Amyloid β peptide enhanced bradykinin-mediated inositol (1,4,5)trisphosphate formation and cytosolic free calcium

Huang, Hsueh‐Meei; Ou, Hsio-Chung; Hsueh, Shon-Jean

doi:10.1016/s0024-3205(98)00260-4

Cited by 19 publications

(9 citation statements)

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“…However, the widespread distribution of bradykinin receptors in regions to which no known functions can be attributed currently will likely provide the most fascinating and fruitful avenues for investigators. Just as bradykinin might play a diverse role in the normal function of the CNS, it might play an equally important role in pathological processes, including traumatic brain injury (Ellis et al, 1989), ischemia (Kamiya et al, 1993;Relton et al, 1997a-c), nerve regeneration (Petersen et al, 1998), and the neurodegeneration seen in the brain during Alzheimer's disease (Huang et al, 1991(Huang et al, , 1995(Huang et al, , 1998Racchi et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

B2 bradykinin receptor immunoreactivity in rat brain

et al. 2000

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Bradykinin has long been known to exist in the central nervous system and has been hypothesized to mediate specific functions. Despite an increasing understanding of the functions of bradykinin, little is known about the cell types expressing the bradykinin receptor within the brain. The present investigation employed a monoclonal antibody directed against the 15-amino-acid portion of the C-terminal of the human bradykinin B2 receptor to establish the cellular distribution of bradykinin B2 receptor immunoreactivity in the rat brain. Bradykinin B2 receptor immunoreactivity was ubiquitously and selectively observed in neurons, including those within the olfactory bulb, cerebral cortex, hippocampus, basal forebrain, basal ganglia, thalamus, hypothalamus, cerebellum, and brainstem nuclei. Bradykinin B2 receptor immunoreactivity was also present in the circumventricular organs including choroid plexus, subfornical organ, median eminence, and area postrema. Double-labeling experiments colocalizing the bradykinin B2 receptor with the neuronal marker NeuN or the astrocytic marker glial fibrillary acidic protein revealed that virtually 100% of the bradykinin B2 receptor-immunoreactive positive cells were neurons. The widespread distribution of bradykinin B2 receptor immunoreactivity in neuronal compartments suggests a greater than previously appreciated role for this peptide in neuronal function.

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Section: Discussionmentioning

confidence: 99%

B2 bradykinin receptor immunoreactivity in rat brain

et al. 2000

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“…Extracellular Ab influences intracellular Ca 2þ homeostasis in vitro (33,53) and in vivo (6,7,38,39). In addition to disrupting APP processing, many FAD-linked PS mutations have been shown to affect Ca 2þ homeostasis by Ab independent mechanisms (40,64).…”

Section: Disrupted Intracellular Camentioning

confidence: 99%

Enhanced ROS Generation Mediated by Alzheimer's Disease Presenilin Regulation of InsP₃R Ca²⁺ Signaling

Müller

Cheung

Foskett

2011

Antioxidants & Redox Signaling

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Familial Alzheimer's disease (FAD) is caused by mutations in amyloid precursor protein and presenilins (PS1, PS2). Many FAD-linked PS mutations affect intracellular calcium (Ca 2+ ) homeostasis by proximal mechanisms independent of amyloid production by dramatically enhancing gating of the inositol trisphosphate receptor (InsP 3 R) intracellular Ca 2+ release channel by a gain-of-function effect that mirrors genetics of FAD and is independent of secretase activity. Electrophysiological recordings of InsP 3 R in FAD patient B cells, cortical neurons of asymptomatic PS1-AD mice, and other cells revealed they have higher occupancy in a high open probability burst mode, resulting in enhanced Ca 2+ signaling. Exaggerated Ca 2+ signaling through this mechanism results in enhanced generation of reactive oxygen species, believed to be an important component in AD pathogenesis. Exaggerated Ca 2+ signaling through InsP 3 R-PS interaction is a disease specific and robust proximal mechanism in AD that may contribute to the pathology of AD by enhanced generation of reactive oxygen species.

