scholarly journals An Extract from the PlantDeschampsia antarcticaProtects Fibroblasts from Senescence Induced by Hydrogen Peroxide

2017 ◽  
Vol 2017 ◽  
pp. 1-16 ◽  
Author(s):  
Ana Ortiz-Espín ◽  
Esther Morel ◽  
Ángeles Juarranz ◽  
Antonio Guerrero ◽  
Salvador González ◽  
...  

The Antarctic plantDeschampsia antarctica(DA) is able to survive in extreme conditions thanks to its special mechanism of protection against environmental aggressions. In this work, we investigated whether an aqueous extract of the plant (EDA) retains some of its defensive properties and is able to protect our skin against common external oxidants. We evaluated EDA over young human fibroblasts and exposed to H2O2, and we measured cell proliferation, viability, and senescence-associatedβ-galactosidase (SA-β-Gal). We also tested the expression of several senescence-associated proteins including sirtuin1, lamin A/C, the replicative protein PCNA, and the redox protein thioredoxin 2. We found that EDA promotedper secell proliferation and viability and increased the expression of anti-senescence-related markers. Then, we selected a dose of H2O2as an inductor of senescence in human fibroblasts, and we found that an EDA treatment 24 h prior H2O2exposure increased fibroblast proliferation. EDA significantly inhibited the increase in SA-β-Gal levels induced by H2O2and promoted the expression of sirtuin 1 and lamin A/C proteins. Altogether, these results suggest that EDA protects human fibroblasts from cellular senescence induced by H2O2, pointing to this compound as a potential therapeutic agent to treat or prevent skin senescence.

2021 ◽  
Vol 22 (4) ◽  
pp. 2047
Author(s):  
Nina Schmid ◽  
Kim-Gwendolyn Dietrich ◽  
Ignasi Forne ◽  
Alexander Burges ◽  
Magdalena Szymanska ◽  
...  

Sirtuins (SIRTs) are NAD+-dependent deacetylases that regulate proliferation and cell death. In the human ovary, granulosa cells express sirtuin 1 (SIRT1), which has also been detected in human tumors derived from granulosa cells, i.e., granulosa cell tumors (GCTs), and in KGN cells. KGN cells are an established cellular model for the majority of GCTs and were used to explore the role of SIRT1. The SIRT1 activator SRT2104 increased cell proliferation. By contrast, the inhibitor EX527 reduced cell numbers, without inducing apoptosis. These results were supported by the outcome of siRNA-mediated silencing studies. A tissue microarray containing 92 GCTs revealed nuclear and/or cytoplasmic SIRT1 staining in the majority of the samples, and also, SIRT2-7 were detected in most samples. The expression of SIRT1–7 was not correlated with the survival of the patients; however, SIRT3 and SIRT7 expression was significantly correlated with the proliferation marker Ki-67, implying roles in tumor cell proliferation. SIRT3 was identified by a proteomic analysis as the most abundant SIRT in KGN. The results of the siRNA-silencing experiments indicate involvement of SIRT3 in proliferation. Thus, several SIRTs are expressed by GCTs, and SIRT1 and SIRT3 are involved in the growth regulation of KGN. If transferable to GCTs, these SIRTs may represent novel drug targets.


2005 ◽  
Vol 98 (2) ◽  
pp. 732-738 ◽  
Author(s):  
Mark F. Banks ◽  
Evgenia V. Gerasimovskaya ◽  
Doug A. Tucker ◽  
Maria G. Frid ◽  
Todd C. Carpenter ◽  
...  

