Generation of ROS in response to CCK-8 stimulation in mouse pancreatic acinar cells

Granados, María P.; Salido, Ginés M.; Pariente, José A.; González, Antonio

doi:10.1016/j.mito.2004.02.003

Cited by 41 publications

(29 citation statements)

References 47 publications

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“…More recently, ROS have been recognised as intracellular messengers, which are required for the activation of a larger number of signal transduction mechanisms. Excessive production of ROS nevertheless leads to oxidative stress, loss of cell function, and ultimately apoptosis or necrosis [18][19][20]. In this study, NAC reserved the apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Notice of Retraction: Musca domestica Larvae Lectin Induced Apoptosis in Human Breast Cancer MCF-7 Cells through ROS-JNK Mediated Caspase Pathway and ROS-Ca²+ Pathway

Wang

Cao

Hou

et al. 2011

2011 5th International Conference on Bioinformatics and Biomedical Engineering

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Musca domestica larvae lectin (38kDa) was shown to induce apoptosis of MCF-7 cells, but the mechanism of lectin in apoptosis remained elusive. In this study, generation of ROS and [Ca 2+ ]c were caused by lectin. Rise of [Ca 2+ ]c was inhibited by antioxidants NAC (inhibitor of ROS). Results suggested involvement of ROS and [Ca 2+ ]c generation in lectin induced cell death. Moreover, [Ca 2+ ]c was regulated by ROS. Lectin induced a continuous activation of the phosphorylation of JNK which was blocked by NAC. These results demonstrated that the action of lectin induced MCF-7 cells apoptosis was via JNK activation. And JNK depended on signaling of ROS. Caspase apoptosis pathway was triggered by lectin through expression of Bax andBcl-2, then cytc was released and caspase was activated. Taken together, these studies considered that lectin induced apoptosis through a ROS-JNK mediated caspase pathway and increase of [Ca 2+ ]c .

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Section: Discussionmentioning

confidence: 99%

Notice of Retraction: Musca domestica Larvae Lectin Induced Apoptosis in Human Breast Cancer MCF-7 Cells through ROS-JNK Mediated Caspase Pathway and ROS-Ca²+ Pathway

Wang

Cao

Hou

et al. 2011

2011 5th International Conference on Bioinformatics and Biomedical Engineering

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“…6), in which Ca 2+ influx and uptake of Ca 2+ by mitochondria generates ROS (see Fig. 1 and Table 1) [23]. This leads to inhibition of PTP1B (see Fig.…”

Section: Ca 2+ Influx Following Store Depletion Is Increased By Ros Amentioning

confidence: 98%

“…ROS generation by mitochondria in response to Ca 2+ has been described [19,20,23]. Ca 2+ enhances ROS generation in mitochondria by stimulating the tricarbonic acid (TCA)-cycle and oxidative phosphorylation [19].…”

Section: Mitochondrial Electron Transport Chainmentioning

confidence: 99%

Inhibition of protein tyrosine phosphatase 1B by reactive oxygen species leads to maintenance of Ca2+ influx following store depletion in HEK 293 cells

et al. 2006

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“…What remains unclear is whether oxidative stress is the trigger or a downstream consequence of an inflammatory response, which promotes the release of further oxidants from activated neutrophils at the site of injury (22,50). However, there is substantial evidence that acinar cells can be a source of oxidant generation (7,17,42). In addition, in some pancreatitis models, lipid peroxidation products were detected prior to any inflammatory changes, suggesting that oxidative stress is an early event, if not the trigger of the disease (32).…”

mentioning

confidence: 99%

Oxidant-impaired intracellular Ca²⁺ signaling in pancreatic acinar cells: role of the plasma membrane Ca²⁺-ATPase

Bruce¹,

Elliott²

2007

American Journal of Physiology-Cell Physiology

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Pancreatitis is an inflammatory disease of pancreatic acinar cells whereby intracellular calcium concentration ([Ca(2+)](i)) signaling and enzyme secretion are impaired. Increased oxidative stress has been suggested to mediate the associated cell injury. The present study tested the effects of the oxidant, hydrogen peroxide, on [Ca(2+)](i) signaling in rat pancreatic acinar cells by simultaneously imaging fura-2, to measure [Ca(2+)](i), and dichlorofluorescein, to measure oxidative stress. Millimolar concentrations of hydrogen peroxide increased cellular oxidative stress and irreversibly increased [Ca(2+)](i), which was sensitive to antioxidants and removal of external Ca(2+), and ultimately led to cell lysis. Responses were also abolished by pretreatment with (sarco)endoplasmic reticulum Ca(2+)-ATPase inhibitors, unless cells were prestimulated with cholecystokinin to promote mitochondrial Ca(2+) uptake. This suggests that hydrogen peroxide promotes Ca(2+) release from the endoplasmic reticulum and the mitochondria and that it promotes Ca(2+) influx. Lower concentrations of hydrogen peroxide (10-100 muM) increased [Ca(2+)](i) and altered cholecystokinin-evoked [Ca(2+)](i) oscillations with marked heterogeneity, the severity of which was directly related to oxidative stress, suggesting differences in cellular antioxidant capacity. These changes in [Ca(2+)](i) also upregulated the activity of the plasma membrane Ca(2+)-ATPase in a Ca(2+)-dependent manner, whereas higher concentrations (0.1-1 mM) inactivated the plasma membrane Ca(2+)-ATPase. This may be important in facilitating "Ca(2+) overload," resulting in cell injury associated with pancreatitis.

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Generation of ROS in response to CCK-8 stimulation in mouse pancreatic acinar cells

Cited by 41 publications

References 47 publications

Notice of Retraction: Musca domestica Larvae Lectin Induced Apoptosis in Human Breast Cancer MCF-7 Cells through ROS-JNK Mediated Caspase Pathway and ROS-Ca²+ Pathway

Notice of Retraction: Musca domestica Larvae Lectin Induced Apoptosis in Human Breast Cancer MCF-7 Cells through ROS-JNK Mediated Caspase Pathway and ROS-Ca²+ Pathway

Inhibition of protein tyrosine phosphatase 1B by reactive oxygen species leads to maintenance of Ca2+ influx following store depletion in HEK 293 cells

Oxidant-impaired intracellular Ca²⁺ signaling in pancreatic acinar cells: role of the plasma membrane Ca²⁺-ATPase

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Generation of ROS in response to CCK-8 stimulation in mouse pancreatic acinar cells

Cited by 41 publications

References 47 publications

Notice of Retraction: Musca domestica Larvae Lectin Induced Apoptosis in Human Breast Cancer MCF-7 Cells through ROS-JNK Mediated Caspase Pathway and ROS-Ca²+ Pathway

Notice of Retraction: Musca domestica Larvae Lectin Induced Apoptosis in Human Breast Cancer MCF-7 Cells through ROS-JNK Mediated Caspase Pathway and ROS-Ca²+ Pathway

Inhibition of protein tyrosine phosphatase 1B by reactive oxygen species leads to maintenance of Ca2+ influx following store depletion in HEK 293 cells

Oxidant-impaired intracellular Ca2+ signaling in pancreatic acinar cells: role of the plasma membrane Ca2+-ATPase

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Oxidant-impaired intracellular Ca²⁺ signaling in pancreatic acinar cells: role of the plasma membrane Ca²⁺-ATPase