Chlorella vulgaris modulates the expression of senescence-associated genes in replicative senescence of human diploid fibroblasts

2019 ◽  
Vol 47 (1) ◽  
pp. 369-379 ◽  
Author(s):  
Faizul Jaafar ◽  
Lina Wati Durani ◽  
Suzana Makpol
2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Lina Wati Durani ◽  
Shy Cian Khor ◽  
Jen Kit Tan ◽  
Kien Hui Chua ◽  
Yasmin Anum Mohd Yusof ◽  
...  

Piper betle (PB) is a traditional medicine that is widely used to treat different diseases around Asian region. The leaf extracts contain various bioactive compounds, which were reported to have antidiabetic, antibacterial, anti-inflammatory, antioxidant, and anticancer effects. In this study, the effect of PB aqueous extracts on replicative senescent human diploid fibroblasts (HDFs) was investigated by determining the expressions of senescence-associated genes using quantitative PCR. Our results showed that PB extracts at 0.4 mg/ml can improve cell proliferation of young (143%), presenescent (127.3%), and senescent (157.3%) HDFs. Increased expressions of PRDX6, TP53, CDKN2A, PAK2, and MAPK14 were observed in senescent HDFs compared to young and/or presenescent HDFs. Treatment with PB extracts modulates the transcriptional profile changes in senescent HDFs. By contrast, expressions of SOD1 increased, whereas GPX1, PRDX6, TP53, CDKN2A, PAK2, and MAPK14 were decreased in PB-treated senescent HDFs compared to untreated senescent HDFs. In conclusion, this study indicates the modulation of PB extracts on senescence-associated genes expression of replicative senescent HDFs. Further studies warrant determining the mechanism of PB in modulating replicative senescence of HDFs through these signaling pathways.


2007 ◽  
Vol 120 (22) ◽  
pp. 2028-2035 ◽  
Author(s):  
Pei-chang WANG ◽  
Jian ZHANG ◽  
Zong-yu ZHANG ◽  
Tan-jun TONG

2020 ◽  
Vol 44 (2) ◽  
pp. 341-349 ◽  
Author(s):  
Kyeong-Eun Yang ◽  
Hyun-Jin Jang ◽  
In-Hu Hwang ◽  
Eun Mi Hong ◽  
Min-Goo Lee ◽  
...  

Aging ◽  
2010 ◽  
Vol 2 (6) ◽  
pp. 333-343 ◽  
Author(s):  
Bernard S. Marasa ◽  
Subramanya Srikantan ◽  
Jennifer L. Martindale ◽  
Mihee M. Kim ◽  
Eun Kyung Lee ◽  
...  

2003 ◽  
Vol 124 (10-12) ◽  
pp. 1025-1034 ◽  
Author(s):  
Peichang Wang ◽  
Zongyu Zhang ◽  
Xiaofeng Ma ◽  
Yu Huang ◽  
Xinwen Liu ◽  
...  

2008 ◽  
Vol 44 (10) ◽  
pp. 1817-1832 ◽  
Author(s):  
Florence Debacq-Chainiaux ◽  
Thierry Pascal ◽  
Emmanuelle Boilan ◽  
Coralie Bastin ◽  
Emilie Bauwens ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Masatoshi Suzuki ◽  
Keiji Suzuki ◽  
Seiji Kodama ◽  
Shunichi Yamashita ◽  
Masami Watanabe

Foci of phosphorylated histone H2AX and ATM are the surrogate markers of DNA double strand breaks. We previously reported that the residual foci increased their size after irradiation, which amplifies DNA damage signals. Here, we addressed whether amplification of DNA damage signal is involved in replicative senescence of normal human diploid fibroblasts. Large phosphorylated H2AX foci (>1.5 μm diameter) were specifically detected in presenescent cells. The frequency of cells with large foci was well correlated with that of cells positive for senescence-associatedβ-galactosidase staining. Hypoxic cell culture condition extended replicative life span of normal human fibroblast, and we found that the formation of large foci delayed in those cells. Our immuno-FISH analysis revealed that large foci partially localized at telomeres in senescent cells. Importantly, large foci of phosphorylated H2AX were always colocalized with phosphorylated ATM foci. Furthermore, Ser15-phosphorylated p53 showed colocalization with the large foci. Since the treatment of senescent cells with phosphoinositide 3-kinase inhibitor, wortmannin, suppressed p53 phosphorylation, it is suggested that amplification of DNA damage signaling sustains persistent activation of ATM-p53 pathway, which is essential for replicative senescence.


FEBS Letters ◽  
1998 ◽  
Vol 427 (2) ◽  
pp. 203-208 ◽  
Author(s):  
Daishiro Kato ◽  
Kazuhiro Miyazawa ◽  
Marugarida Ruas ◽  
Maria Starborg ◽  
Ikuo Wada ◽  
...  

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