Distribution and Cellular Localization of KCC2 in the Ferret Neocortex

2018 ◽  
Vol 40 (1) ◽  
pp. 39-53
Author(s):  
Francis T. Djankpa ◽  
Oluwole B. Akinola ◽  
Sharon L. Juliano
Keyword(s):  
Cerebral Cortex ◽  
Expression Pattern ◽  
Cellular Localization ◽  
Regional Distribution ◽  
Neuronal Markers ◽  
Chloride Homeostasis ◽  
Mature Neurons ◽  
Laminar Pattern ◽  
Differential Pattern ◽  
Cellular Compartments

KCC2 (a brain-specific potassium-chloride cotransporter) affects development of the cerebral cortex, including aspects of neuronal migration and cellular maturation and differentiation. KCC2 also modulates chloride homeostasis by influencing the switch of GABA from depolarizing in young neurons to hyperpolarizing in mature neurons. We describe the expression pattern, regional distribution, and cellular colocalization of KCC2 in the ferret cortex in normal kits and those treated with methylazoxymethanol acetate (MAM). We earlier developed a model of impaired cortical development by injecting MAM during mid-cortical gestation, which briefly interferes with neuronal production and additionally results in increased levels of KCC2 at P0. Using immunohistochemistry, we show a shift in KCC2 expression during development, being high in the subplate at P0, repositioning into a subtle laminar pattern in the neocortex at P7-P14, and becoming homogeneous at P35. KCC2 colocalizes with neuronal markers in the developing and mature cerebral cortex of normal ferrets and those treated with MAM, but shows a differential pattern of expression at different ages and locates in distinct cellular compartments during development. Subcellular localization shows that KCC2 predominantly situates in the membrane fraction of neocortical samples. These findings reveal that KCC2 colocalizes differentially with neurons and its expression pattern alters during development.

scholarly journals Regulation of Mineralocorticoid Receptor Expression during Neuronal Differentiation of Murine Embryonic Stem Cells

Endocrinology ◽  
2010 ◽  
Vol 151 (5) ◽  
pp. 2244-2254 ◽  
Author(s):  
Mathilde Munier ◽  
Geri Meduri ◽  
Say Viengchareun ◽  
Philippe Leclerc ◽  
Damien Le Menuet ◽  
...  
Keyword(s):  
Neuronal Differentiation ◽  
Mineralocorticoid Receptor ◽  
Fluorescent Protein ◽  
Morphological Changes ◽  
Critical Role ◽  
Embryonic Stem ◽  
Embryoid Bodies ◽  
Receptor Expression ◽  
Neuronal Markers ◽  
Mature Neurons

Mineralocorticoid receptor (MR) plays a critical role in brain function. However, the regulatory mechanisms controlling neuronal MR expression that constitutes a key element of the hormonal response are currently unknown. Two alternative P1 and P2 promoters drive human MR gene transcription. To examine promoter activities and their regulation during neuronal differentiation and in mature neurons, we generated stably transfected recombinant murine embryonic stem cell (ES) lines, namely P1-GFP and P2-GFP, in which each promoter drove the expression of the reporter gene green fluorescent protein (GFP). An optimized protocol, using embryoid bodies and retinoic acid, permitted us to obtain a reproducible neuronal differentiation as revealed by the decrease in phosphatase alkaline activity, the concomitant appearance of morphological changes (neurites), and the increase in the expression of neuronal markers (nestin, β-tubulin III, and microtubule-associated protein-2) as demonstrated by immunocytochemistry and quantitative PCR. Using these cell-based models, we showed that MR expression increased by 5-fold during neuronal differentiation, MR being preferentially if not exclusively expressed in mature neurons. Although the P2 promoter was always weaker than the P1 promoter during neuronal differentiation, their activities increased by 7- and 5-fold, respectively, and correlated with MR expression. Finally, although progesterone and dexamethasone were ineffective, aldosterone stimulated both P1 and P2 activity and MR expression, an effect that was abrogated by knockdown of MR by small interfering RNA. In conclusion, we provide evidence for a tight transcriptional control of MR expression during neuronal differentiation. Given the neuroprotective and antiapoptotic role proposed for MR, the neuronal differentiation of ES cell lines opens potential therapeutic perspectives in neurological and psychiatric diseases.

scholarly journals Multiple cellular compartments engagement in Nicotiana benthamiana-peanut stunt virus-satRNA interactions revealed by systems biology approach

2021 ◽  
Author(s):  
Barbara Wrzesińska ◽  
Agnieszka Zmienko ◽  
Lam Dai Vu ◽  
Ive De Smet ◽  
Aleksandra Obrępalska-Stęplowska
Keyword(s):  
Virus Infection ◽  
Nicotiana Benthamiana ◽  
Cellular Localization ◽  
Plant Interactions ◽  
Satellite Rna ◽  
Functional Connections ◽  
Cell Compartments ◽  
Wide Range ◽  
Peanut Stunt Virus ◽  
Cellular Compartments

