Stepwise up-regulation of MicroRNA expression levels from replicating to reversible and irreversible growth arrest states in WI-38 human fibroblasts

2009 ◽  
Vol 221 (1) ◽  
pp. 109-119 ◽  
Author(s):  
Olivier C. Maes ◽  
Harshini Sarojini ◽  
Eugenia Wang
2010 ◽  
Vol 21 (1) ◽  
pp. 68-73 ◽  
Author(s):  
C. Borel ◽  
S. Deutsch ◽  
A. Letourneau ◽  
E. Migliavacca ◽  
S. B. Montgomery ◽  
...  

2013 ◽  
Vol 18 (4) ◽  
pp. 273-287 ◽  
Author(s):  
Loris De Cecco ◽  
Matteo Dugo ◽  
Silvana Canevari ◽  
Maria Grazia Daidone ◽  
Maurizio Callari

Author(s):  
Yanbing Li ◽  
Yu Geng ◽  
Boda Zhou ◽  
Xuejiao Wu ◽  
Ou Zhang ◽  
...  

AbstractIt is formerly conducted that long non-coding RNA growth arrest-specific 5 (GAS5) is involved in the process of coronary atherosclerosis (AS). The regulatory effects of GAS5 on the microRNA (miR)-194-3p/thioredoxin-interacting protein (TXNIP) axis in AS have been insufficiently explored yet. Thereafter, this work is started from GAS5/miR-194-3p/TXNIP axis in AS. AS rats were modeled to obtain their coronary vascular tissues and endothelial cells (ECs), in which GAS5, miR-194-3p, and TXNIP expression were tested. ECs were identified by immunohistochemistry. The mechanism among GAS5, miR-194-3p, and TXNIP was determined. ECs were transfected with inhibited GAS5 or overexpressed miR-194-3p to decipher their functions in proliferation and apoptosis of ECs in AS. Raised GAS5 and TXNIP and degraded miR-194-3p expression levels exhibited in AS. GAS5 bound to miR-194-3p while miR-194-3p targeted TXNIP. Depleting GAS5 or restoring miR-194-3p enhanced proliferation and depressed apoptosis of ECs in AS. This work clearly manifests that inhibited GAS5 facilitates the growth of ECs through miR-194-3p-targeted TXNIP in AS, consolidating the basal reference to the curing for AS.


Oncotarget ◽  
2017 ◽  
Vol 8 (42) ◽  
pp. 73345-73361 ◽  
Author(s):  
Patrick Wald ◽  
X. Shawn Liu ◽  
Cory Pettit ◽  
Mary Dillhoff ◽  
Andrei Manilchuk ◽  
...  

2013 ◽  
Vol 112 (3) ◽  
pp. 347-354 ◽  
Author(s):  
Aysegül Ilhan-Mutlu ◽  
Adelheid Wöhrer ◽  
Anna Sophie Berghoff ◽  
Georg Widhalm ◽  
Christine Marosi ◽  
...  

2007 ◽  
Vol 81 (23) ◽  
pp. 12740-12747 ◽  
Author(s):  
Christy Hebner ◽  
Melanie Beglin ◽  
Laimonis A. Laimins

ABSTRACT The high-risk human papillomavirus (HPV) E6 and E7 proteins act cooperatively to mediate multiple activities in viral pathogenesis. For instance, E7 acts to increase p53 levels while E6 accelerates its rate of turnover through the binding of the cellular ubiquitin ligase E6AP. Interferons are important antiviral agents that modulate both the initial and persistent phases of viral infection. The expression of HPV type 16 E7 was found to sensitize keratinocytes to the growth-inhibitory effects of interferon, while coexpression of E6 abrogates this inhibition. Treatment of E7-expressing cells with interferon ultimately resulted in cellular senescence through a process that is dependent upon acetylation of p53 by p300/CBP at lysine 382. Cells expressing mutant forms of E6 that are unable to bind p300/CBP or bind p53 failed to block acetylation of p53 at lysine 382 and were sensitive to growth arrest by interferon. In contrast, mutant forms of E6 that are unable to bind E6AP remain resistant to the effects of interferon, demonstrating that the absolute levels of p53 are not the major determinants of this activity. Finally, p53 acetylation at lysine 382 was found not to be an essential determinant of other types of senescence such as that induced by overexpression of Ras in human fibroblasts. This study identifies an important physiological role for E6 binding to p300/CBP in blocking growth arrest of human keratinocytes in the presence of interferon and so contributes to the persistence of HPV-infected cells.


2001 ◽  
Vol 21 (20) ◽  
pp. 6748-6757 ◽  
Author(s):  
Wenyi Wei ◽  
Ruth M. Hemmer ◽  
John M. Sedivy

ABSTRACT Following a proliferative phase of variable duration, most normal somatic cells enter a growth arrest state known as replicative senescence. In addition to telomere shortening, a variety of environmental insults and signaling imbalances can elicit phenotypes closely resembling senescence. We used p53−/− and p21−/− human fibroblast cell strains constructed by gene targeting to investigate the involvement of the Arf-Mdm2-p53-p21 pathway in natural as well as premature senescence states. We propose that in cell types that upregulate p21 during replicative exhaustion, such as normal human fibroblasts, p53, p21, and Rb act sequentially and constitute the major pathway for establishing growth arrest and that the telomere-initiated signal enters this pathway at the level of p53. Our results also revealed a number of significant differences between human and rodent fibroblasts in the regulation of senescence pathways.


2017 ◽  
Vol 61 (12) ◽  
pp. 2153-2158 ◽  
Author(s):  
C. Giannitti ◽  
A. De Palma ◽  
N. A. Pascarelli ◽  
S. Cheleschi ◽  
N. Giordano ◽  
...  

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