Involvement of calmodulin in neuronal cell death

Shirasaki, Yasufumi; Kanazawa, Yoshito; Morishima, Yasuo; Makino, Mitsuhiro

doi:10.1016/j.brainres.2006.01.123

Cited by 14 publications

(11 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, calmodulin can increase the activity of phospholipase [ 40 ]. The activation of phospholipase causes the overload of Ca 2+ and the excessive activation of calmodulin signaling pathway, thereby resulting in nerve cell death [ 41 ]. The activation of CaM in our study might increase the Ca 2+ concentration inside cells and trigger nerve cell death, which further causes the death of mites.…”

Section: Discussionmentioning

confidence: 99%

RNA-Seq Analysis Reveals Candidate Targets for Curcumin againstTetranychus cinnabarinus

Liu

Zhang

et al. 2016

BioMed Research International

View full text Add to dashboard Cite

Tetranychus cinnabarinus is an important agricultural pest with a broad host range. We previously identified curcumin as a promising acaricidal compound against T. cinnabarinus. However, the acaricidal mechanism of curcumin remains unknown. In this study, RNA-seq was employed to analyze the transcriptome changes in T. cinnabarinus treated with curcumin or the solvent. A total of 105,706,297 clean sequence reads were generated by sequencing, with more than 90% of the reads successfully mapped to the reference sequence. The RNA-seq identified 111 and 96 differentially expressed genes between curcumin- and solvent-treated mites at 24 and 48 h after treatment, respectively. GO enrichment analysis of differentially expressed genes showed that the cellular process was the dominant group at both time points. Finally, we screened 23 differentially expressed genes that were functionally identical or similar to the targets of common insecticide/acaricides or genes that were associated with mite detoxification and metabolism. Calmodulin, phospholipase A2, and phospholipase C were activated upon curcumin treatment suggesting that the calcium channel related genes might play important roles in mite's response to curcumin. Overall our results revealed the global transcriptional changes in T. cinnabarinus after curcumin treatment to enable further identification of the targets of curcumin in mites.

show abstract

Section: Discussionmentioning

confidence: 99%

RNA-Seq Analysis Reveals Candidate Targets for Curcumin againstTetranychus cinnabarinus

Liu

Zhang

et al. 2016

BioMed Research International

View full text Add to dashboard Cite

show abstract

“…Calmodulin is an endogenous Ca 2+ buffer in neurons (Baimbridge et al 1992). Increases in Ca 2+ concentrations activate Ca 2+ -calmodulindependent pathways that may lead to cell death, while blocking calmodulin has been shown to inhibit brain injury after ischaemia (Shirasaki et al 2006). Calmodulin expression increased significantly in MS rats, reflecting a greater risk of cellular damage.…”

Section: Apoptosis and Calcium Signalling Proteinsmentioning

confidence: 99%

Exercise normalizes altered expression of proteins in the ventral hippocampus of rats subjected to maternal separation

Daniels

Marais

Stein³

et al. 2011

Experimental Physiology

View full text Add to dashboard Cite

Many studies have reported on the detrimental effects of early life adversity and the beneficial effects of exercise on brain function. However, the molecular mechanisms that underpin these various effects remain poorly understood. The advent of advanced proteomic analysis techniques has enabled simultaneous measurement of protein expression in a wide range of biological systems. We therefore used iTRAQ proteomic analysis of protein expression to determine whether exercise counteracts the detrimental effects of early life adversity in the form of maternal separation on protein expression in the brain. Rat pups were subjected to maternal separation from postnatal day 2 to 14 for 3 h day −1 or normally reared. At 40 days of age, half of the rats in each group (maternal separation and normally reared) were allowed to exercise voluntarily (access to a running wheel) for 6 weeks and the remainder kept as sedentary control animals. At 83 days of age, rats were killed and the ventral hippocampus was dissected for quantitative proteomic (iTRAQ) analysis. The iTRAQ proteomic analysis identified several proteins that had been altered by maternal separation, including proteins involved in neuronal structure, metabolism, signalling, anti-oxidative stress and neurotransmission, and that many of these proteins were restored to normal by subsequent exposure to voluntary exercise in adolescence. Our data show that a broad range of proteins play a role in the complex consequences of adversity and exercise.

