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 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 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

Transcriptional response of skeletal muscle to a low-protein gestation diet in porcine offspring accumulates in growth- and cell cycle-regulating pathways

2012 ◽  
Vol 44 (16) ◽  
pp. 811-818 ◽  
Author(s):  
Michael Oster ◽  
Eduard Murani ◽  
Cornelia C. Metges ◽  
Siriluck Ponsuksili ◽  
Klaus Wimmers
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Skeletal Muscle ◽  
Signaling Pathways ◽  
Cell Cycle Regulation ◽  
Acid Metabolism ◽  
Energy Utilization ◽  
Nucleic Acid Metabolism ◽  
Growth Factor Signaling ◽  
Cycle Regulation

Inadequate maternal protein supply during gestation represents an environmental factor that affects physiological signaling pathways with long-term consequences for growth, function, and structure of various tissues. Hypothesizing that the offspring's transcriptome is persistently altered by maternal diets, we used a porcine model to monitor the longitudinal expression changes in muscle to identify pathways relevant to fetal initiation of postnatal growth and development. German Landrace gilts were fed isoenergetic gestational diets containing 6.5% (LP) or 12.1% protein. The longissimus dorsi samples were collected from offspring at 94 days postconception (dpc) and 1, 28, and 188 days postnatum (dpn) for expression profiling. At 94 dpc, 1 dpn, and 28 dpn relatively few transcripts (<130) showed an altered abundance between the dietary groups. In fact, at 94 dpc genes of G2/M checkpoint regulation and mitotic roles of Polo-like kinases showed lowered transcript abundance in LP. At 188 dpn 677 transcripts were altered including those related to oxidative phosphorylation, citrate cycle, fatty acid metabolism (higher abundance in LP) and cell cycle regulation (lower abundance in LP). Correspondingly, transcriptional alterations during pre and postnatal development differed considerably among dietary groups, particularly for genes related to cell cycle regulation (G1/S and G2/M checkpoint regulation; cyclines), growth factor signaling (GH, IGF1, mTOR, RAN, VEGF, INSR), lipid metabolism, energy metabolism, and nucleic acid metabolism. In skeletal muscle, fetal programming related to maternal LP diets disturbed gene expression in growth-related pathways into adulthood. Diet-dependent gene expression may hamper proper development, thereby affecting signaling pathways related to energy utilization.

Ageing Affects Cell Cycle Regulation In Human Skeletal Muscle Undergoing Atrophy And Regrowth

2017 ◽  
Vol 49 (5S) ◽  
pp. 236
Author(s):  
Ulrik Frandsen ◽  
Tatyana Prokhorova ◽  
Line Jensen ◽  
Lars G. Hvid ◽  
Peter Scherling ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Skeletal Muscle ◽  
Cell Cycle Regulation ◽  
Human Skeletal Muscle ◽  
Cycle Regulation

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.

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