A Novel Cre Transgenic Mouse to Label Cardiac Purkinje Fibersduring Ischemic Injury
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PROVIDER: PRJNA641684 | ENA |
REPOSITORIES: ENA
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Project description:Purkinje fibers form a network of specializedventricularmyocardial cells to assure a coordinatedpropagation of the electrical impulseduring normalforheartefficientcontractionof the heart.Thedevelopmental origins of Purkinje fibers and their roles during cardiac arrhythmia have been reported.However, theresponse of Purkinje fibers to ischemic injury and theirfunctionrolesduring myocardialregenerationare still illusive. Here we introduceda novel inducibleCreallelemouse linethat specificallylabelsthemousecardiac conduction system. Fate mappingshowed Cre activity in different componentsofindicatedspecific labeling ofthe cardiac conduction system, including the sinoatrial and atrioventricularnodes,as well as the Purkinje fibersdifferentknown and unknowncomponents ofthecardiac conductionsystem. RNA-Seqof laser-captured Purkinje fibers showed a uniqueinjuryresponse occurredafterischemic injuryin thisventricularpart of the conductionsystemand corresponding changes in.Ccellularcompositionchange inofPurkinje fibersafter ischemic injury waswereobserved using immunostaining
2021-07-16 | GSE153182 | GEO
Project description:Affymetrix array gene expression analysis using RNA isolated from Purkinje cells and ventricular myocytes from the Cntn2-EGFP/ a-MHC-Cre/ floxed-tdTomato compound transgenic dual fluorescence reporter mouse Cardiac Purkinje cells are important triggers of ventricular arrhythmias associated with heritable and acquired syndromes. The mechanisms responsible for this pro-arrhythmic behavior are incompletely understood. Here, through transcriptional profiling of genetically labeled cardiomyocytes, we identified expression of Purkinje cell protein-4 (Pcp4), a putative regulator of calmodulin and Ca2+/calmodulin-dependent kinase II (CaMKII) signaling, exclusively within the His-Purkinje network. Using Pcp4-null mice and acquired cardiomyopathy models, we demonstrate that reduced expression of PCP4 is associated with CaMKII activation, abnormal electrophysiology, dysregulated intracellular calcium handling and pro-arrhythmic behavior in isolated Purkinje cells. We also show that Pcp4-null mice display profound autonomic dysregulation and arrhythmic behavior in vivo. Together, these results demonstrate that PCP4 regulates cardiac excitability through both Purkinje cell autonomous and central mechanisms and identify this modulator of CaMKII signaling as a potential arrhythmia-susceptibility candidate.
2014-11-30 | GSE60987 | GEO
Project description:We performed gene-expression analysis of mouse Purkinje cells as a model M-bM-^@M-^\single-type neuronM-bM-^@M-^]. DNA microarray analysis detected at least 7,055 genes in Purkinje cells, most of which are classified into functional molecule categories. Our comparative analysis between Purkinje cells and the granule cell layer showed that the characteristic expression pattern in Purkinje cells was particularly represented by M-bM-^@M-^\the neural communication systemM-bM-^@M-^] components. Pukinje cells and granule cell layer of the mouse cerebellum were collected by laser microdissection for RNA extraction and hybridization on Affymetrix microarrays.
2013-01-17 | E-GEOD-26749 | biostudies-arrayexpress
Project description:We performed gene-expression analysis of mouse Purkinje cells as a model “single-type neuron”. DNA microarray analysis detected at least 7,055 genes in Purkinje cells, most of which are classified into functional molecule categories. Our comparative analysis between Purkinje cells and the granule cell layer showed that the characteristic expression pattern in Purkinje cells was particularly represented by “the neural communication system” components.
2013-01-17 | GSE26749 | GEO
Project description:To elucidate the molecular features of craniofacial versus trunk neural crest cells (NCCs), we utilized P0-Cre/Floxed-EGFP mice that specifically label NCCs (Yamauchi et al., 1999 (PMID 10419695)). Craniofacial and trunk regions were isolated from P0-Cre/Floxed-EGFP mouse embryos at embryonic day E12.5, and dissociated cells were analyzed by flow cytometory in regard to the intensity of EGFP.
2014-08-01 | GSE39191 | GEO
Project description:Microarray profiling of cardiac biopsies from the area at at risk and remote myocardium of mice subjected to ischemic preconditioning. Mice were subjected to ischemic preconditioning (IPC) through reversible ligation of the left coronary artery or a sham procedure. The procedure consisted of 4 minutes of ischemia followed by 4 minutes of reperfusion, repeated 4 times and then followed by a 30 minute reperfusion period. Biopsies were taken from the area at risk (AAR) and remote myocardium (RM) from two IPC mice and two sham control mice.
2016-06-24 | E-GEOD-83659 | biostudies-arrayexpress
Project description:The signalling protein PKCγ is a major regulator of Purkinje cell development and synaptic function. We have shown previously that increased PKCγ activity impairs dendritic development of cerebellar Purkinje cells. Mutations in the protein kinase Cγ gene (PRKCG) cause spinocerebellar ataxia type 14 (SCA14). In a transgenic mouse model of SCA14 expressing the human S361G mutation, Purkinje cell dendritic development is impaired in cerebellar slice cultures similar to pharmacological activation of PKC. The mechanisms of PKCγ-driven inhibition of dendritic growth are still unclear. Using immunoprecipitation-coupled mass spectrometry analysis we have identified Collapsin Response Mediator Protein 2 (CRMP2) as a protein interacting with constitutive active PKCγ(S361G) and confirmed the interaction with the Duolink™ proximity ligation assay. We show that in cerebellar slice cultures from PKCγ(S361G)- mice, phosphorylation of CRMP2 at the known PKC target site Thr555 is increased in Purkinje cells confirming phosphorylation of CRMP2 by PKCγ. miRNA-mediated CRMP2 knockdown decreased Purkinje cell dendritic outgrowth in dissociated cerebellar cultures as did the transfection of CRMP2 mutants with a modified Thr555 site. In contrast, dendritic development was normal after wildtype CRMP2 overexpression. In a novel knock-in mouse expressing only the phospho-defective T555A-mutant CRMP2, Purkinje cell dendritic development was reduced in dissociated cultures. This reduction could be rescued by transfecting wildtype CRMP2 but only partially by the phospho-mimetic T555D-mutant. Our findings establish CRMP2 as an important target of PKCγ phosphorylation in Purkinje cells mediating its control of dendritic development. Dynamic regulation of CRMP2 phosphorylation via PKCγ is required for its correct function.
2022-02-24 | PXD020124 | Pride
Project description:H3K9me2 ChIP-Seq of cardiac biopsies from the area at at risk and remote myocardium of mice subjected to ischemic preconditioning. Mice were subjected to ischemic preconditioning (IPC) through reversible ligation of the left coronary artery or a sham procedure. The procedure consisted of 5 minutes of ischemia followed by 5 minutes of reperfusion, repeated 4 times and then followed by a 30 minute reperfusion period. Biopsies were taken from the area at risk (AAR) and remote myocardium (RM) from six IPC mice
2016-07-04 | E-GEOD-83979 | biostudies-arrayexpress
Project description:Interventions: No Group:No intervention
Primary outcome(s): CRE screening results
Study Design: Sequential
| 2699279 | ecrin-mdr-crc
Project description:Microarray profiling of cardiac biopsies from the area at at risk and remote myocardium of mice subjected to ischemic preconditioning.
2016-06-24 | GSE83659 | GEO