scholarly journals Main Active Components and Cell Cycle Regulation Mechanism of Astragali Radix and Angelicae Sinensis Radix in the Treatment of Ox-LDL-Induced HUVECs Injury and Inhibition of Their Cell Cycle

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Cai-Xia Liu ◽  
Ying-Zi Tan ◽  
Chang-Qing Deng
Keyword(s):  
Cell Cycle ◽  
Oxidative Damage ◽  
Cell Cycle Regulation ◽  
Regulation Mechanism ◽  
Active Components ◽  
Astragali Radix ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Angelicae Sinensis ◽  
Cycle Regulation

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.

scholarly journals Erratum to: Effects of flavonoids on expression of genes involved in cell cycle regulation and DNA replication in human fibroblasts

2016 ◽  
Vol 424 (1-2) ◽  
pp. 211-211
Author(s):  
Marta Moskot ◽  
Joanna Jakóbkiewicz-Banecka ◽  
Elwira Smolińska ◽  
Ewa Piotrowska ◽  
Grzegorz Węgrzyn ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Replication ◽  
Cell Cycle Regulation ◽  
Human Fibroblasts ◽  
Expression Of Genes ◽  
Cycle Regulation

scholarly journals Changes in the expression of genes involved in cell cycle regulation and the relative telomere length in the process of canceration induced by omethoate

Tumor Biology ◽  
2017 ◽  
Vol 39 (7) ◽  
pp. 101042831771978 ◽  
Author(s):  
Xiaoran Duan ◽  
Yongli Yang ◽  
Sihua Wang ◽  
Xiaolei Feng ◽  
Tuanwei Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Telomere Length ◽  
Cell Cycle Regulation ◽  
Relative Telomere Length ◽  
Expression Of Genes ◽  
Cycle Regulation

scholarly journals IUGR impairs cardiomyocyte growth and maturation in fetal sheep

2018 ◽  
Vol 239 (2) ◽  
pp. 253-265 ◽  
Author(s):  
Sonnet S Jonker ◽  
Daniel Kamna ◽  
Dan LoTurco ◽  
Jenai Kailey ◽  
Laura D Brown
Keyword(s):  
Cell Cycle ◽  
Skeletal Muscle ◽  
Cell Cycle Regulation ◽  
Striated Muscle ◽  
Placental Insufficiency ◽  
Growth Restriction ◽  
Fetal Sheep ◽  
Ambient Temperatures ◽  
Expression Of Genes ◽  
Cycle Regulation

Placental insufficiency causes intrauterine growth restriction (IUGR), a common complication of pregnancy. In skeletal muscle, IUGR reduces fetal myofibril size, reduces myoblast proliferation and reduces expression of genes in cell cycle regulation clusters. The myocardium is striated like skeletal muscle, and IUGR also reduces cell cycle activity and maturation in cardiomyocytes, despite cardiac output preferentially directed to the coronary circulation. We hypothesized that cardiomyocyte growth restriction would be accompanied by similar changes in cell cycle regulation genes and would reduce cardiomyocyte cell cycle activity, number, maturity and size. Pregnant ewes were housed in elevated ambient temperatures from ~40 to ~115 days of gestation (dGA) to produce placental insufficiency and IUGR; fetal hearts were studied at ~134 dGA. Hearts were biopsied for mRNA analysis and then dissociated into individual myocytes (Control n = 8; IUGR n = 15) or dissected (Control n = 9; IUGR n = 13). IUGR fetuses had low circulating insulin and insulin-like growth factor 1 (IGF1) and high circulating cortisol. Bodies and hearts of IUGR fetuses were lighter than those of Controls. Cardiomyocytes of IUGR fetuses were smaller, less mature, less active in the cell cycle and less numerous than in Controls. Further, there was a pattern of downregulation of cell cycle genes in IUGR ventricles. IUGR growth profiles in heart and skeletal muscle suggest similar regulation despite differences in blood and nutrient delivery prioritization. IGF1 signaling is suggested as a mechanism regulating altered growth in IUGR striated muscle and a potential therapeutic candidate.

scholarly journals Effects of flavonoids on expression of genes involved in cell cycle regulation and DNA replication in human fibroblasts

