scholarly journals The Pancreatic Homeodomain Transcription Factor IDX1/IPF1 Is Expressed in Neural Cells during Brain Development

Endocrinology ◽  
1999 ◽  
Vol 140 (8) ◽  
pp. 3857-3860 ◽  
Author(s):  
Beatriz Perez-Villamil ◽  
Petra T. Schwartz ◽  
Mario Vallejo

Abstract Expression of the homeodomain transcription factor IDX1/IPF1 has been shown to be restricted to cells in the developing foregut that form the pancreatic primordium. In the adult, IDX1/IPF1 is expressed in the duodenum and pancreatic islets. The IDX1/IPF1 gene is required for pancreatic development, and in the human, heterozygous mutations have been linked to diabetes mellitus. In the present communication, we report that IDX1/IPF1 is expressed in discrete cells of the rat central nervous system during embryonic development. Using RT-PCR, IDX1/IPF1 mRNA was detected in neural precursor RC2.E10 cells, as well as in both forebrain and hindbrain of developing rats at embryonic day 15 (E15). The presence of IDX1/IPF1 protein was confirmed by Western immunoblotting. Immunohistochemical analyses of sagittal sections of E15 rats demonstrated the presence of scattered IDX1/IPF1-immunopositive cells in the forebrain. Finally, electrophoretic mobility shift assays using nuclear extracts from neural cells revealed the presence of IDX1/IPF1 bound to a putative homeodomain protein DNA-binding site present in the promoter of the glial fibrillary acidic protein gene. Our results suggest that IDX1/IPF1 may have previously unsuspected extrapancreatic functions during development of neural cells in the central nervous system.

Open Biology ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 190245
Author(s):  
Eléanor Simon ◽  
Sergio Fernández de la Puebla ◽  
Isabel Guerrero

Specific neuropeptides regulate in arthropods the shedding of the old cuticle (ecdysis) followed by maturation of the new cuticle. In Drosophila melanogaster , the last ecdysis occurs at eclosion from the pupal case, with a post-eclosion behavioural sequence that leads to wing extension, cuticle stretching and tanning. These events are highly stereotyped and are controlled by a subset of crustacean cardioactive peptide (CCAP) neurons through the expression of the neuropeptide Bursicon (Burs). We have studied the role of the transcription factor Odd-paired (Opa) during the post-eclosion period. We report that opa is expressed in the CCAP neurons of the central nervous system during various steps of the ecdysis process and in peripheral CCAP neurons innerving the larval muscles involved in adult ecdysis. We show that its downregulation alters Burs expression in the CCAP neurons. Ectopic expression of Opa, or the vertebrate homologue Zic2 , in the CCAP neurons also affects Burs expression, indicating an evolutionary functional conservation. Finally, our results show that, independently of its role in Burs regulation, Opa prevents death of CCAP neurons during larval development.


2010 ◽  
Vol 79 (3) ◽  
pp. 1363-1373 ◽  
Author(s):  
Jianchun Xiao ◽  
Lorraine Jones-Brando ◽  
C. Conover Talbot ◽  
Robert H. Yolken

ABSTRACTStrain type is one of the key factors suspected to play a role in determining the outcome ofToxoplasmainfection. In this study, we examined the transcriptional profile of human neuroepithelioma cells in response to representative strains ofToxoplasmaby using microarray analysis to characterize the strain-specific host cell response. The study of neural cells is of interest in light of the ability ofToxoplasmato infect the brain and to establish persistent infection within the central nervous system. We found that the extents of the expression changes varied considerably among the three strains. Neuroepithelial cells infected withToxoplasmatype I exhibited the highest level of differential gene expression, whereas type II-infected cells had a substantially smaller number of genes which were differentially expressed. Cells infected with type III exhibited intermediate effects on gene expression. The three strains also differed in the individual genes and gene pathways which were altered following cellular infection. For example, gene ontology (GO) analysis indicated that type I infection largely affects genes related to the central nervous system, while type III infection largely alters genes which affect nucleotide metabolism; type II infection does not alter the expression of a clearly defined set of genes. Moreover, Ingenuity Pathways Analysis (IPA) suggests that the three lineages differ in the ability to manipulate their host; e.g., they employ different strategies to avoid, deflect, or subvert host defense mechanisms. These observed differences may explain some of the variation in the neurobiological effects of different strains ofToxoplasmaon infected individuals.


2001 ◽  
Vol 81 (2) ◽  
pp. 871-927 ◽  
Author(s):  
Nicole Baumann ◽  
Danielle Pham-Dinh

Oligodendrocytes, the myelin-forming cells of the central nervous system (CNS), and astrocytes constitute macroglia. This review deals with the recent progress related to the origin and differentiation of the oligodendrocytes, their relationships to other neural cells, and functional neuroglial interactions under physiological conditions and in demyelinating diseases. One of the problems in studies of the CNS is to find components, i.e., markers, for the identification of the different cells, in intact tissues or cultures. In recent years, specific biochemical, immunological, and molecular markers have been identified. Many components specific to differentiating oligodendrocytes and to myelin are now available to aid their study. Transgenic mice and spontaneous mutants have led to a better understanding of the targets of specific dys- or demyelinating diseases. The best examples are the studies concerning the effects of the mutations affecting the most abundant protein in the central nervous myelin, the proteolipid protein, which lead to dysmyelinating diseases in animals and human (jimpy mutation and Pelizaeus-Merzbacher disease or spastic paraplegia, respectively). Oligodendrocytes, as astrocytes, are able to respond to changes in the cellular and extracellular environment, possibly in relation to a glial network. There is also a remarkable plasticity of the oligodendrocyte lineage, even in the adult with a certain potentiality for myelin repair after experimental demyelination or human diseases.


