Altered Expression of Genes Encoding Neurotransmitter Receptors in GnRH Neurons of Proestrous Mice

ABSTRACTRationaleThe heart continues to develop and mature after birth and into adolescence. Accordingly, cardiac maturation is likely to include a progressive refinement in both organ morphology and function during the postnatal period. Yet, age-dependent changes in cardiac electrophysiology and calcium handling have not yet been fully characterized.ObjectiveThe objective of this study, was to examine the relationship between cardiac maturation, electrophysiology, and calcium handling throughout postnatal development in a rat model.MethodsPostnatal rat cardiac maturation was determined by measuring the expression of genes involved in cell-cell coupling, electrophysiology, and calcium handling. In vivo electrocardiograms were recorded from neonatal, juvenile, and adult animals. Simultaneous dual optical mapping of transmembrane voltage and calcium transients was performed on isolated, Langendorff-perfused rat hearts (postnatal day 0–3, 4-7, 8-14, adult).ResultsYounger, immature hearts displayed slowed electrical conduction, prolonged action potential duration and increased ventricular refractoriness. Slowed calcium handling in the immature heart increased the propensity for calcium transient alternans which corresponded to alterations in the expression of genes encoding calcium handling proteins. Developmental changes in cardiac electrophysiology were associated with the altered expression of genes encoding potassium channels and intercalated disc proteins.ConclusionUsing an intact whole heart model, this study highlights chronological changes in cardiac electrophysiology and calcium handling throughout postnatal development. Results of this study can serve as a comprehensive baseline for future studies focused on pediatric cardiac research, safety assessment and/or preclinical testing using rodent models.

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Ablation of sarcolipin results in atrial remodeling

AJP Cell Physiology ◽

10.1152/ajpcell.00425.2011 ◽

2012 ◽

Vol 302 (12) ◽

pp. C1762-C1771 ◽

Cited By ~ 24

Author(s):

Lai-Hua Xie ◽

Mayilvahanan Shanmugam ◽

Ji Yeon Park ◽

Zhenghang Zhao ◽

Hairuo Wen ◽

...

Keyword(s):

Interstitial Fibrosis ◽

Calcium Transient ◽

Atrial Remodeling ◽

Atrial Myocytes ◽

Long Term Effects ◽

Sodium Calcium Exchanger ◽

Altered Expression ◽

Expression Of Genes ◽

Genes Encoding ◽

Intracellular Ca

Sarcolipin (SLN) is a key regulator of sarco(endo)plasmic reticulum (SR) Ca2+-ATPase (SERCA), and its expression is altered in diseased atrial myocardium. To determine the precise role of SLN in atrial Ca2+ homeostasis, we developed a SLN knockout ( sln−/−) mouse model and demonstrated that ablation of SLN enhances atrial SERCA pump activity. The present study is designed to determine the long-term effects of enhanced SERCA activity on atrial remodeling in the sln−/− mice. Calcium transient measurements show an increase in atrial SR Ca2+ load and twitch Ca2+ transients. Patch-clamping experiments demonstrate activation of the forward mode of sodium/calcium exchanger, increased L-type Ca2+ channel activity, and prolongation of action potential duration at 90% repolarization in the atrial myocytes of sln−/− mice. Spontaneous Ca2+ waves, delayed afterdepolarization, and triggered activities are frequent in the atrial myocytes of sln−/− mice. Furthermore, loss of SLN in atria is associated with increased interstitial fibrosis and altered expression of genes encoding collagen and other extracellular matrix proteins. Our results also show that the sln−/− mice are susceptible to atrial arrhythmias upon aging. Together, these findings indicate that ablation of SLN results in increased SERCA activity and SR Ca2+ load, which, in turn, could cause abnormal intracellular Ca2+ handling and atrial remodeling.

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Relation between Biofilm and Virulence in Vibrio tapetis: A Transcriptomic Study

Pathogens ◽

10.3390/pathogens7040092 ◽

2018 ◽

Vol 7 (4) ◽

pp. 92 ◽

Cited By ~ 4

Author(s):

Sophie Rodrigues ◽

Christine Paillard ◽

Sabine Van Dillen ◽

Ali Tahrioui ◽

Jean-Marc Berjeaud ◽

...

