Protective effects of galantamine against Aβ-induced PC12 cell apoptosis by preventing mitochondrial dysfunction and endoplasmic reticulum stress

Liu, Xiaoyu; Xu, Kedi; Yan, M.; Wang, Yongping; Zheng, Xiaoxiang

doi:10.1016/j.neuint.2010.07.007

Cited by 67 publications

(29 citation statements)

References 55 publications

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“…ER and mitochondria respond coordinately in a variety of scenarios, such as arsenic poisoning [106], cholesterol overloading [107], protein aggregation [108] and neurodegenerative disorders [109]. Under these conditions oxidative stress is a common factor providing extensive opportunities for ER-mitochondrial crosstalk, as both organelles participate in maintaining, initiating and responding to changes in redox state [110, 111].…”

Section: Pathophysiological Implications Of the Er-mitochondria Inmentioning

confidence: 99%

Cell Death and Survival Through the Endoplasmic Reticulum- Mitochondrial Axis

Bravo-Sagua¹,

Rodríguez²,

Kuzmicic³

et al. 2013

Current Molecular Medicine

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Section: Pathophysiological Implications Of the Er-mitochondria Inmentioning

confidence: 99%

Cell Death and Survival Through the Endoplasmic Reticulum- Mitochondrial Axis

Bravo-Sagua¹,

Rodríguez²,

Kuzmicic³

et al. 2013

Current Molecular Medicine

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“…Alzheimer's disease Tau hyperphosphorylation and formation of protein aggregates of Aβ peptide Presenilin-2, which generates Aβ, increases the interaction and calcium transfer at MAM [108].…”

Section: Diseasementioning

confidence: 99%

Cell Death and Survival Through the Endoplasmic Reticulum- Mitochondrial Axis

Bravo-Sagua¹,

Rodriguez²,

Kuzmicic³

et al. 2012

CMM

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The endoplasmic reticulum has a central role in biosynthesis of a variety of proteins and lipids. Mitochondria generate ATP, synthesize and process numerous metabolites, and are key regulators of cell death. The architectures of endoplasmic reticulum and mitochondria change continually via the process of membrane fusion, fission, elongation, degradation, and renewal. These structural changes correlate with important changes in organellar function. Both organelles are capable of moving along the cytoskeleton, thus changing their cellular distribution. Numerous studies have demonstrated coordination and communication between mitochondria and endoplasmic reticulum. A focal point for these interactions is a zone of close contact between them known as the mitochondrial-associated endoplasmic reticulum membrane (MAM), which serves as a signaling juncture that facilitates calcium and lipid transfer between organelles. Here we review the emerging data on how communication between endoplasmic reticulum and mitochondria can modulate organelle function and determine cellular fate. KeywordsCell death; endoplasmic reticulum; metabolism; mitochondria CONFLICT OF INTERESTThe authors confirm that this article content has no conflicts of interest. NIH Public Access Author ManuscriptCurr Mol Med. Author manuscript; available in PMC 2014 July 21. Published in final edited form as:Curr Mol Med. 2013 February ; 13(2): 317-329. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript ORGANELLE FUNCTIONThe endoplasmic reticulum (ER) is an organelle whose primary function is protein synthesis and folding [1]. One third of cellular proteins are synthesized by ER-associated ribosomes, particularly those destined for secretion [2]. In the ER lumen, nascent polypeptides are modified with N-linked glycans and made accessible to proteins involved in proper protein folding and quality control [3,4]. In addition, the ER is the main site for biosynthesis of a variety of lipids such as phospholipids, cholesterol, and ceramides, which are transported to other organelles and cellular membranes via vesicles of the secretory pathway [5].ER is composed of a series of continuous membranous structures that are organized into subdomains that include the rough ER, smooth ER, transitional ER and the nuclear envelope [6]. The architecture of the ER changes continually according to cellular demand through the processes of fusion, fission, elongation and membrane degradation [6]. Structural differences correlate with differences in ER function [6]. The rough ER is mainly laminal and associated with polyribosomes for protein synthesis. The smooth ER is primarily composed of tubular structures. This is the site of phospholipid biosynthesis and is the chief point of contact with other organelles [6]. Changes in ER membrane curvature and structure are facilitated by several proteins, including GTPases and reticulons [6]. For a detailed view of ER structure and related processes, readers are referred to a recent excellent review by Park ...

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“…Afterwards, the released cytochrome c would blind to apoptotic protease activating factor-1 (Apaf-1) and ATP as the activited apoptosome, which results in caspases activities and leads to the characteristic morphological changes of cerebral neurons. 14) For this reasons above, the aim of this study was to investigate whether ginkgolide K possesses the protective effect on H 2 O 2 -induced PC12 cells injury or not and further explore the potential mechanisms of protective effect of ginkgolide K.…”

mentioning

confidence: 99%

Neuroprotective Effect of Ginkgolide K against H<sub>2</sub>O<sub>2</sub>-Induced PC12 Cell Cytotoxicity by Ameliorating Mitochondrial Dysfunction and Oxidative Stress

Liu

Xun

et al. 2014

Biological & Pharmaceutical Bulletin

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Mitochondria and oxidative stress play important roles in neuronal cell death associated with cerebral ischemia. Elevated level of reactive oxygen species (ROS) and mitochondrial dysfunction are thought to be responsible for cerebral ischemia injury along with neural cells death through several apoptotic mechanisms. In this study, exposure of rat pheochromocytoma (PC12) cells to hydrogen peroxide (H 2 O 2 ) at the concentration of 0.3 mM for 24 h caused significant loss of cell viability, lactate dehydrogenase (LDH) release from cells, ascent of ROS level and mitochondrial membrane potential (MMP) decrease. Moreover, the activities of caspase-9, caspase-8 and caspase-3 all were increased in H 2 O 2 -induced PC12 cells. However, pretreatment with ginkgolide K (GK) solutions of different concentrations (10, 50, 100 µM) for 24 h prior to exposuring to H 2 O 2 significantly increased cells viability, suppressed LDH release, attenuated ROS level, prevented cytochrome c release from mitochondria and boosted MMP expression. In addition, ginkgolide K notably inhibited the caspase-3 and caspase-9 but not caspase-8 activities in exogenous H 2 O 2 -treated PC12 cells. These results demonstrated that ginkgolide K protected PC12 cells from H 2 O 2 -induced apoptosis by restoring MMP expression, ameliorating oxidative stress and subsequently leading to inhibit the activity of caspase-3 protein. Therefore, the present study supported that ginkgolide K may be a promising neuroprotective compound for cerebral ischemia treatment.

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Protective effects of galantamine against Aβ-induced PC12 cell apoptosis by preventing mitochondrial dysfunction and endoplasmic reticulum stress

Cited by 67 publications

References 55 publications

Cell Death and Survival Through the Endoplasmic Reticulum- Mitochondrial Axis

Cell Death and Survival Through the Endoplasmic Reticulum- Mitochondrial Axis

Cell Death and Survival Through the Endoplasmic Reticulum- Mitochondrial Axis

Neuroprotective Effect of Ginkgolide K against H<sub>2</sub>O<sub>2</sub>-Induced PC12 Cell Cytotoxicity by Ameliorating Mitochondrial Dysfunction and Oxidative Stress

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