Altered Expression of Genes Profiles Modulated by a Combination of Astragali Radix and Angelicae Sinensis Radix in Obstructed Rat Kidney

To explore the main active components and effects of cell cycle regulation mechanism of Astragali radix (AR) and Angelicae sinensis radix (ASR) on oxidative damage in vascular endothelial cells, a model of oxidative damage in human umbilical vein endothelial cells (HUVECs) induced by oxidized low-density lipoprotein (ox-LDL) treatment was developed. Based on the “knock-out/knock-in” model of the target component, cell viability, intracellular reactive oxygen species (ROS), and lactate dehydrogenase (LDH) leakage were assessed by Cell Counting Kit-8 assay, fluorescent probe 2,7-dichlorodihydrofluorescein diacetate (DCFH-DA), and colorimetric assay, respectively, to evaluate the protective effect of the active components of AR and ASR (astragaloside IV (AS IV), astragaloside I (AS I), formononetin (FRM), calycosin (CAL), calycosin-7-O-β-D glucoside (CLG), and ferulic acid (FRA)) against oxidative damage. The cell cycle and expression of genes encoding cyclins and cyclin-dependent kinases (CDKs) were observed using flow cytometry and quantitative real-time polymerase chain reaction. The results showed that the combination of active components (ACC) significantly inhibited the decrease in cell viability as well as the increase in ROS and LDH release in HUVECs induced by ox-LDL treatment. AS IV and FRM promoted the proliferation of HUVECs but the proliferation index was decreased in the AS I and FRA groups; this inhibitory effect was counteracted by the ACC. The ACC reduced and increased the proportion of positive cells in G1 and S phases, respectively, followed by the upregulation of cyclin A (CCNA), cyclin E (CCNE), and CDK2 mRNA expression and downregulation of cyclin B (CCNB), cyclin D1 (CCND1), CDK1, CDK4, and CDK6 mRNA expression, which significantly mitigated inhibition of HUVECs proliferation induced by ox-LDL treatment. Taken together, AS IV, AS I, FRM, CAL, CLG, and FRA were the primary pharmacodynamic substances of AR and ASR that alleviated oxidative injury in HUVECs. ACC mitigated the upregulation of intracellular ROS levels and LDH release induced by ox-LDL treatment, which promoted the cell cycle procession of HUVECs by regulating the expression of genes encoding cyclins and CDKs and thus preventing oxidative damage in HUVECs.

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Herpesvirus-Associated Proliferative Skin Disease in Frogs and Toads: Proposed Pathogenesis

Veterinary Pathology ◽

10.1177/03009858211006385 ◽

2021 ◽

pp. 030098582110063

Author(s):

Francesco C. Origgi ◽

Patricia Otten ◽

Petra Lohmann ◽

Ursula Sattler ◽

Thomas Wahli ◽

...

Keyword(s):

Molecular Mechanisms ◽

Rana Temporaria ◽

Skin Lesions ◽

Bufo Bufo ◽

Careful Examination ◽

Altered Expression ◽

Expression Of Genes ◽

Cell Remodeling ◽

Tissue Changes

A comparative study was carried out on common and agile frogs ( Rana temporaria and R. dalmatina) naturally infected with ranid herpesvirus 3 (RaHV3) and common toads ( Bufo bufo) naturally infected with bufonid herpesvirus 1 (BfHV1) to investigate common pathogenetic pathways and molecular mechanisms based on macroscopic, microscopic, and ultrastructural pathology as well as evaluation of gene expression. Careful examination of the tissue changes, supported by in situ hybridization, at different stages of development in 6 frogs and 14 toads revealed that the skin lesions are likely transient, and part of a tissue cycle necessary for viral replication in the infected hosts. Transcriptomic analysis, carried out on 2 naturally infected and 2 naïve common frogs ( Rana temporaria) and 2 naturally infected and 2 naïve common toads ( Bufo bufo), revealed altered expression of genes involved in signaling and cell remodeling in diseased animals. Finally, virus transcriptomics revealed that both RaHV3 and BfHV1 had relatively high expression of a putative immunomodulating gene predicted to encode a decoy receptor for tumor necrosis factor in the skin of the infected hosts. Thus, the comparable lesions in infected frogs and toads appear to reflect a concerted epidermal and viral cycle, with presumptive involvement of signaling and gene remodeling host and immunomodulatory viral genes.

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Matching the Heart to Heat-Induced Circulatory Load: Heat-Acclimatory Responses

Physiology ◽

10.1152/nips.01453.2003 ◽

2003 ◽

Vol 18 (6) ◽

pp. 215-221 ◽

Cited By ~ 5

Author(s):

Michal Horowitz

Keyword(s):

Heart Rate ◽

Oxygen Demand ◽

Heat Acclimation ◽

Regulatory Proteins ◽

Contractile Apparatus ◽

Cardiac Efficiency ◽

Cross Tolerance ◽

Altered Expression ◽

Expression Of Genes ◽

Cardiac Adaptation

Heat acclimation enhances cardiac efficiency by increasing stroke volume and decreasing heart rate. These adaptations involve biochemical changes in the contractile apparatus, switched on by altered expression of genes coding contractile and calcium-regulatory proteins and partially mediated by persistent low thyroxine. Heat acclimation also produces cross-tolerance to oxygen deprivation, thus reinforcing cardiac adaptation to oxygen demand/supply mismatching via energy-sparing pathways.

