Increased expression of calponin-3 in epileptic patients and experimental rats

Han, Yanbing; Yin, Huan; Xu, Yali; Luo, Jie; Wang, Xuefeng; Chen, Guojun

doi:10.1016/j.expneurol.2011.11.014

Cited by 18 publications

(9 citation statements)

References 30 publications

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“…Along these lines, in this study reactive astrocyte strongly expressing GFAP was preferentially observed in the penumbral region and these astrocytes were co-labeled with calponin 3. Previously, it has been reported that in case of epileptic patients expression level of calponin 3 was increased in MAP2-positive neurons [7]. In addition, in animal models of epilepsy with pilocarpine, calponin 3 immunoreactivity was specifically increased in the inner one-third of the molecular layer of the dentate gyrus and double immunolabeling revealed that calponin 3 was localized in the dendritic spines.…”

Section: Discussionmentioning

confidence: 83%

“…For example, it was reported that calponin 3 is expressed in radial glia, glia limitans, Bergmann glia and mature astrocytes in postnatal rat brains, although it was absent in mature astrocytes in culture [11]. In addition, in the human cortices faint calponin-3 staining was reported in astrocytes [7]. Further, cultured cortical astrocytes express calponin heterogeneously [16].…”

Section: Discussionmentioning

confidence: 99%

“…In addition, the elevation level of calponin 3 in the cerebrospinal fluid (CSF) was highly correlated with disease duration [7]. Further, calponin 3 immunoreactivity was clearly increased in the inner one-third of the molecular layer of the dentate gyrus at 1 and 2 weeks after pilocarpine-induced seizures, which indicates that calponin 3 is involved in mossy fiber sprouting and neo-synaptogenesis [5].…”

Section: Introductionmentioning

confidence: 98%

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Expression of Calponin 3 in the Striatum Following 3-Nitropropionic Acid-induced Neurotoxicity

Choi¹

2013

Journal of Life Science

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Calponin 3 is an F-actin-binding protein and plays a key role in regulating spine plasticity and synaptic activity in neurons. Unlike the other subtypes, calponin 1 and 2, which are expressed in smooth and cardiac muscle cells, calponin 3 is highly expressed in the brain. The goal of this study was to elucidate the spatiotemporal expression pattern of calponin 3 following repeated administration of 3-nitropropionic acid in mice. The repeated administration of 3-nitropropionic acid generated necrotic neuronal cell death in the striatum. Calponin 3 was up-regulated in the neuroprotective penimbral region from 1.5 days after the last injection and thereafter. Double immunofluorescence study revealed that calponin 3 was induced in GFAP-positive astrocytes. These results suggest that calponin 3 induction in the neuroprotective penumbral area following 3-nitropropionic acid intoxication may play a key role in reactive astrogliosis in the striatum.

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

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Expression of Calponin 3 in the Striatum Following 3-Nitropropionic Acid-induced Neurotoxicity

Choi¹

2013

Journal of Life Science

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“…Similarly, we found an upregulation of CNN3 expression in the ZNF711 patients. Significant upregulation of Calponin-3 was also found in the temporal cortices and cerebrospinal fluid of epilepsy patients when compared to non-epileptic controls (Han et al, 2012). In ZNF711 patients, the only significantly downregulated gene was FYN, encoding a nonreceptor protein tyrosine kinase expressed in neurons and glia (Bare et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Mutations in two large pedigrees highlight the role of ZNF711 in X-linked intellectual disability

Werf

Dijck

Reyniers

et al. 2017

Gene

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Intellectual disability (ID) affects approximately 1-2% of the general population and is characterized by impaired cognitive abilities. ID is both clinically as well as genetically heterogeneous, up to 2000 genes are estimated to be involved in the emergence of the disease with various clinical presentations. For many genes, only a few patients have been reported and causality of some genes has been questioned upon the discovery of apparent loss-offunction mutations in healthy controls. Description of additional patients strengthens the evidence for the involvement of a gene in the disease and can clarify the clinical phenotype associated with mutations in a particular gene. Here, we present two large four-generation families with a total of 11 males affected with ID caused by mutations in ZNF711, thereby expanding the total number of families with ID and a ZNF711 mutation to four. Patients with mutations in ZNF711 all present with mild to moderate ID and poor speech accompanied by additional features in some patients, including autistic features and mild facial dysmorphisms, suggesting that ZNF711 mutations cause non-syndromic ID.

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“…The lithium‐pilocarpine‐induced rat epilepsy model, which has been used widely and was described previously (Han et al, ; Xu et al, ), is applied here to investigate the expression level and pattern of HIF‐1α. All animals were randomly divided into the normal control group ( n = 5) and the experimental groups ( n = 35).…”

Section: Methodsmentioning

confidence: 99%

Altered expression of hypoxia‐Inducible factor‐1α participates in the epileptogenesis in animal models

Jiang²,

Chen

et al. 2014

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Although epilepsy is a common neurological disorder, its mechanism(s) are still not completely understood. Hypoxia can lead to neuronal cell death and angiogenesis, and the same mechanisms were also found in epilepsy. Hypoxia-inducible factor-1α (HIF-1α) is an important transcription protein that regulates gene expression in the brain and other tissues in response to decreases in oxygen availability. However, little is known regarding the expression of HIF-1α in the epileptic brain and whether HIF-1α interventions affect the epileptic process. The aims of this study are to investigate the expression profile of HIF-1α in rat models and to explore the role of HIF-1α in epilepsy. We performed Western blots and immunofluorescence in a lithium-pilocarpine rat epilepsy model. To determine the role of HIF-1α in epilepsy, we used the HIF-1α agonist DMOG and inhibitor KC7F2 to detect changes in the animal behavior in pentylenetetrazole (PTZ) and lithium-pilocarpine epilepsy models. The expression of HIF-1α was significantly increased after pilocarpine-induced status epilepticus. DMOG significantly prolonged the latent period in the PTZ kindling model and decreased the rate of spontaneous recurrent seizures during the chronic stage in the lithium-pilocarpine model. Conversely, the inhibitor KC7F2 produced an opposite behavioral change. Interestingly, both KC7F2 and DMOG had no effect on the acute stage of pilocarpine model and PTZ convulsive model. Our study suggests that upregulated HIF-1α may be involved in the process of epileptogenesis but not in the acute stage of epilepsy. The modulation of HIF-1α may offer a novel therapeutic target in epilepsy.

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Increased expression of calponin-3 in epileptic patients and experimental rats

Cited by 18 publications

References 30 publications

Expression of Calponin 3 in the Striatum Following 3-Nitropropionic Acid-induced Neurotoxicity

Expression of Calponin 3 in the Striatum Following 3-Nitropropionic Acid-induced Neurotoxicity

Mutations in two large pedigrees highlight the role of ZNF711 in X-linked intellectual disability

Altered expression of hypoxia‐Inducible factor‐1α participates in the epileptogenesis in animal models

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