scholarly journals A set of miRNAs participates in the cellular senescence program in human diploid fibroblasts

2011 ◽  
Vol 19 (4) ◽  
pp. 713-721 ◽  
Author(s):  
R Faraonio ◽  
P Salerno ◽  
F Passaro ◽  
C Sedia ◽  
A Iaccio ◽  
...  

Aging Cell ◽  
2015 ◽  
Vol 15 (2) ◽  
pp. 245-255 ◽  
Author(s):  
Kyeong Eun Yang ◽  
Hyun‐Jin Jang ◽  
In‐Hu Hwang ◽  
Young‐Ho Chung ◽  
Jong‐Soon Choi ◽  
...  


PLoS ONE ◽  
2008 ◽  
Vol 3 (3) ◽  
pp. e1710 ◽  
Author(s):  
Jing Huang ◽  
Qini Gan ◽  
Limin Han ◽  
Jian Li ◽  
Hai Zhang ◽  
...  


1989 ◽  
Vol 9 (7) ◽  
pp. 3088-3092 ◽  
Author(s):  
W E Wright ◽  
O M Pereira-Smith ◽  
J W Shay

IMR-90 normal human diploid fibroblasts, transfected with a steroid inducible mouse mammary tumor virus-driven simian virus 40 T antigen, were carried through crisis to yield an immortal cell line. Growth was dependent on the presence of the inducer (dexamethasone) during both the extended precrisis life span of the cells and after immortalization. After dexamethasone removal, immortal cells divided once or twice and then accumulated in G1. These results are best explained by a two-stage model for cellular senescence. Mortality stage 1 (M1) causes a loss of mitogen responsiveness and arrest near the G1/S interface and can be bypassed or overcome by the cellular DNA synthesis-stimulating activity of T antigen. Mortality stage 2 (M2) is an independent mechanism that is responsible for the failure of cell division during crisis. The inactivation of M2 is a rare event, probably of mutational origin in human cells, independent of or only indirectly related to the expression of T antigen. Under this hypothesis, T-antigen-immortalized cells contain an active but bypassed M1 mechanism and an inactivated M2 mechanism. These cells are dependent on the continued expression of T antigen for the maintenance of immortality for the same reason that precrisis cells are dependent on T antigen for growth: both contain an active M1 mechanism.



2011 ◽  
Vol 286 (38) ◽  
pp. 33447-33456 ◽  
Author(s):  
Xiaoxiao Cao ◽  
Lixiang Xue ◽  
Limin Han ◽  
Liwei Ma ◽  
Tianda Chen ◽  
...  


1994 ◽  
Vol 201 (1) ◽  
pp. 409-414 ◽  
Author(s):  
X.T. Liu ◽  
C.A. Stewart ◽  
R.L. King ◽  
D.A. Danner ◽  
R.T. Dellorco ◽  
...  


2008 ◽  
Vol 121 (13) ◽  
pp. 2235-2245 ◽  
Author(s):  
Q. Gan ◽  
J. Huang ◽  
R. Zhou ◽  
J. Niu ◽  
X. Zhu ◽  
...  


Aging ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 3731-3749 ◽  
Author(s):  
Hyun-Jin Jang ◽  
Kyeong Eun Yang ◽  
Won Keun Oh ◽  
Song-I Lee ◽  
In-Hu Hwang ◽  
...  


2000 ◽  
Vol 119 (3) ◽  
pp. 113-130 ◽  
Author(s):  
In Kyoung Lim ◽  
Kwang Won Hong ◽  
In Hae Kwak ◽  
Gyesoon Yoon ◽  
Sang Chul Park


2016 ◽  
Author(s):  
Hyun-Jin Jang ◽  
Eunbi Jo ◽  
Young-Ho Chung ◽  
JunSoo Park ◽  
Sung-Jun Park ◽  
...  


2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Sharon Gwee Sian Khee ◽  
Yasmin Anum Mohd Yusof ◽  
Suzana Makpol

Emerging evidences highlight the implication of microRNAs as a posttranscriptional regulator in aging. Several senescence-associated microRNAs (SA-miRNAs) are found to be differentially expressed during cellular senescence. However, the role of dietary compounds on SA-miRNAs remains elusive. This study aimed to elucidate the modulatory role of tocotrienol-rich fraction (TRF) on SA-miRNAs (miR-20a, miR-24, miR-34a, miR-106a, and miR-449a) and established target genes of miR-34a (CCND1, CDK4, and SIRT1) during replicative senescence of human diploid fibroblasts (HDFs). Primary cultures of HDFs at young and senescent were incubated with TRF at 0.5 mg/mL. Taqman microRNA assay showed significant upregulation of miR-24 and miR-34a and downregulation of miR-20a and miR-449a in senescent HDFs (P<0.05). TRF reduced miR-34a expression in senescent HDFs and increased miR-20a expression in young HDFs and increased miR-449a expression in both young and senescent HDFs. Our results also demonstrated that ectopic expression of miR-34a reduced the expression of CDK4 significantly (P<0.05). TRF inhibited miR-34a expression thus relieved its inhibition on CDK4 gene expression. No significant change was observed on the expression of CCND1, SIRT1, and miR-34a upstream transcriptional regulator, TP53. In conclusion tocotrienol-rich fraction prevented cellular senescence of human diploid fibroblasts via modulation of SA-miRNAs and target genes expression.



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