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Metabolomics and molecular docking to compare of the efficacies of wild-simulated and transplanted Astragali Radix based on its compatibility with Angelicae Sinensis Radix against blood deficiency

Journal of Chromatography B ◽

10.1016/j.jchromb.2021.122682 ◽

2021 ◽

pp. 122682

Author(s):

YueTao Liu ◽

ZiYing Wang ◽

XueMei Qin

Keyword(s):

Molecular Docking ◽

Astragali Radix ◽

Angelicae Sinensis

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Altered expression of genes regulating angiogenesis in experimental androgen-independent prostate cancer

The Prostate ◽

10.1002/pros.20672 ◽

2007 ◽

Vol 68 (2) ◽

pp. 161-170 ◽

Cited By ~ 31

Author(s):

Heléne Gustavsson ◽

Karin Jennbacken ◽

Karin Welén ◽

Jan-Erik Damber

Keyword(s):

Prostate Cancer ◽

Altered Expression ◽

Expression Of Genes ◽

Androgen Independent

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Depletion of KNL2 Results in Altered Expression of Genes Involved in Regulation of the Cell Cycle, Transcription, and Development in Arabidopsis

International Journal of Molecular Sciences ◽

10.3390/ijms20225726 ◽

2019 ◽

Vol 20 (22) ◽

pp. 5726 ◽

Cited By ~ 1

Author(s):

Anastassia Boudichevskaia ◽

Andreas Houben ◽

Anne Fiebig ◽

Klara Prochazkova ◽

Ales Pecinka ◽

...

Keyword(s):

Cell Cycle ◽

Critical Role ◽

Histone H3 ◽

Global Gene Expression ◽

Proper Function ◽

Knockout Mutant ◽

Flower Bud ◽

Altered Expression ◽

Expression Of Genes ◽

Histone H3 Variant

Centromeres contain specialized nucleosomes at which histone H3 is partially replaced by the centromeric histone H3 variant cenH3 that is required for the assembly, maintenance, and proper function of kinetochores during mitotic and meiotic divisions. Previously, we identified a KINETOCHORE NULL 2 (KNL2) of Arabidopsis thaliana that is involved in the licensing of centromeres for the cenH3 recruitment. We also demonstrated that a knockout mutant for KNL2 shows mitotic and meiotic defects, slower development, reduced growth rate, and fertility. To analyze an effect of KNL2 mutation on global gene transcription of Arabidopsis, we performed RNA-sequencing experiments using seedling and flower bud tissues of knl2 and wild-type plants. The transcriptome data analysis revealed a high number of differentially expressed genes (DEGs) in knl2 plants. The set was enriched in genes involved in the regulation of the cell cycle, transcription, development, and DNA damage repair. In addition to comprehensive information regarding the effects of KNL2 mutation on the global gene expression, physiological changes in plants are also presented, which provides an integrated understanding of the critical role played by KNL2 in plant growth and development.

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Age-dependent changes in electrophysiology and calcium handling – implications for pediatric cardiac research

10.1101/657551 ◽

2019 ◽

Author(s):

Luther M. Swift ◽

Morgan Burke ◽

Devon Guerrelli ◽

Manelle Ramadan ◽

Marissa Reilly ◽

...

Keyword(s):

Postnatal Development ◽

Cardiac Electrophysiology ◽

Calcium Handling ◽

Cell Coupling ◽

Altered Expression ◽

Expression Of Genes ◽

Age Dependent ◽

Genes Encoding ◽

Cardiac Maturation

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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BRCA1 Haploinsufficiency Leads to Altered Expression of Genes Involved in Cellular Proliferation and Development

PLoS ONE ◽

10.1371/journal.pone.0100068 ◽

2014 ◽

Vol 9 (6) ◽

pp. e100068 ◽

Cited By ~ 9

Author(s):

Harriet E. Feilotter ◽

Claire Michel ◽

Paolo Uy ◽

Lauren Bathurst ◽

Scott Davey

Keyword(s):

Cellular Proliferation ◽

Altered Expression ◽

Expression Of Genes

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Maternal iron deficiency alters trophoblast differentiation and placental development in rat pregnancy

Endocrinology ◽

10.1210/endocr/bqab215 ◽

2021 ◽

Author(s):

Hannah Roberts ◽

Andrew G Woodman ◽

Kelly J Baines ◽

Mariyan J Jeyarajah ◽

Stephane L Bourque ◽

...

Keyword(s):

Iron Deficiency ◽

Fetal Growth ◽

Growth And Development ◽

Iron Homeostasis ◽

Junctional Zone ◽

Altered Expression ◽

Expression Of Genes ◽

Iron Deficient ◽

Increased Risk ◽

Maternal Iron

Abstract Iron deficiency occurs when iron demands chronically exceed intake, and is prevalent in pregnant women. Iron deficiency during pregnancy poses major risks for the baby, including fetal growth restriction and long-term health complications. The placenta serves as the interface between a pregnant mother and her baby, and ensures adequate nutrient provisions for the fetus. Thus, maternal iron deficiency may impact fetal growth and development by altering placental function. We used a rat model of diet-induced iron deficiency to investigate changes in placental growth and development. Pregnant Sprague-Dawley rats were fed either a low-iron or iron-replete diet starting two weeks before mating. Compared to controls, both maternal and fetal hemoglobin were reduced in dams fed low-iron diets. Iron deficiency decreased fetal liver and body weight, but not brain, heart or kidney weight. Placental weight was increased in iron deficiency, due primarily to expansion of the placental junctional zone. The stimulatory effect of iron deficiency on junctional zone development was recapitulated in vitro, as exposure of rat trophoblast stem cells to the iron chelator deferoxamine increased differentiation toward junctional zone trophoblast subtypes. Gene expression analysis revealed 464 transcripts changed at least 1.5-fold (P<0.05) in placentas from iron-deficient dams, including altered expression of genes associated with oxygen transport and lipoprotein metabolism. Expression of genes associated with iron homeostasis was unchanged despite differences in levels of their encoded proteins. Our findings reveal robust changes in placentation during maternal iron deficiency, which could contribute to the increased risk of fetal distress in these pregnancies.

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