scholarly journals Preventive Effects of Epigallocatechin-3-O-Gallate against Replicative Senescence Associated with p53 Acetylation in Human Dermal Fibroblasts

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Dong-Wook Han ◽  
Mi Hee Lee ◽  
Bongju Kim ◽  
Jun Jae Lee ◽  
Suong-Hyu Hyon ◽  
...  
Keyword(s):  
Cell Cycle Progression ◽  
Replicative Senescence ◽  
Nuclear Translocation ◽  
Articular Chondrocytes ◽  
Underlying Mechanism ◽  
Serial Passage ◽  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Primary Cells ◽  
Preventive Effects

Considering the various pharmacological activities of epigallocatechin-3-O-gallate (EGCG) including anticancer, and anti-inflammatory, antidiabetic, and so forth, relatively less attention has been paid to the antiaging effect of EGCG on primary cells. In this study, the preventive effects of EGCG against serial passage-induced senescence were investigated in primary cells including rat vascular smooth muscle cells (RVSMCs), human dermal fibroblasts (HDFs), and human articular chondrocytes (HACs). The involvement of Sirt1 and acetylated p53 was examined as an underlying mechanism for the senescence preventive activity of EGCG in HDFs. All cells were employed with the initial passage number (PN) between 3 and 7. For inducing senescence, the cells were serially passaged at the predetermined times and intervals in the absence or presence of EGCG (50 or 100 μM). Serial passage-induced senescence in RVSMCs and HACs was able to be significantly prevented at 50 μM EGCG, while in HDFs, 100 μM EGCG could significantly prevent senescence and recover their cell cycle progression close to the normal level. Furthermore, EGCG was found to prevent serial passage- and H2O2-induced senescence in HDFs by suppressing p53 acetylation, but the Sirt1 activity was unaffected. In addition, proliferating HDFs showed similar cellular uptake of FITC-conjugated EGCG into the cytoplasm with their senescent counterparts but different nuclear translocation of it from them, which would partly account for the differential responses to EGCG in proliferating versus senescent cells. Taking these results into consideration, it is suggested that EGCG may be exploited to craft strategies for the development of an antiaging or age-delaying agent.

Photobiomodulation with 590 nm Wavelength Delays the Telomere Shortening and Replicative Senescence of Human Dermal Fibroblasts In Vitro

2020 ◽  
Vol 38 (11) ◽  
pp. 656-660
Author(s):  
Borislav Arabadjiev ◽  
Roumen Pankov ◽  
Ivelina Vassileva ◽  
Lyuben Sashov Petrov ◽  
Ivan Buchvarov
Keyword(s):  
Replicative Senescence ◽  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Telomere Shortening

LncRNA RP11-670E13.6 Regulates Cell Cycle Progression in UVB Damaged Human Dermal Fibroblasts

2018 ◽  
Vol 94 (3) ◽  
pp. 589-597 ◽  
Author(s):  
Mengna Li ◽  
Li Li ◽  
Xiaofeng Zhang ◽  
Yan Yan ◽  
Baoxi Wang
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Cycle Progression

scholarly journals Antiphotoaging Effect of 3,5-Dicaffeoyl-epi-quinic Acid against UVA-Induced Skin Damage by Protecting Human Dermal Fibroblasts In Vitro

2020 ◽  
Vol 21 (20) ◽  
pp. 7756
Author(s):  
Jung Hwan Oh ◽  
Fatih Karadeniz ◽  
Chang-Suk Kong ◽  
Youngwan Seo
Keyword(s):  
Molecular Mechanisms ◽  
Type I Collagen ◽  
Nuclear Translocation ◽  
Quinic Acid ◽  
Dermal Fibroblasts ◽  
Type I ◽  
Human Dermal Fibroblasts ◽  
Skin Damage ◽  
Chronological Aging

Cutaneous aging is divided into intrinsic and exogenous aging correspondingly contributing to the complex biological phenomenon in skin. Intrinsic aging is also termed chronological aging, which is the accumulation of inevitable changes over time and is largely genetically determined. Superimposed on this intrinsic process, exogenous aging is associated with environmental exposure, mainly to ultraviolet (UV) radiation and more commonly termed as photoaging. UV-induced skin aging induces increased expression of matrix metalloproteinases (MMPs) which in turn causes the collagen degradation. Therefore, MMP inhibitors of natural origin are regarded as a primary approach to prevent or treat photoaging. This study investigated the effects of 3,5-dicaffeoyl-epi-quinic acid (DEQA) on photoaging and elucidated its molecular mechanisms in UVA-irradiated human dermal fibroblasts (HDFs). The results show that treatment with DEQA decreases MMP-1 production and increases type I collagen production in UVA-damaged HDFs. In addition, treatment of UVA-irradiated HDFs with DEQA downregulates MMP-1, MMP-3 and MMP-9 expression via blocking MAPK-cascade-regulated AP-1 transcriptional activity in UVA-irradiated HDFs. Furthermore, DEQA relieves the UVA-mediated suppression of type I procollagen and collagen expression through stimulating TGF-β/Smad signaling, leading to activation of the Smad 2/3 and Smad 4 nuclear translocation. These results suggest that DEQA could be a potential cosmetic agent for prevention and treatment of skin photoaging.