Abstract Key message PSV infection changed the abundance of host plant’s transcripts and proteins associated with various cellular compartments, including ribosomes, chloroplasts, mitochondria, the nucleus and cytosol, affecting photosynthesis, translation, transcription, and splicing. Abstract Virus infection is a process resulting in numerous molecular, cellular, and physiological changes, a wide range of which can be analyzed due to development of many high-throughput techniques. Plant RNA viruses are known to replicate in the cytoplasm; however, the roles of chloroplasts and other cellular structures in the viral replication cycle and in plant antiviral defense have been recently emphasized. Therefore, the aim of this study was to analyze the small RNAs, transcripts, proteins, and phosphoproteins affected during peanut stunt virus strain P (PSV-P)–Nicotiana benthamiana interactions with or without satellite RNA (satRNA) in the context of their cellular localization or functional connections with particular cellular compartments to elucidate the compartments most affected during pathogenesis at the early stages of infection. Moreover, the processes associated with particular cell compartments were determined. The ‘omic’ results were subjected to comparative data analyses. Transcriptomic and small RNA (sRNA)–seq data were obtained to provide new insights into PSV-P–satRNA–plant interactions, whereas previously obtained proteomic and phosphoproteomic data were used to broaden the analysis to terms associated with cellular compartments affected by virus infection. Based on the collected results, infection with PSV-P contributed to changes in the abundance of transcripts and proteins associated with various cellular compartments, including ribosomes, chloroplasts, mitochondria, the nucleus and the cytosol, and the most affected processes were photosynthesis, translation, transcription, and mRNA splicing. Furthermore, sRNA-seq and phosphoproteomic analyses indicated that kinase regulation resulted in decreases in phosphorylation levels. The kinases were associated with the membrane, cytoplasm, and nucleus components.

Protein kinase C-α and the regulation of diverse cell responses

2017 ◽  
Vol 8 (3-4) ◽  
pp. 143-153 ◽  
Author(s):  
Rishi Kant Singh ◽  
Sanjay Kumar ◽  
Pramod Kumar Gautam ◽  
Munendra Singh Tomar ◽  
Praveen Kumar Verma ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Cellular Localization ◽  
Cellular Transformation ◽  
Cell Types ◽  
Adapter Proteins ◽  
Cellular Functions ◽  
Cell Responses ◽  
Kinase C ◽  
Cellular Compartments

AbstractProtein kinase C (PKC) comprises a family of lipid-sensitive enzymes that have been involved in a broad range of cellular functions. PKC-α is a member of classical PKC with ubiquitous expression and different cellular localization. This unique PKC isoform is activated by various signals which evoke lipid hydrolysis, after activation it interacts with various adapter proteins and is localized to specific cellular compartments where it is devised to work. The universal expression and activation by various stimuli make it a perfect player in uncountable cellular functions including differentiation, proliferation, apoptosis, cellular transformation, motility, adhesion and so on. However, these functions are not intrinsic properties of PKC-α, but depend on cell types and conditions. The activities of PKC-α are managed by the various pharmacological activators/inhibitors and antisense oligonucleotides. The aim of this review is to elaborate the structural feature, and provide an insight into the mechanism of PKC-α activation and regulation of its key biological functions in different cellular compartments to develop an effective pharmacological approach to regulate the PKC-α signal array.

scholarly journals The laminar pattern of resting state in human cerebral cortex

2021 ◽  
Vol 76 ◽  
pp. 8-16
Author(s):  
Anna Rita Egbert ◽  
Emilia Łojek ◽  
Bharat Biswal ◽  
Agnieszka Pluta
Keyword(s):  
Cerebral Cortex ◽  
Resting State ◽  
Human Cerebral Cortex ◽  
Laminar Pattern

scholarly journals Effect of Mitochondrial and Cytosolic FXN Isoform Expression on Mitochondrial Dynamics and Metabolism

2020 ◽  
Vol 21 (21) ◽  
pp. 8251
Author(s):  
Mauro Agrò ◽  
Javier Díaz-Nido
Keyword(s):  
Cross Talk ◽  
Cellular Localization ◽  
Mitochondrial Dynamics ◽  
In Vitro Models ◽  
Mitochondrial Network ◽  
Functional Roles ◽  
Cellular Models ◽  
Recessive Mutations ◽  
Cellular Compartments

