scholarly journals Repression of Osmr and Fgfr1 by miR-1/133a prevents cardiomyocyte dedifferentiation and cell cycle entry in the adult heart

2021 ◽  
Vol 7 (42) ◽  
Author(s):  
Melissa Valussi ◽  
Johannes Besser ◽  
Katharina Wystub-Lis ◽  
Sven Zukunft ◽  
Manfred Richter ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Adult Heart ◽  
Cell Cycle Entry

scholarly journals RAE-1 ligands for the NKG2D receptor are regulated by E2F transcription factors, which control cell cycle entry

2012 ◽  
Vol 209 (13) ◽  
pp. 2409-2422 ◽  
Author(s):  
Heiyoun Jung ◽  
Benjamin Hsiung ◽  
Kathleen Pestal ◽  
Emily Procyk ◽  
David H. Raulet
Keyword(s):  
Cell Cycle ◽  
Transcription Factors ◽  
Stress Responses ◽  
Transcriptional Activation ◽  
Posttranscriptional Regulation ◽  
Cellular Proliferation ◽  
Control Cell ◽  
T Cell Subsets ◽  
Cell Cycle Entry

The NKG2D stimulatory receptor expressed by natural killer cells and T cell subsets recognizes cell surface ligands that are induced on transformed and infected cells and facilitate immune rejection of tumor cells. We demonstrate that expression of retinoic acid early inducible gene 1 (RAE-1) family NKG2D ligands in cancer cell lines and proliferating normal cells is coupled directly to cell cycle regulation. Raet1 genes are directly transcriptionally activated by E2F family transcription factors, which play a central role in regulating cell cycle entry. Induction of RAE-1 occurred in primary cell cultures, embryonic brain cells in vivo, and cells in healing skin wounds and, accordingly, wound healing was delayed in mice lacking NKG2D. Transcriptional activation by E2Fs is likely coordinated with posttranscriptional regulation by other stress responses. These findings suggest that cellular proliferation, as occurs in cancer cells but also other pathological conditions, is a key signal tied to immune reactions mediated by NKG2D-bearing lymphocytes.

Abstract 347: Identification and Characterization of a miRNA Cohort Initiated Transitional Program That Controls Cell Cycle Arrest of the Perinatal Heart

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Patrick G Burgon ◽  
Jonathan J Weldrick
Keyword(s):  
Cell Cycle ◽  
Empirical Bayes ◽  
Molecular Mechanisms ◽  
Fetal Heart ◽  
Micro Rna ◽  
Bayes Estimation ◽  
Oligonucleotide Array ◽  
Array Analysis ◽  
Adult Heart ◽  
Perinatal Heart

During fetal and early perinatal development the myocardium undergoes a period of hyperplastic growth, which results in an exponential increase in the number of cardiomyocytes (CM) that will constitute the adult heart. Soon after birth, CMs proceed through a final round of cell division in the absence cytokinesis that results in binucleation of >95% of adult CMs. Fetal heart genes are re-activated with the onset of pathological hypertrophic or dilated cardiomyopathies, yet there is no evidence of CM re-entry into the cell cycle. Despite the importance of this phenomenon, little is known about the molecular basis for the transition from hyperplastic to hypertrophic-based myocardial growth. Hypothesis: A perinatal heart gene program is necessary for the normal transition from a fetal heart gene program to an adult heart gene program. To identify the molecular mechanisms and pathways involved in CM differentiation during the perinatal transition, RNA was isolated from E18, and 1, 3, 5, 7, 10 and 35d old mouse hearts. CM gene expression and micro-RNA profiles (n=3 arrays/time point) were determined by oligonucleotide array analysis. The raw array data was normalized by Robust Multi-array analysis. Empirical Bayes estimation of gene-specific variances was performed between each of the time points in order to identify genes that are transiently and significantly changed at days 3 and 5 as compare to E18 and 10d post-birth. The analysis identified 2,799 genes (E18 v 5d) and 3,347 genes (5d v 10d) that were then clustered to determine significant pathway enrichment (p<0.05) with Ingenuity Pathway Analysis. Our analysis confirmed previous observations of a down regulation of glucose oxidative metabolism (p=0.02) with an up-regulation of fatty acid metabolism (p=0.0001) between E18 and 5d post-birth. Also, 63 cell cycle genes are collectively down regulated (p=4.3x10-4) between 5d and 10d post-birth. We identified 131 genes that are transiently up regulated at 5d compared to E18 and 10d and this transition was proceeded by a specific cohort of miRNAs. The data generated from this study provide new insight into the molecular mechanisms by which CMs regulate and permanently exit from the cell cycle.

scholarly journals Phosphoinositide 3-Kinases p110α and p110β Regulate Cell Cycle Entry, Exhibiting Distinct Activation Kinetics in G1 Phase

2008 ◽  
Vol 28 (8) ◽  
pp. 2803-2814 ◽  
Author(s):  
Miriam Marqués ◽  
Amit Kumar ◽  
Isabel Cortés ◽  
Ana Gonzalez-García ◽  
Carmen Hernández ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Tyrosine Kinases ◽  
Control Cell ◽  
Growth Factor Receptor ◽  
Maximum Activity ◽  
S Phase ◽  
Selective Action ◽  
Cell Cycle Entry ◽  
Phosphoinositide 3 Kinase ◽  
Phase Entry

ABSTRACT Phosphoinositide 3-kinase (PI3K) is an early signaling molecule that regulates cell growth and cell cycle entry. PI3K is activated immediately after growth factor receptor stimulation (at the G0/G1 transition) and again in late G1. The two ubiquitous PI3K isoforms (p110α and p110β) are essential during embryonic development and are thought to control cell division. Nonetheless, it is presently unknown at which point each is activated during the cell cycle and whether or not they both control S-phase entry. We found that p110α was activated first in G0/G1, followed by a minor p110β activity peak. In late G1, p110α activation preceded that of p110β, which showed the maximum activity at this time. p110β activation required Ras activity, whereas p110α was first activated by tyrosine kinases and then further induced by active Ras. Interference with p110α and -β activity diminished the activation of downstream effectors with different kinetics, with a selective action of p110α in blocking early G1 events. We show that inhibition of either p110α or p110β reduced cell cycle entry. These results reveal that PI3Kα and -β present distinct activation requirements and kinetics in G1 phase, with a selective action of PI3Kα at the G0/G1 phase transition. Nevertheless, PI3Kα and -β both regulate S-phase entry.

Changes in p21Cip1 and p27Kip1 expression are not required for cell cycle entry and progression to S phase in Swiss 3T3 cells

2000 ◽  
Vol 12 (9-10) ◽  
pp. 619-627 ◽  
Author(s):  
Waraporn Promwikorn ◽  
Shaun R Hawley ◽  
Stephen R Pennington
Keyword(s):  
Cell Cycle ◽  
S Phase ◽  
3T3 Cells ◽  
P27kip1 Expression ◽  
Cell Cycle Entry ◽  
Swiss 3T3
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