-7 serve a function in the membrane-expansion process in autophagosome formation, and overexpression of Atg-5 and Atg-7 may facilitate the activation of autophagy (36). The present results were consistent with this and indicated that let-7a overexpression further promoted the increased levels of Atg-5 and Atg-7 induced by Aβ1-40.…”

Section: Discussionsupporting

confidence: 90%

Overexpression of let-7a increases neurotoxicity in a PC12 cell model of Alzheimer's disease via regulating autophagy

Zhao

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Increased deposition of β-amyloid (Aβ) protein is one of the typical characteristics of Alzheimer's disease (AD). Recent evidence has demonstrated that the microRNA let-7 family, which is highly expressed in the central nervous system, participates in the regulation of pathologic processes of AD. In the present study, the effect of let-7a overexpression on Aβ1-40-induced neurotoxicity was evaluated in PC12 and SK-N-SH cells. The results indicated that overexpression of let-7a enhanced the neurotoxicity induced by Aβ1-40 in PC12 and SK-N-SH cells. In addition, the apoptosis induced by Aβ1-40 in PC12 and SK-N-SH cells was increased by let-7a overexpression. Furthermore, Aβ1-40 treatment increased the protein levels of microtubule-associated protein 1A/1B-light chain 3 (LC3) and beclin-1 and increased the LC3 II/I ratio. The mRNA expression levels of beclin-1, autophagy protein 5 (Atg-5) and Atg-7 were also increased by Aβ1-40 treatment in PC12 cells. Let-7a overexpression further upregulated the above autophagy-related markers. Furthermore, the protein level of p62 was increased by Aβ1-40 treatment, and this was further enhanced by let-7a overexpression. Finally, the present results demonstrated that the phosphoinositide-3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathway was involved in the autophagy regulation by let-7a. In conclusion, the present study demonstrates that the neurotoxicity induced by Aβ1-40 is augmented by let-7a overexpression via regulation of autophagy, and the PI3K/Akt/mTOR signaling pathway also serves a function in this process.

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“…We found that autophagic vesicles in the cytoplasm containing extensively degraded organelles such as mitochondria and endoplasmic reticulum increased significantly after the cells were treated with TOCP. However, there might be different in other kinds of animals; Song et al (2012Song et al ( , 2014 showed that the number of autophagosomes was markedly increased in the myelinated and unmyelinated axons of hen spinal cords after treatment of hens with TOCP, while the protein levels of LC3, beclin 1, and ATG5 were significantly decreased, which suggested that the administration of TOCP resulted in a disruption of autophagy-regulated machinery in hens.…”

Section: Discussionmentioning

confidence: 99%

Tri-ortho-cresyl phosphate induces autophagy of rat spermatogonial stem cells

Liu¹,

Wang²,

Wei³

et al. 2015

Reproduction

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Tri-ortho-cresyl phosphate (TOCP) has been widely used as plasticizers, plastic softeners, and flame retardants in industry and reported to have a deleterious effect on the male reproductive system in animals besides delayed neurotoxicity. Our preliminary results found that TOCP could disrupt the seminiferous epithelium in the testis and inhibit spermatogenesis, but the precise mechanism is yet to be elucidated. This study shows that TOCP inhibited viability of rat spermatogonial stem cells in a dose-dependent manner. TOCP could not lead to cell cycle arrest in the cells; the mRNA levels of p21, p27, p53, and cyclin D1 in the cells were also not affected by TOCP. Meanwhile, TOCP did not induce apoptosis of rat spermatogonial stem cells. After treatment with TOCP, however, both LC3-II and the ratio of LC3-II/LC3-I were markedly increased; autophagy proteins ATG5 and beclin 1 were also increased after treatment with TOCP, indicating that TOCP could induce autophagy in the cells. Ultrastructural observation under the transmission electron microscopy indicated that autophagic vesicles in the cytoplasm containing extensively degraded organelles such as mitochondria and endoplasmic reticulum increased significantly after the cells were treated with TOCP. In summary, we have shown that TOCP can inhibit viability of rat spermatogonial stem cells and induce autophagy of the cells, without affecting cell cycle and apoptosis.

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Involvement of autophagy in tri-ortho-cresyl phosphate- induced delayed neuropathy in hens

Cited by 21 publications

References 46 publications

RETRACTED ARTICLE: Apelin-13 Prevents the Delayed Neuropathy Induced by Tri-ortho-cresyl Phosphate Through Regulation the Autophagy Flux in Hens

RETRACTED ARTICLE: Apelin-13 Prevents the Delayed Neuropathy Induced by Tri-ortho-cresyl Phosphate Through Regulation the Autophagy Flux in Hens

Overexpression of let-7a increases neurotoxicity in a PC12 cell model of Alzheimer's disease via regulating autophagy

Tri-ortho-cresyl phosphate induces autophagy of rat spermatogonial stem cells

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