scholarly journals Organogermanium suppresses cell death due to oxidative stress in normal human dermal fibroblasts

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Tomoya Takeda ◽  
Sota Doiyama ◽  
Junya Azumi ◽  
Yasuhiro Shimada ◽  
Yoshihiko Tokuji ◽  
...  
Keyword(s):  
Cell Death ◽  
Expression Analysis ◽  
Dermal Fibroblasts ◽  
Water Soluble ◽  
Gene Profiling ◽  
Human Dermal Fibroblasts ◽  
Ros Scavenging ◽  
Normal Human ◽  
Preventive Effects ◽  
Normal Human Dermal Fibroblasts

Abstract Reactive oxygen species (ROS) are very harmful to dermal cells, and it is thus important to develop cosmetics that protect the skin from ROS and other stimuli. Repagermanium is a synthetic water-soluble organogermanium polymer, and in this study, we attempted to visualize the incorporation of germanium into normal human dermal fibroblasts (NHDFs) using isotope microscopy. In addition, the content of 3-(trihydroxygermyl)propanoic acid (THGP), a hydrolyzed monomer of repagermanium, in NHDFs was determined through liquid chromatography mass spectrometry (LC-MS/MS), and the dose-dependent incorporation of THGP was confirmed. We then evaluated the preventive effects of THGP against ROS-induced NHDF death and confirmed the observed preventive effects through gene profiling and expression analysis. The addition of 0.59–5.9 mM THGP reduced cell death resulting from ROS damage caused by the reaction between xanthine oxidase and hypoxanthine and the direct addition of H2O2. Furthermore, this study provides the first demonstration that the effect of THGP was not due to the direct scavenging of ROS, which indicates that the mechanism of THGP differs from that of general antioxidants, such as ascorbic acid. The gene profiling and expression analysis showed that THGP suppressed the expression of the nuclear receptor subfamily 4 group A member 2 (NR4A2) gene, which is related to cell death, and the interleukin 6 (IL6) and chemokine (C-X-C motif) ligand 2 (CXCL2) genes, which are related to the inflammatory response. Furthermore, the production of IL6 induced by H2O2 was suppressed by the THGP treatment. Our data suggest that the preventive effect of THGP against ROS-induced cell death is not due to antioxidant enzymes or ROS scavenging.

Replicative senescence of human dermal fibroblasts affects structural and functional aspects of the Golgi apparatus

2019 ◽  
Vol 28 (8) ◽  
pp. 922-932 ◽  
Author(s):  
Julie Despres ◽  
Yasmina Ramdani ◽  
Marine di Giovanni ◽  
Magalie Bénard ◽  
Abderrakib Zahid ◽  
...  
Keyword(s):  
Golgi Apparatus ◽  
Replicative Senescence ◽  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Functional Aspects

scholarly journals CSIG Inhibits PTEN Translation in Replicative Senescence

2008 ◽  
Vol 28 (20) ◽  
pp. 6290-6301 ◽  
Author(s):  
Liwei Ma ◽  
Na Chang ◽  
Shuzhen Guo ◽  
Qian Li ◽  
Zongyu Zhang ◽  
...  
Keyword(s):  
Cellular Senescence ◽  
Cell Cycle Progression ◽  
Replicative Senescence ◽  
Subtractive Hybridization ◽  
Underlying Mechanism ◽  
Suppressive Subtractive Hybridization ◽  
Luciferase Reporter ◽  
Hek 293 ◽  
293 Cells ◽  
Pten Mrna

ABSTRACT Using a suppressive subtractive hybridization system, we identified CSIG (cellular senescence-inhibited gene protein; RSL1D1) that was abundant in young human diploid fibroblast cells but declined upon replicative senescence. Overexpression or knockdown of CSIG did not influence p21Cip1 and p16INK4a expressions. Instead, CSIG negatively regulated PTEN and p27Kip1 expressions, in turn promoting cell proliferation. In PTEN-silenced HEK 293 cells and PTEN-deficient human glioblastoma U87MG cells, the effect of CSIG on p27Kip1 expression and cell division was abolished, suggesting that PTEN was required for the role of CSIG on p27Kip1 regulation and cell cycle progression. Investigation into the underlying mechanism revealed that the regulation of PTEN by CSIG was achieved through a translational suppression mechanism. Further study showed that CSIG interacted with PTEN mRNA in the 5′ untranslated region (UTR) and that knockdown of CSIG led to increased luciferase activity of a PTEN 5′ UTR-luciferase reporter. Moreover, overexpression of CSIG significantly delayed the progression of replicative senescence, while knockdown of CSIG expression accelerated replicative senescence. Knockdown of PTEN diminished the effect of CSIG on cellular senescence. Our findings indicate that CSIG acts as a novel regulatory component of replicative senescence, which requires PTEN as a mediator and involves in a translational regulatory mechanism.

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