Pretreatment with PTD-Calbindin D 28k Alleviates Rat Brain Injury Induced by Ischemia and Reperfusion

Fan, Yuding; Shi, Langfeng; Gu, Yuehua; Zhao, Yanxin; Xie, Jun; Qiao, Jie; Yang, Guo‐Yuan; Wang, Yang; Lü, Chuan-Zhen

doi:10.1038/sj.jcbfm.9600373

Cited by 36 publications

(23 citation statements)

References 56 publications

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“…Over-expression of calbindin reduces oxidative stress and preserves mitochondrial function in Alzheimer's disease model [22]. Mover, calbindin over-expression protects neurons from focal cerebral ischemia and protein transduction domain (PTD)-calbindin D 28k pretreatment attenuates rat brain injury induced by ischemia and reperfusion [23,24]. RT-PCR and Western blot analyses showed decreases in calbindin protein during MCAO-induced brain injury.…”

Section: Discussionmentioning

confidence: 99%

Focal cerebral ischemic injury decreases calbindin expression in brain tissue and HT22 cells

et al. 2013

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Calbindin is a calcium binding protein that controls intracellular calcium levels and has a neuroprotective function against apoptotic stimuli. We investigated the expression of calbindin in ischemic brain injury. Focal cerebral ischemia was induced in male rats by middle cerebral artery occlusion (MCAO) and cerebral cortices were collected 24 h after MCAO. Cerebral ischemia significantly increased infarct volume. RT-PCR and Western blot analyses showed that MCAO injury induced a decrease of calbindin expression. Moreover, immunohistochemical staining showed that the number of calbindin-positive cells decreased in ischemic regions of MCAO-operated animals. In cultured hippocampal-derived cell lines, glutamate exposure increased intracellular Ca2+ concentrations and decreased calbindin expression. Taken together, both in vivo and in vitro results demonstrated decreases of calbindin after neuronal cell injury. These results suggest that decreases of calbindin in ischemic brain injury contribute to neuronal cell death.

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Section: Discussionmentioning

confidence: 99%

Focal cerebral ischemic injury decreases calbindin expression in brain tissue and HT22 cells

et al. 2013

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“…In rat models of ischemic brain injury, Calb1 over-expression or pretreatment led to an improvement in neuronal survival and a decrease in infarct volume [8, 34]. The involvement of Calb1 in learning and memory, as well as neurodegenerative disorders, has also been explored in animal models.…”

Section: Introductionmentioning

confidence: 99%

Hippocampal calbindin-1 immunoreactivity correlate of recognition memory performance in aged mice

Soontornniyomkij

Risbrough

Young

et al. 2012

Neuroscience Letters

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Aging-related dysregulation of neuronal calcium metabolism, which not only involves the control of calcium fluxes but also the cytosolic calcium buffering system such as calbindin-1 (Calb1), may disturb synaptic plasticity and thereby memory functioning. Calb1 expression has been shown to affect hippocampal long-term potentiation and learning and to play a neuroprotective role in animal models of ischemic brain injury and neurodegenerative disorders. We hypothesize that memory performance in aged mice correlates with neuronal Calb1 protein expression in the hippocampal formation. We studied a set of 18 aged and 22 young male C57BL/6N mice, in which the aged group performed poorer than the young in single-trial novel object recognition testing (two-tailed p=0.005, U test). Apparent decreases in the Calb1 immunoreactivity (measured by quantitative immunohistochemistry) in aged mice compared to that in young mice were not statistically significant either in the hippocampal CA1 subfield or dentate gyrus. In the aged mouse group, levels of Calb1 immunoreactivity both in the CA1 subfield and dentate gyrus correlated directly with the measure of recognition memory performance (Spearman rank correlation rs=0.47 and 0.48, two-tailed p=0.047 and 0.044, respectively). Our results suggest that hippocampal Calb1 expression affects memory performance in aged mice probably via its role in maintaining neuronal calcium homeostasis. Alternatively, our finding of lower Calb1 immunoreactivity with poorer memory performance in aged mice might be attributed to saturation of Calb1 protein by higher levels of intracellular calcium, due to aging-related dysregulation of neuronal calcium fluxes.

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“…Calbindin, a major calcium-binding protein in the cytosol, plays a critical role during intracellular Ca 2þ homeostasis and is implicated in neuroprotection (when expressed at high levels) owing to its ability to buffer free intracellular Ca 2þ [109][110][111]. Dopamine-D1 receptor signalling is modulated by calcium level and NO [2,67].…”

Section: (A) Mechanisms Linking No With Cox2 Expressionmentioning

confidence: 99%

Are cyclooxygenase-2 and nitric oxide involved in the dyskinesia of Parkinson's disease induced byl-DOPA?

Bortolanza

Padovan-Neto

Cavalcanti-Kiwiatkoski

et al. 2015

Phil. Trans. R. Soc. B

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Inflammatory mechanisms are proposed to play a role in l -DOPA-induced dyskinesia. Cyclooxygenase-2 (COX2) contributes to inflammation pathways in the periphery and is constitutively expressed in the central nervous system. Considering that inhibition of nitric oxide (NO) formation attenuates l -DOPA-induced dyskinesia, this study aimed at investigating if a NO synthase (NOS) inhibitor would change COX2 brain expression in animals with l -DOPA-induced dyskinesia. To this aim, male Wistar rats received unilateral 6-hydroxydopamine microinjection into the medial forebrain bundle were treated daily with l -DOPA (21 days) combined with 7-nitroindazole or vehicle. All hemi-Parkinsonian rats receiving l -DOPA showed dyskinesia. They also presented increased neuronal COX2 immunoreactivity in the dopamine-depleted dorsal striatum that was directly correlated with dyskinesia severity. Striatal COX2 co-localized with choline-acetyltransferase, calbindin and DARPP-32 (dopamine-cAMP-regulated phosphoprotein-32), neuronal markers of GABAergic neurons. NOS inhibition prevented l -DOPA-induced dyskinesia and COX2 increased expression in the dorsal striatum. These results suggest that increased COX2 expression after l -DOPA long-term treatment in Parkinsonian-like rats could contribute to the development of dyskinesia.

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Pretreatment with PTD-Calbindin D 28k Alleviates Rat Brain Injury Induced by Ischemia and Reperfusion

Cited by 36 publications

References 56 publications

Focal cerebral ischemic injury decreases calbindin expression in brain tissue and HT22 cells

Focal cerebral ischemic injury decreases calbindin expression in brain tissue and HT22 cells

Hippocampal calbindin-1 immunoreactivity correlate of recognition memory performance in aged mice

Are cyclooxygenase-2 and nitric oxide involved in the dyskinesia of Parkinson's disease induced byl-DOPA?

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