show abstract

“…NMDA receptor allows nNOS to uncouple from its scaffolding protein and begin NO generation (1,35). Previous studies (48,50) have shown that a concentration of 100 M glutamate is toxic to neurons. On the basis of all of these findings, we tested various concentrations of glutamate to stimulate NMDA receptors.…”

Section: Effect Of Induced Hypotension On Perivascular and Tissuementioning

confidence: 99%

Cerebral microvascular dilation during hypotension and decreased oxygen tension: a role for nNOS

Bauser‐Heaton¹,

Bohlen²

2007

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Bauser-Heaton HD, Bohlen HG. Cerebral microvascular dilation during hypotension and decreased oxygen tension: a role for nNOS. Am J Physiol Heart Circ Physiol 293: H2193-H2201, 2007. First published July 13, 2007; doi:10.1152/ajpheart.00190.2007 and neuronal nitric oxide synthase (nNOS) are implicated as important contributors to cerebral vascular regulation through nitric oxide (NO). However, direct in vivo measurements of NO in the brain have not been used to dissect their relative roles, particularly as related to oxygenation of brain tissue. We found that, in vivo, rat cerebral arterioles had increased NO concentration ([NO]) and diameter at reduced periarteriolar oxygen tension (PO 2) when either bath oxygen tension or arterial pressure was decreased. Using these protocols with highly selective blockade of nNOS, we tested the hypothesis that brain tissue nNOS could donate NO to the arterioles at rest and during periods of reduced perivascular oxygen tension, such as during hypotension or reduced local availability of oxygen. The decline in periarteriolar PO 2 by bath manipulation increased [NO] and vessel diameter comparable with responses at similarly decreased PO 2 during hypotension. To determine whether the nNOS provided much of the vascular wall NO, nNOS was locally suppressed with the highly selective inhibitor N-(4S)- (4-amino-5-[aminoethyl]aminopentyl)-NЈ-nitroguanidine. After blockade, resting [NO], PO 2, and diameters decreased, and the increase in [NO] during reduced PO 2 or hypotension was completely absent. However, flow-mediated dilation during occlusion of a collateral arteriole did remain intact after nNOS blockade and the vessel wall [NO] increased to ϳ80% of normal. Therefore, nNOS predominantly increased NO during decreased periarteriolar oxygen tension, such as that during hypotension, but eNOS was the dominant source of NO for flow shear mechanisms. nitric oxide; brain; arterioles; in vivo; microelectrode; neuronal nitric oxide synthase SUPPRESSION OF NITRIC OXIDE (NO) formation by an intravascular arginine analog decreases cerebral blood flow by 10 -40% (17,18,40,42). This indicates that a source of NO actively influences cerebral resistance vessels at rest. Furthermore, Jones et al. (25) and Kajita et al. (26) found that, during hypotension, the lower limit of brain blood flow autoregulation was increased to ϳ90 mmHg in the presence of nitroarginine compared with ϳ65 mmHg in the natural state. The observations of reduced resting blood flow and impaired flow autoregulation indicate that NO regulation has important roles in both maintaining brain resting blood flow and dilatory responses to hypotension. These various observations would predict that, when the various NO synthase (NOS) isoforms are inhibited, even a mild reduction in arterial blood pressure would compromise brain blood flow and tissue oxygenation.Exactly how NO mechanisms are involved in brain blood flow regulation are difficult to predict but may involve feedback processes linked to oxygen. In studies of the small int...

show abstract

Involvement of calmodulin in neuronal cell death

Cited by 14 publications

References 41 publications

RNA-Seq Analysis Reveals Candidate Targets for Curcumin againstTetranychus cinnabarinus

RNA-Seq Analysis Reveals Candidate Targets for Curcumin againstTetranychus cinnabarinus

Exercise normalizes altered expression of proteins in the ventral hippocampus of rats subjected to maternal separation

Cerebral microvascular dilation during hypotension and decreased oxygen tension: a role for nNOS

Contact Info

Product

Resources

About