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“…Rat pheochromocytoma cells (PC12) were grown in NUNC T75 flasks (Naperville, IL) in DMEM supplemented with 5% horse serum and 10% FBS, and were maintained in a 10% CO 2 humidified incubator at 37°C as previously described [Huang et al, 1998[Huang et al, , 1999. The cells were subcultured and grown on 12-well plates, 3.5-cm Petri dishes for 2 days before the experiments.…”

Section: Cell Culturesmentioning

confidence: 99%

“…[Ca 2ϩ ] i was determined as described previously [Huang et al, 1998]. Briefly, cells on polylysine-coated glass coverslips were loaded with 2 M fura-2AM at 37°C for 30 min, then they were rinsed with HEPES buffer.…”

Section: Measurement Of [Ca 2؉ ] Imentioning

confidence: 99%

“…After incubation, the cultured media were collected and centrifuged at 10,000g for 5 min. Fifty microliters of the supernatants were transferred to microtiter plates and the activity of LDH released into the medium was measured at 492 nm at a reference wavelength of 630 nm using a spectrophotometric plate reader (MRX, Dynatech, Chantilly, VA) as previously described [Huang et al, 1998]. …”

Section: Measurement Of Ldhmentioning

confidence: 99%

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Differential alteration of catecholamine release during chemical hypoxia is correlated with cell toxicity and is blocked by protein kinase C inhibitors in PC12 cells

et al. 2000

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Release of neurotransmitters, including dopamine and glutamate, has been implicated in hypoxia/ischemia-induced alterations in neuronal function and in subsequent tissue damage. Although extensive studies have been done on the mechanism underlying the changes in glutamate release, few have examined the mechanism that is responsible for the changes in catecholamines. Rat pheochromocytoma-12 (PC12) cells synthesize, store, and release catecholamines including DA and NE. Therefore, we used HPLC and ED to evaluate extracellular DA and NE concentrations in a medium during chemical hypoxia in PC12 cells. Chemical hypoxia produced by KCN induced differential release of DA and NE. Under normal glucose conditions, KCN induced release of NE, but not DA. Under glucose-free conditions, KCN-induced release of DA was elevated transiently, whereas the release of NE increased progressively. Under parallel conditions, KCN biphasically elevated the level of cytosolic free calcium ([CA(2+)](i)) in glucose-free DMEM, peaking at 95 +/- 18 nM at 1,107 +/- 151 s, followed by a new plateau level at 249 +/- 24 nM sustained from 4,243 +/- 466 to 5,263 +/- 440 s. Cell toxicity, as measured by LDH release, was increased significantly by KCN in glucose-free DMEM but was diminished in the presence of glucose, and was correlated with DA release by chemical hypoxia. The protein kinase C (PKC) inhibitor GO6976 or staurosporine inhibited KCN-induced LDH release as well as the release of NE and DA. Taken together, selective activation of DA but not NE was correlated with the LDH release by chemical hypoxia, and was diminished with GO6976 or staurosporine. These results suggest that selective activation of PKC isoforms is involved in the chemical hypoxia-induced DA release, which may lead to neuronal cell toxicity.

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Amyloid β peptide enhanced bradykinin-mediated inositol (1,4,5)trisphosphate formation and cytosolic free calcium

Cited by 19 publications

References 19 publications

B2 bradykinin receptor immunoreactivity in rat brain

B2 bradykinin receptor immunoreactivity in rat brain

Enhanced ROS Generation Mediated by Alzheimer's Disease Presenilin Regulation of InsP₃R Ca²⁺ Signaling

Differential alteration of catecholamine release during chemical hypoxia is correlated with cell toxicity and is blocked by protein kinase C inhibitors in PC12 cells

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Amyloid β peptide enhanced bradykinin-mediated inositol (1,4,5)trisphosphate formation and cytosolic free calcium

Cited by 19 publications

References 19 publications

B2 bradykinin receptor immunoreactivity in rat brain

B2 bradykinin receptor immunoreactivity in rat brain

Enhanced ROS Generation Mediated by Alzheimer's Disease Presenilin Regulation of InsP3R Ca2+ Signaling

Differential alteration of catecholamine release during chemical hypoxia is correlated with cell toxicity and is blocked by protein kinase C inhibitors in PC12 cells

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Enhanced ROS Generation Mediated by Alzheimer's Disease Presenilin Regulation of InsP₃R Ca²⁺ Signaling