Aluminum maltolate induces primary rat astrocyte apoptosis via overactivation of the class III PI3K/Beclin 1-dependent autophagy signal

Zeng, Ke‐Wu; Fu, Hong En; Liu, Gengxin; Wang, Xuemei

doi:10.1016/j.tiv.2011.11.010

Cited by 33 publications

(14 citation statements)

References 38 publications

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“…3-MA blocks autophagosome formation via inhibition of type III PI3K and inhibits autophagy. Type III PI3K is crucial for vesicle nucleation and the formation of the preautophagosome, which is a very early event of autophagy (50). In our present study, pretreatment of cells with 3-MA before colistin treatment significantly decreased the viability of cells and promoted chromatin condensation and cytoplasmic vacuolization.…”

Section: Discussionsupporting

confidence: 55%

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: 55%

Autophagy Regulates Colistin-Induced Apoptosis in PC-12 Cells

Zhang

Zhao

Ding

et al. 2015

Antimicrob Agents Chemother

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“…The phosphorylation state of JNK has been increased by Al (Li et al, 2012a). And autophagy-related protein (Beclin 1 and LC3II) expressions has been induced by Al (Zeng et al, 2012). The inhibition of the ERK-MAPK, PI3K/AKT and JNK signaling pathway may be the key for AlCl3-induced lower osteoblasts viability.…”

Section: Discussionmentioning

confidence: 96%

Ginsenoside Rb1 alleviates aluminum chloride-induced rat osteoblasts dysfunction

Zhu

Zheng

et al. 2016

Toxicology

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Osteoblasts dysfunction, induced by aluminum (Al), plays a critical role in the osteoporosis etiology. Ginsenoside Rb1 (Rb1) has the therapeutic properties for osteoporosis. This study aimed to assess the efficiency of Rb1 in ameliorating Al-induced osteoblasts dysfunction. The osteoblasts were divided into four groups: Rb1-treated group (RG, 0.0145mg/mL Rb1), control group (CG, 0), AlCl-treated group (AG, 0.126mg/mL AlCl·6HO), AlCl+Rb1-treated group (ARG, 0.0145mg/mL Rb1 and 0.126mg/mL AlCl·6HO). After 24h of culture, the osteoblasts viability, the transforming growth factor-β1 (TGF-), bone morphogenetic protein-2 (BMP-2), the insulin-like growth factor I (IGF-I), core-binding factor α1 (Cbfα1) mRNA expressions, glutathione perioxidase (GSH-P and superoxide dismutase (SOD) activities, and reactive oxygen species (ROS) concentration were determined. The osteoblasts ultrastructural features were also observed. In the ARG, the osteoblasts viability, TGF-, BMP-2, IGF-I and Cbfα1 mRNA expressions and the GSH-P and SOD activities were significantly increased, the ROS concentration was significantly decreased, and osteoblasts histology lesion was attenuated compared with the AG. These results demonstrated that Rb1 could significantly reverse osteoblasts viability and osteoblasts growth regulation factor, inhibit oxidative stress, and attenuate histology lesion in the osteoblasts with AlCl. These results indicate that Rb1 can effectively alleviate the AlCl-induced osteoblasts dysfunction.

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“…Although autophagy and apoptosis can coexist in the same damaged RGC, they do not necessarily overlap and can occur independently [58,92]. Autophagy can occur before neuronal apoptosis in aluminum-insulted astrocytes, a chronic hypertensive glaucoma model, and an optic nerve axotomy mouse model [46,93,94]. Similarly, in a chronic glaucoma model, autophagy activation occurs earlier than RGC loss [58].…”

Section: Cross-talk Between Autophagy and Apoptosismentioning

confidence: 99%

Autophagy: A Role in the Apoptosis, Survival, Inflammation, and Development of the Retina

Lin

2018

Ophthalmic Res

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Autophagy is a lysosomal degradation process that maintains cellular homeostasis by removing dysfunctional organelles and unfolded proteins. Increasing evidence has shown that autophagy proteins are involved in retinal physiology and pathology and that defective autophagy contributes to retinal degeneration. In retinal diseases, autophagy plays a dual role: promoting retinal cell survival and death. Autophagy at a normal level helps retinal cells defend themselves against harmful stress; however, excessive autophagy results in retinal deterioration. Both synergistic and antagonistic roles of autophagy and apoptosis in the retina have been reported in the literature. In this review, we summarize the roles of autophagy in the development of the retina and retinal diseases. This review highlights the importance of autophagy in retinal diseases, and targeting autophagy may provide a new therapeutic approach for retinal diseases.

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Aluminum maltolate induces primary rat astrocyte apoptosis via overactivation of the class III PI3K/Beclin 1-dependent autophagy signal

Cited by 33 publications

References 38 publications

Autophagy Regulates Colistin-Induced Apoptosis in PC-12 Cells

Autophagy Regulates Colistin-Induced Apoptosis in PC-12 Cells

Ginsenoside Rb1 alleviates aluminum chloride-induced rat osteoblasts dysfunction

Autophagy: A Role in the Apoptosis, Survival, Inflammation, and Development of the Retina

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