Friedreich’s ataxia (FRDA) is a neurodegenerative disease caused by recessive mutations in the frataxin gene that lead to a deficiency of the mitochondrial frataxin (FXN) protein. Alternative forms of frataxin have been described, with different cellular localization and tissue distribution, including a cerebellum-specific cytosolic isoform called FXN II. Here, we explored the functional roles of FXN II in comparison to the mitochondrial FXN I isoform, highlighting the existence of potential cross-talk between cellular compartments. To achieve this, we transduced two human cell lines of patient and healthy subjects with lentiviral vectors overexpressing the mitochondrial or the cytosolic FXN isoforms and studied their effect on the mitochondrial network and metabolism. We confirmed the cytosolic localization of FXN isoform II in our in vitro models. Interestingly, both cytosolic and mitochondrial isoforms have an effect on mitochondrial dynamics, affecting different parameters. Accordingly, increases of mitochondrial respiration were detected after transduction with FXN I or FXN II in both cellular models. Together, these results point to the existence of a potential cross-talk mechanism between the cytosol and mitochondria, mediated by FXN isoforms. A more thorough knowledge of the mechanisms of action behind the extra-mitochondrial FXN II isoform could prove useful in unraveling FRDA physiopathology.

The effects of low-level lead exposure in developing rats: changes in circadian locomotor activity and hippocampal noradrenaline turnover

1984 ◽  
Vol 62 (4) ◽  
pp. 430-435 ◽  
Author(s):  
M. F. Collins ◽  
P. D. Hrdina ◽  
E. Whittle ◽  
R. L. Singhal
Keyword(s):  
Cerebral Cortex ◽  
Locomotor Activity ◽  
Lead Exposure ◽  
Turnover Rate ◽  
Regional Distribution ◽  
Spontaneous Locomotor Activity ◽  
Noradrenaline Turnover ◽  
Noradrenaline Content ◽  
Noradrenergic Function ◽  
Noradrenaline Levels

The circadian spontaneous locomotor activity of rats exposed to 0.1 mg lead/kg, po from 3 days until 4 and 6 weeks of age was similar to that of controls. However, hyperactivity during initial hours of recording was observed in rats that were treated with lead (Pb) until 8 weeks of age. When treatment was discontinued for 2 weeks, previously Pb-exposed rats had a tendency to be hypoactive. The elevated locomotor activity in 8-week-old lead-treated rats was not accompanied by any significant changes of noradrenaline levels in the cerebral cortex or hippocampus. Alterations in noradrenaline content of the hippocampus were, however, observed in rats that had been treated with Pb for 4 and 6 weeks. The turnover rate of noradrenaline in the hippocampus was also found to be significantly reduced following treatment for 6 weeks. Regional distribution of Pb in the brains of lead-exposed rats showed a large accumulation of the metal in the hippocampus. The alterations of the noradrenergic function in the hippocampus may be associated with the preferential storage of lead in this region.

scholarly journals The Progression and Topographic Distribution of Interleukin-1β Expression after Permanent Middle Cerebral Artery Occlusion in the Rat

1999 ◽  
Vol 19 (1) ◽  
pp. 87-98 ◽  
Author(s):  
Christine A. Davies ◽  
Sarah A. Loddick ◽  
Sylvie Toulmond ◽  
R. Paul Stroemer ◽  
Joanne Hunt ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Corpus Callosum ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cellular Localization ◽  
Interleukin 1 ◽  
Artery Occlusion ◽  
Interleukin 1Β ◽  
Surrounding Tissue ◽  
Topographic Distribution

The cytokine interleukin-1 (IL-1) has been implicated in the exacerbation of ischemic damage in the brains of rodents. This study has ascertained the cellular localization and chronologic and topographic distribution of pro/mature interleukin-1β (IL-1β) protein 0.5, 1, 2, 6, 24, and 48 hours after ischemia by subjecting rats to permanent unilateral occlusion of the middle cerebral artery. Interleukin-1β was localized immunocytochemically in vibratome sections of perfusion-fixed brains. The cells that expressed IL-1β had the morphologic features of microglia and macrophages. Interleukin-1β was first detected 1 hour after occlusion in ipsilateral meningeal macrophage-like cells. By 6 hours, pro/mature IL-1β-immunoreactive (IL-1βir) putative microglia were present in the ischemic cerebral cortex, corpus callosum, caudoputamen, and surrounding tissue. By 24 and 48 hours after ischemia, the number and spread of IL-1βir cells increased greatly, including those resembling activated microglia and macrophages, as the core of the infarct became infiltrated. Interleukin-1βir cells also were present in apparently undamaged tissue, adjacent to the lesion ipsilaterally, and contralaterally in the cerebral cortex, dorsal corpus callosum, dorsal caudoputamen, and hippocampus. These results support the functional role of IL-1 in ischemic brain damage and reveal a distinct temporal and spatial expression of IL-1β protein in cells believed to be microglia and macrophages.

Sign in / Sign up

Export Citation Format

Share Document