2018 ◽  
Vol 98 (1) ◽  
pp. 239-389 ◽  
Author(s):  
Alexei Verkhratsky ◽  
Maiken Nedergaard

Astrocytes are neural cells of ectodermal, neuroepithelial origin that provide for homeostasis and defense of the central nervous system (CNS). Astrocytes are highly heterogeneous in morphological appearance; they express a multitude of receptors, channels, and membrane transporters. This complement underlies their remarkable adaptive plasticity that defines the functional maintenance of the CNS in development and aging. Astrocytes are tightly integrated into neural networks and act within the context of neural tissue; astrocytes control homeostasis of the CNS at all levels of organization from molecular to the whole organ.


2016 ◽  
Vol 74 (8) ◽  
pp. 671-678 ◽  
Author(s):  
Roberto E. Sica ◽  
Roberto Caccuri ◽  
Cecilia Quarracino ◽  
Francisco Capani

ABSTRACT Experimental evidence suggests that astrocytes play a crucial role in the physiology of the central nervous system (CNS) by modulating synaptic activity and plasticity. Based on what is currently known we postulate that astrocytes are fundamental, along with neurons, for the information processing that takes place within the CNS. On the other hand, experimental findings and human observations signal that some of the primary degenerative diseases of the CNS, like frontotemporal dementia, Parkinson’s disease, Alzheimer’s dementia, Huntington’s dementia, primary cerebellar ataxias and amyotrophic lateral sclerosis, all of which affect the human species exclusively, may be due to astroglial dysfunction. This hypothesis is supported by observations that demonstrated that the killing of neurons by non-neural cells plays a major role in the pathogenesis of those diseases, at both their onset and their progression. Furthermore, recent findings suggest that astrocytes might be involved in the pathogenesis of some psychiatric disorders as well.


2020 ◽  
Vol 20 (5) ◽  
pp. 335-340 ◽  
Author(s):  
Mubeena P.M. Mariyath ◽  
Mehdi H. Shahi ◽  
Shirin Farheen ◽  
Mohd Tayyab ◽  
Nabeela Khanam ◽  
...  

Background: Complex central nervous system (CNS) is made up of neuronal cells and glial cells. Cells of central nervous system are able to regenerate after injury and during repairing. Sonic hedgehog pathway initiated by Shh-N a glycoprotein plays vital role in CNS patterning growth, development and now tumorigenesis. Nkx2.2 homeodomain transcription factor is an effecter molecule, which is positively regulated by Shh during normal growth. Nkx2.2 is essential for V3 domain specification during neural tube patterning at embryonic stage. MBP + oligodendrocytes are differentiated from progenitor cells which express Olig2. Nx2.2 is co-expressed with Olig2 in oligodendrocytes and is essential for later stage of oligodendrocyte maturation. Objective: This review paper explores the potential role of Nkx2.2 transcription factor in glioblastoma development. Conclusion: Shh pathway plays a vital role in oligodendrocytes differentiation and Nkx2.2 transcription factor is essential for oligodendrocytes differentiation and maturation. Intriguingly, down regulation of Nkx2.2 transcription factor with aberrant Shh signaling pathway is reported in glioma samples. So here it is suggested that Nkx2.2 expression pattern could be used as a potential biomarker for the early diagnosis of glioma.


2007 ◽  
Vol 306 (1) ◽  
pp. 360
Author(s):  
Amir M. Ashique ◽  
Mattias Karlen ◽  
Youngshik Choe ◽  
Johan Ericson ◽  
John L. Rubenstein ◽  
...  

2019 ◽  
Vol 204 ◽  
pp. 04008 ◽  
Author(s):  
Munkhbaatar Batmunkh ◽  
Lkhagvaa Bayarchimeg ◽  
Aleksandr N. Bugay ◽  
Oidov Lkhagva

Simulating the biological damage induced by charged particles trajectories (tracks) in the central nervous system (CNS) at different levels of its organization (molecular, cellular, and tissue) is a challenge of modern radiobiology studies. According to the recent experimental studies at particle accelerators, the most radiation-sensitive area of the CNS is the hippocampus. In this regards, the development of measurement-based Monte Carlo simulation of radiation-induced alterations in the hippocampus is of great interest to understand the radiobiological effects on the CNS. The present work investigates the influence of charged particles on the hippocampal cells of the rat brain using the Geant4 Monte Carlo radiation transport code. The applied computer simulation provides a method to simulate physics processes and chemical reactions in the developed model of the rat hippocampus, which contains different types of neural cells - pyramidal cells, mature and immature granular cells, mossy cells, and neural stem cells. The distribution of stochastic energy depositions has been obtained and analyzed in critical structures of the hippocampal neurons after irradiation with 600 MeV/u iron particles. The computed energy deposition in irradiated hippocampal neurons following a track of iron ion suggests that most of the energy is accumulated by granular cells. The obtained quantities at the level of molecular targets also assume that NMDA and GABA receptors belong to the most probable targets in the irradiated neural cells.


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