scholarly journals Comparison of the effects of 40% oxygen and two atmospheric absolute air pressure conditions on stress-induced premature senescence of normal human diploid fibroblasts

2008 ◽  
Vol 13 (4) ◽  
pp. 447-458 ◽  
Author(s):  
Sangnam Oh ◽  
Eunil Lee ◽  
Joohyun Lee ◽  
Yongchul Lim ◽  
Joonhee Kim ◽  
...  
Keyword(s):  
Air Pressure ◽  
Premature Senescence ◽  
Diploid Fibroblasts ◽  
Human Diploid Fibroblasts ◽  
Normal Human ◽  
Stress Induced Premature Senescence

scholarly journals Inhibition of Mitochondrial CytochromecRelease and Suppression of Caspases by Gamma-Tocotrienol Prevent Apoptosis and Delay Aging in Stress-Induced Premature Senescence of Skin Fibroblasts

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Suzana Makpol ◽  
Norhazira Abdul Rahim ◽  
Chua Kien Hui ◽  
Wan Zurinah Wan Ngah
Keyword(s):  
Caspase 3 ◽  
Annexin V ◽  
Telomerase Activity ◽  
Cellular Aging ◽  
Premature Senescence ◽  
Caspase 9 ◽  
Diploid Fibroblasts ◽  
Human Diploid Fibroblasts ◽  
Apoptotic Effect ◽  
Stress Induced Premature Senescence

In this study, we determined the molecular mechanism ofγ-tocotrienol (GTT) in preventing cellular aging by focusing on its anti-apoptotic effect in stress-induced premature senescence (SIPS) model of human diploid fibroblasts (HDFs). Results obtained showed that SIPS exhibited senescent-phenotypic characteristic, increased expression of senescence-associatedβ-galactosidase (SAβ-gal) and promoted G0/G1cell cycle arrest accompanied by shortening of telomere length with decreased telomerase activity. Both SIPS and senescent HDFs shared similar apoptotic changes such as increased Annexin V-FITC positive cells, increased cytochromecrelease and increased activation of caspase-9 and caspase-3 (P<0.05). GTT treatment resulted in a significant reduction of Annexin V-FITC positive cells, inhibited cytochromecrelease and decreased activation of caspase-9 and caspase-3 (P<0.05). Gene expression analysis showed that GTT treatment down regulated BAX mRNA, up-regulated BCL2A1 mRNA and decreased the ratio of Bax/Bcl-2 protein expression (P<0.05) in SIPS. These findings suggested that GTT inhibits apoptosis by modulating the upstream apoptosis cascade, causing the inhibition of cytochromecrelease from the mitochondria with concomitant suppression of caspase-9 and caspase-3 activation. In conclusion, GTT delays cellular senescence of human diploid fibroblasts through the inhibition of intrinsic mitochondria-mediated pathway which involved the regulation of pro- and anti-apoptotic genes and proteins.

scholarly journals Comparative Effects of Biodynes, Tocotrienol-Rich Fraction, and Tocopherol in Enhancing Collagen Synthesis and Inhibiting Collagen Degradation in Stress-Induced Premature Senescence Model of Human Diploid Fibroblasts

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Suzana Makpol ◽  
Faidruz Azura Jam ◽  
Shy Cian Khor ◽  
Zahariah Ismail ◽  
Yasmin Anum Mohd Yusof ◽  
...  
Keyword(s):  
Collagen Synthesis ◽  
Skin Aging ◽  
Collagen Degradation ◽  
Type I ◽  
Premature Senescence ◽  
Diploid Fibroblasts ◽  
Human Diploid Fibroblasts ◽  
Protein Levels ◽  
Stress Induced Premature Senescence ◽  
Tocotrienol Rich Fraction

Biodynes, tocotrienol-rich fraction (TRF), and tocopherol have shown antiaging properties. However, the combined effects of these compounds on skin aging are yet to be investigated. This study aimed to elucidate the skin aging effects of biodynes, TRF, and tocopherol on stress-induced premature senescence (SIPS) model of human diploid fibroblasts (HDFs) by determining the expression of collagen and MMPs at gene and protein levels. Primary HDFs were treated with biodynes, TRF, and tocopherol prior to hydrogen peroxide (H2O2) exposure. The expression ofCOL1A1, COL3A1, MMP1, MMP2, MMP3,andMMP9genes was determined by qRT-PCR. Type I and type III procollagen proteins were measured by Western blotting while the activities of MMPs were quantified by fluorometric Sensolyte MMP Kit. Our results showed that biodynes, TRF, and tocopherol upregulated collagen genes and downregulatedMMPgenes (P<0.05). Type I procollagen and type III procollagen protein levels were significantly increased in response to biodynes, TRF, and tocopherol treatment (P<0.05) with reduction in MMP-1, MMP-2, MMP-3, and MMP-9 activities (P<0.05). These findings indicated that biodynes, TRF, and tocopherol effectively enhanced collagen synthesis and inhibited collagen degradation and therefore may protect the skin from aging.

scholarly journals Reversible cellular senescence: implications for immortalization of normal human diploid fibroblasts.

1989 ◽  
Vol 9 (7) ◽  
pp. 3088-3092 ◽  
Author(s):  
W E Wright ◽  
O M Pereira-Smith ◽  
J W Shay
Keyword(s):  
Cellular Senescence ◽  
Rare Event ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
T Antigen ◽  
Diploid Fibroblasts ◽  
Human Diploid Fibroblasts ◽  
Normal Human ◽  
Immortal Cells ◽  
Cellular Dna

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.

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