Keyword(s):

Pathogenic Bacteria ◽

Cell System ◽

Ruditapes Philippinarum ◽

Differentially Expressed ◽

Type Vi Secretion System ◽

Altered Expression ◽

Expression Of Genes ◽

Polysaccharide Synthesis ◽

Genes Encoding ◽

Genetic Level

Marine pathogenic bacteria are able to form biofilms on many surfaces, such as mollusc shells, and they can wait for the appropriate opportunity to induce their virulence. Vibrio tapetis can develop such biofilms on the inner surface of shells of the Ruditapes philippinarum clam, leading to the formation of a brown conchiolin deposit in the form of a ring, hence the name of the disease: Brown Ring Disease. The virulence of V. tapetis is presumed to be related to its capacity to form biofilms, but the link has never been clearly established at the physiological or genetic level. In the present study, we used RNA-seq analysis to identify biofilm- and virulence-related genes displaying altered expression in biofilms compared to the planktonic condition. A flow cell system was employed to grow biofilms to obtain both structural and transcriptomic views of the biofilms. We found that 3615 genes were differentially expressed, confirming that biofilm and planktonic lifestyles are very different. As expected, the differentially expressed genes included those involved in biofilm formation, such as motility- and polysaccharide synthesis-related genes. The data show that quorum sensing is probably mediated by the AI-2/LuxO system in V. tapetis biofilms. The expression of genes encoding the Type VI Secretion System and associated exported proteins are strongly induced, suggesting that V. tapetis activates this virulence factor when living in biofilm.

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Global gene expression and secondary metabolite changes in Arabidopsis thaliana ABI4 over-expression lines

Botany ◽

10.1139/cjb-2016-0043 ◽

2016 ◽

Vol 94 (8) ◽

pp. 615-634 ◽

Cited By ~ 1

Author(s):

Bianyun Yu ◽

Margaret Y. Gruber ◽

Shu Wei ◽

Rong Zhou ◽

Dwayne Hegedus ◽

...

Keyword(s):

Arabidopsis Thaliana ◽

Secondary Metabolite ◽

Plant Development ◽

Global Gene Expression ◽

Comprehensive Overview ◽

Altered Expression ◽

Transcript Levels ◽

Over Expression ◽

Expression Of Genes ◽

Genes Encoding

Despite numerous studies on ABI4, its role in plant secondary metabolism has not been fully investigated. Here, we used metabolite profiling together with transcriptome analysis to demonstrate that ABI4 transcript levels regulate a host of secondary metabolite pathways and growth modalities in ABI4 over-expression (ABI4_OE) lines of Arabidopsis thaliana. This strategy provided a unique and comprehensive overview of the regulation of metabolic shifts in response to ABI4 transcription. We show that enhancement of ABI4 transcript levels changed seed proanthocyanidin (PA), flavonoid, and carotenoid levels in ABI4_OE seeds and 30-day-old shoots, as well as the expression of genes encoding enzymes involved in the production of these and other secondary metabolites in ABI4_OE shoots. In seeds, PA accumulated in very large uneven patches, which was dramatically different from the even distribution of PA in wild-type seeds. Shoots of ABI4_OE lines also exhibited altered expression of a range of genes involved in several aspects of plant development, including hormone and cell-wall synthesis. Alteration of such disparate secondary metabolite pathways, along with hormone and developmental pathways, suggests that ABI4 is a master regulator integrating these compounds with plant development.

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Human islet preparations distributed for research exhibit a variety of insulin-secretory profiles

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00437.2014 ◽

2015 ◽

Vol 308 (7) ◽

pp. E592-E602 ◽

Cited By ~ 50

Author(s):

Nora S. Kayton ◽

Gregory Poffenberger ◽

Joseph Henske ◽

Chunhua Dai ◽

Courtney Thompson ◽

...

Keyword(s):

Insulin Secretion ◽

Human Islets ◽

Glucose Sensing ◽

Human Islet ◽

Altered Expression ◽

Expression Of Genes ◽

Genes Encoding ◽

Basal Insulin Secretion ◽

The Many

Human islet research is providing new insights into human islet biology and diabetes, using islets isolated at multiple US centers from donors with varying characteristics. This creates challenges for understanding, interpreting, and integrating research findings from the many laboratories that use these islets. In what is, to our knowledge, the first standardized assessment of human islet preparations from multiple isolation centers, we measured insulin secretion from 202 preparations isolated at 15 centers over 11 years and noted five distinct patterns of insulin secretion. Approximately three quarters were appropriately responsive to stimuli, but one quarter were dysfunctional, with unstable basal insulin secretion and/or an impairment in stimulated insulin secretion. Importantly, the patterns of insulin secretion by responsive human islet preparations (stable Baseline and Fold stimulation of insulin secretion) isolated at different centers were similar and improved slightly over the years studied. When all preparations studied were considered, basal and stimulated insulin secretion did not correlate with isolation center, biological differences of the islet donor, or differences in isolation, such as Cold Ischemia Time. Dysfunctional islet preparations could not be predicted from the information provided by the isolation center and had altered expression of genes encoding components of the glucose-sensing pathway, but not of insulin production or cell death. These results indicate that insulin secretion by most preparations from multiple centers is similar but that in vitro responsiveness of human islets cannot be predicted, necessitating preexperimental human islet assessment. These results should be considered when one is designing, interpreting, and integrating experiments using human islets.