2015 ◽  
Vol 407 (1-2) ◽  
pp. 97-109 ◽  
Author(s):  
Marta Moskot ◽  
Joanna Jakóbkiewicz-Banecka ◽  
Elwira Smolińska ◽  
Ewa Piotrowska ◽  
Grzegorz Węgrzyn ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Replication ◽  
Cell Cycle Regulation ◽  
Human Fibroblasts ◽  
Expression Of Genes ◽  
Cycle Regulation

scholarly journals Golgi Oncoprotein GOLPH3 Gene Expression Is Regulated by Functional E2F and CREB/ATF Promoter Elements

Genes ◽  
2019 ◽  
Vol 10 (3) ◽  
pp. 247 ◽  
Author(s):  
Beatriz Peñalver-González ◽  
Jon Vallejo-Rodríguez ◽  
Gartze Mentxaka ◽  
Asier Fullaondo ◽  
Ainhoa Iglesias-Ara ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Messenger Rna ◽  
Cell Cycle Regulation ◽  
Luciferase Reporter ◽  
Luciferase Reporter Construct ◽  
Daughter Cells ◽  
Genes Encoding ◽  
E2f Transcription Factors ◽  
Cycle Regulation ◽  
Interfering Rna

The Golgi organelle duplicates its protein and lipid content to segregate evenly between two daughter cells after mitosis. However, how Golgi biogenesis is regulated during interphase remains largely unknown. Here we show that messenger RNA (mRNA) expression of GOLPH3 and GOLGA2, two genes encoding Golgi proteins, is induced specifically in G1 phase, suggesting a link between cell cycle regulation and Golgi growth. We have examined the role of E2F transcription factors, critical regulators of G1 to S progression of the cell cycle, in the expression of Golgi proteins during interphase. We show that promoter activity for GOLPH3, a Golgi protein that is also oncogenic, is induced by E2F1-3 and repressed by E2F7. Mutation of the E2F motifs present in the GOLPH3 promoter region abrogates E2F1-mediated induction of a GOLPH3 luciferase reporter construct. Furthermore, we identify a critical CREB/ATF element in the GOLPH3 promoter that is required for its steady state and ATF2-induced expression. Interestingly, depletion of GOLPH3 with small interfering RNA (siRNA) delays the G1 to S transition in synchronized U2OS cells. Taken together, our results reveal a link between cell cycle regulation and Golgi function, and suggest that E2F-mediated regulation of Golgi genes is required for the timely progression of the cell cycle.

scholarly journals Altered Gene Expression Encoding Cytochines, Grow Factors and Cell Cycle Regulators in the Endometrium of Women with Chronic Endometritis

Diagnostics ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 471
Author(s):  
Ettore Cicinelli ◽  
Amerigo Vitagliano ◽  
Vera Loizzi ◽  
Dominique De Ziegler ◽  
Margherita Fanelli ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Endometrial Biopsy ◽  
Cell Cycle Regulators ◽  
Chronic Endometritis ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Proliferative Endometrium ◽  
Altered Gene ◽  
Apoptotic Activity ◽  
Cycle Regulation

To evaluate the expression of genes encoding cytokines, grow factors and cell cycle regulators in the proliferative endometrium of women with chronic endometritis (CE) compared to controls. We performed a case-control study on seven women with CE as diagnosed by hysteroscopy and histology (Cases) compared to six women without CE (Controls). All women underwent diagnostic hysteroscopy plus endometrial biopsy during the mid-proliferative phase of the menstrual cycle. Endometrial samples were divided into two different aliquots for histological and molecular analyses. The endometrial expression profile of 16 genes encoding proteins involved in the inflammatory process, proliferation and cell cycle regulation/apoptosis was assessed by using high-throughput qPCR. Study endpoints were between-group differences in the expression of VEGF A, VEGF B, VEGF C, EGF, TNF, TGF B1, IFNG, TP73, TP73L, BAXva, CDC2, CDC2va, CCND3, CCNB1, BAX and IL12. RESULTS: VEGF A, VEGF B, VEGF C, EGF, TNF, TGF B1, IFNG, TP73, TP73L, BAXva, CDC2, CDC2va, CCND3, CCNB1 were significantly overexpressed in women with CE compared to controls, while BAX and IL12 had similar expression between groups. In women with CE, we found an altered endometrial expression of genes involved in inflammatory, cell proliferation, and apoptosis processes. The dominance of proliferative and anti-apoptotic activity in CE may potentially promote the development of polyps and hyperplastic lesions.

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