In most mammalian species, chronic exposure to hypoxia leads to pulmonary hypertension and vascular remodeling. The adventitial fibroblast, because of its ability to proliferate in response to hypoxia, is thought to be a critical cell in the remodeling process. However, the transcription factors driving hypoxia-induced fibroblast proliferation have yet to be elucidated. The early growth response-1 (Egr-1) transcription factor has been shown to be upregulated by hypoxia in pulmonary artery adventitial fibroblasts. We therefore hypothesized that Egr-1 is directly involved in hypoxia-induced adventitial fibroblast proliferation. Immunohistochemical analysis of in vivo lung tissue from animals exposed to chronic hypoxia revealed increased expression of Egr-1 in the pulmonary artery fibroblasts vs. expression shown in normoxic controls. In fibroblasts cultured from chronically hypoxic animals, exposure to 1% oxygen upregulated Egr-1 protein and cell proliferation. To evaluate the role of Egr-1 in hypoxia-induced proliferation, we employed an Egr-1 antisense strategy. Addition of antisense Egr-1 oligonucleotides, but not sense oligonucleotides, attenuated the hypoxia-induced upregulation of Egr-1 protein and reduced hypoxia-induced DNA synthesis by 50%. Cell proliferation was also significantly inhibited by the addition of antisense Egr-1 oligonucleotides but not the sense oligonucleotides. In addition, hypoxia-induced upregulations of cyclin D and epidermal growth factor receptor were attenuated by Egr-1 antisense oligonucleotides. We conclude that Egr-1 protein expression is very sensitive to upregulation by hypoxia in pulmonary artery adventitial fibroblasts and that it plays an important role in the autonomous growth phenotype induced by hypoxia in these cells.


1987 ◽  
Vol 104 (4) ◽  
pp. 1105-1115 ◽  
Author(s):  
K Matuoka ◽  
M Namba ◽  
Y Mitsui

To establish the relation of glycosaminoglycan synthesis to cell proliferation, we investigated the synthesis of individual glycosaminoglycan species by intact cells and in a cell-free system, using normal and transformed human fibroblasts under differing culture conditions. Reducing serum concentration brought about a marked decline in the synthesis of hyaluronate (HA) as well as cell proliferation on both normal and transformed cells. Both HA synthesis and proliferation decreased with increasing cell densities markedly (in inverse proportion to cell density) in normal cells but gradually in transformed cells. This noticeable congruity of the changes in HA synthesis and proliferation indicates that the change in HA synthesis is related primarily to cell proliferation rather than to cell density or cellular transformation. Examination of HA synthesis in a cell-free system demonstrated that the activity of HA synthetase also fluctuated in conjunction with cell proliferation. Furthermore, growth-reduced cells (except crowded transformed cells) inhibited cell-free HA synthesis and this inhibition was induced coincidentally with a decrease in both HA synthetase activity and proliferation. These findings suggest that the change in HA synthesis is significant in the regulation of cell proliferation.


2009 ◽  
Vol 10 (11) ◽  
pp. 1705-1712 ◽  
Author(s):  
N.S. Fedarko ◽  
P. D'Avis ◽  
C.R. Frazier ◽  
M.J. Burrill ◽  
V. Fergusson ◽  
...  

1979 ◽  
Vol 58 (6) ◽  
pp. 1634-1639 ◽  
Author(s):  
R.E. Singer ◽  
W.G. Dutton

The effects of Escherichia coli endotoxin upon mouse L929 cell proliferation, DNA synthesis, protein synthesis, and proline incorporation were determined. It was found that a level of endotoxin which inhibited cell proliferation prompted a similar inhibition of DNA synthesis and overall cell protein synthesis. In contrast, endotoxin was shown to inhibit incorporation of proline into cell protein to a significantly greater extent.


Crystals ◽  
2019 ◽  
Vol 9 (10) ◽  
pp. 537 ◽  
Author(s):  
Ae Kyung Park ◽  
Il-Sup Kim ◽  
Hackwon Do ◽  
Hyun Kim ◽  
Woong Choi ◽  
...  

Ascorbic acid (AsA) is an abundant component of plants and acts as a strong and active antioxidant. In order to maintain the antioxidative capacity of AsA, the rapid regeneration of AsA is regulated by dehydroascorbate reductase (DHAR) and monodehydroascorbate reductase (MDHAR). To understand how MDHAR functions under extreme temperature conditions, this study characterized its biochemical properties and determined the crystal structure of MDHAR from the Antarctic hairgrass Deschampsia antarctica (DaMDHAR) at 2.2 Å resolution. This allowed for a structural comparison with the mesophilic MDHAR from Oryza sativa L. japonica (OsMDHAR). In the functional analysis, yeast cells expressing DaMDHAR were tolerant to freezing and thawing cycles. It is possible that the expression of DaMDHAR in yeast enhanced the tolerance for ROS-induced abiotic stress.


Sign in / Sign up

Export Citation Format

Share Document