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Salt stress induces altered expression of genes encoding antioxidant enzymes in seedlings of a Brazilian indica rice (Oryza sativa L.)

Plant Science ◽

10.1016/j.plantsci.2003.10.001 ◽

2004 ◽

Vol 166 (2) ◽

pp. 323-331 ◽

Cited By ~ 74

Author(s):

Larissa Menezes-Benavente ◽

Felipe Karam Teixeira ◽

Claire Lessa Alvim Kamei ◽

Márcia Margis-Pinheiro

Keyword(s):

Oryza Sativa ◽

Antioxidant Enzymes ◽

Salt Stress ◽

Oryza Sativa L ◽

Indica Rice ◽

Altered Expression ◽

Expression Of Genes ◽

Genes Encoding

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Disruption of pathways regulated by Integrator complex in Galloway–Mowat syndrome due to WDR73 mutations

Scientific Reports ◽

10.1038/s41598-021-84472-7 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

F. C. Tilley ◽

C. Arrondel ◽

C. Chhuon ◽

M. Boisson ◽

N. Cagnard ◽

...

Keyword(s):

Cell Cycle ◽

Transcription Initiation ◽

Transcriptional Control ◽

Cell Cycle Control ◽

Transcriptional Response ◽

Loss Of Function ◽

Altered Expression ◽

Expression Of Genes ◽

Genes Encoding ◽

Cellular Pathways

AbstractSeveral studies have reported WDR73 mutations to be causative of Galloway–Mowat syndrome, a rare disorder characterised by the association of neurological defects and renal-glomerular disease. In this study, we demonstrate interaction of WDR73 with the INTS9 and INTS11 components of Integrator, a large multiprotein complex with various roles in RNA metabolism and transcriptional control. We implicate WDR73 in two Integrator-regulated cellular pathways; namely, the processing of uridylate-rich small nuclear RNAs (UsnRNA), and mediating the transcriptional response to epidermal growth factor stimulation. We also show that WDR73 suppression leads to altered expression of genes encoding cell cycle regulatory proteins. Altogether, our results suggest that a range of cellular pathways are perturbed by WDR73 loss-of-function, and support the consensus that proper regulation of UsnRNA maturation, transcription initiation and cell cycle control are all critical in maintaining the health of post-mitotic cells such as glomerular podocytes and neurons, and preventing degenerative disease.

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RamA, a Member of the AraC/XylS Family, Influences Both Virulence and Efflux in Salmonella enterica Serovar Typhimurium

Journal of Bacteriology ◽

10.1128/jb.01517-09 ◽

2010 ◽

Vol 192 (6) ◽

pp. 1607-1616 ◽

Cited By ~ 71

Author(s):

Andrew M. Bailey ◽

Al Ivens ◽

Rob Kingsley ◽

Jennifer L. Cottell ◽

John Wain ◽

...

Keyword(s):

Salmonella Enterica ◽

Target Genes ◽

Salmonella Enterica Serovar Typhimurium ◽

Consensus Sequence ◽

Altered Expression ◽

Expression Of Genes ◽

Mouse Macrophages ◽

Serovar Typhimurium ◽

Genes Encoding ◽

High Level

ABSTRACT The transcriptomes of Salmonella enterica serovar Typhimurium SL1344 lacking a functional ramA or ramR or with plasmid-mediated high-level overexpression of ramA were compared to those of the wild-type parental strain. Inactivation of ramA led to increased expression of 14 SPI-1 genes and decreased expression of three SPI-2 genes, and it altered expression of ribosomal biosynthetic genes and several amino acid biosynthetic pathways. Furthermore, disruption of ramA led to decreased survival within RAW 264.7 mouse macrophages and attenuation within the BALB/c ByJ mouse model. Highly overexpressed ramA led to increased expression of genes encoding multidrug resistance (MDR) efflux pumps, including acrAB, acrEF, and tolC. Decreased expression of 34 Salmonella pathogenicity island (SPI) 1 and 2 genes, decreased SipC production, decreased adhesion to and survival within macrophages, and decreased colonization of Caenorhabditis elegans were also seen. Disruption of ramR led to the increased expression of ramA, acrAB, and tolC, but not to the same level as when ramA was overexpressed on a plasmid. Inactivation of ramR had a more limited effect on pathogenicity gene expression. In silico analysis of a suggested RamA-binding consensus sequence identified target genes, including ramR, acrA, tolC, sipABC, and ssrA. This study demonstrates that the regulation of a mechanism of MDR and expression of virulence genes show considerable overlap, and we postulate that such a mechanism is dependent on transcriptional activator concentration and promoter sensitivity. However, we have no evidence to support the hypothesis that increased MDR via RamA regulation of AcrAB-TolC gives rise to a hypervirulent strain.

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