Transcriptomic profiling revealed the regulatory mechanism of Arabidopsis seedlings response to oxidative stress from cryopreservation

2015 ◽  
Vol 34 (12) ◽  
pp. 2161-2178 ◽  
Author(s):  
Li Ren ◽  
Di Zhang ◽  
Guan-qun Chen ◽  
Barbara M. Reed ◽  
Xiao-hui Shen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Regulatory Mechanism ◽  
Transcriptomic Profiling

scholarly journals Genomic innovation of ATD alleviates mistranslation associated with multicellularity in Animalia

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Santosh Kumar Kuncha ◽  
Vinitha Lakshmi Venkadasamy ◽  
Gurumoorthy Amudhan ◽  
Priyanka Dahate ◽  
Sankara Rao Kola ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Quality Control ◽  
Cell Death ◽  
Regulatory Mechanism ◽  
Protein Biosynthesis ◽  
Trna Synthetase ◽  
Translation Quality ◽  
Trna Species ◽  
Critical Error

The emergence of multicellularity in Animalia is associated with increase in ROS and expansion of tRNA-isodecoders. tRNA expansion leads to misselection resulting in a critical error of L-Ala mischarged onto tRNAThr, which is proofread by Animalia-specific-tRNA Deacylase (ATD) in vitro. Here we show that in addition to ATD, threonyl-tRNA synthetase (ThrRS) can clear the error in cellular scenario. This two-tier functional redundancy for translation quality control breaks down during oxidative stress, wherein ThrRS is rendered inactive. Therefore, ATD knockout cells display pronounced sensitivity through increased mistranslation of threonine codons leading to cell death. Strikingly, we identify the emergence of ATD along with the error inducing tRNA species starting from Choanoflagellates thus uncovering an important genomic innovation required for multicellularity that occurred in unicellular ancestors of animals. The study further provides a plausible regulatory mechanism wherein the cellular fate of tRNAs can be switched from protein biosynthesis to non-canonical functions.

scholarly journals T-2 Toxin Induces Oxidative Stress, Apoptosis and Cytoprotective Autophagy in Chicken Hepatocytes

Toxins ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 90 ◽  
Author(s):  
Huadong Yin ◽  
Shunshun Han ◽  
Yuqi Chen ◽  
Yan Wang ◽  
Diyan Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Mechanism ◽  
Regulatory Mechanism ◽  
Fusarium Species ◽  
Cereal Grains ◽  
Oxygen Species ◽  
Related Protein ◽  
Pathological Changes ◽  
Toxicological Effect ◽  
Type A Trichothecenes

T-2 toxin is type A trichothecenes mycotoxin, which produced by fusarium species in cereal grains. T-2 toxin has been shown to induce a series of toxic effects on the health of human and animal, such as immunosuppression and carcinogenesis. Previous study has proven that T-2 toxin caused hepatotoxicity in chicken, but the regulatory mechanism is unclear. In the present study, we assessed the toxicological effect of T-2 toxin on apoptosis and autophagy in hepatocytes. The total of 120 1-day-old healthy broilers were allocated randomly into four groups and reared for 21 day with complete feed containing 0 mg/kg, 0.5 mg/kg, 1 mg/kg or 2 mg/kg T-2 toxin, respectively. The results showed that the apoptosis rate and pathological changes degree hepatocytes were aggravated with the increase of T-2 toxin. At the molecular mechanism level, T-2 toxin induced mitochondria-mediated apoptosis by producing reactive oxygen species, promoting cytochrome c translocation between the mitochondria and cytoplasm, and thus promoting apoptosomes formation. Meanwhile, the expression of the autophagy-related protein, ATG5, ATG7 and Beclin-1, and the LC3-II/LC3-I ratio were increased, while p62 was downregulated, suggesting T-2 toxin caused autophagy in hepatocytes. Further experiments demonstrated that the PI3K/AKT/mTOR signal may be participated in autophagy induced by T-2 toxin in chicken hepatocytes. These data suggest a possible underlying molecular mechanism for T-2 toxin that induces apoptosis and autophagy in chicken hepatocytes

Lopimune-induced mitochondrial toxicity is attenuated by increased uncoupling protein-2 level in treated mouse hepatocytes

2015 ◽  
Vol 468 (3) ◽  
pp. 401-407 ◽  
Author(s):  
Sara El Hoss ◽  
Georges M. Bahr ◽  
Karim S. Echtay
Keyword(s):  
Oxidative Stress ◽  
Protease Inhibitor ◽  
Regulatory Mechanism ◽  
Uncoupling Protein ◽  
Uncoupling Protein 2 ◽  
Ros Production ◽  
Mitochondrial Toxicity ◽  
Mouse Hepatocytes ◽  
Proton Leakage ◽  
Feedback Regulatory Mechanism

We have demonstrated that the antiretroviral protease inhibitor Lopimune increases oxidative stress in mouse hepatocytes and subsequently mitochondrial proton leakage. This effect is mediated by increased uncoupling protein-2 expression which in turn inhibits ROS production as a negative feedback regulatory mechanism.

The incorporation of cystine by the soluble carrier family 7 member 11 (SLC7A11) is a component of the redox regulatory mechanism in stallion spermatozoa†

2019 ◽  
Vol 101 (1) ◽  
pp. 208-222 ◽  
Author(s):  
José Manuel Ortiz-Rodriguez ◽  
Francisco E Martín-Cano ◽  
Cristina Ortega-Ferrusola ◽  
Javier Masot ◽  
Eloy Redondo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Regulatory Mechanism ◽  
Specific Inhibitor ◽  
Redox Status ◽  
Control Mechanisms ◽  
Male Factor Infertility ◽  
Male Factor ◽  
Major Mechanism ◽  
Oxidation Reduction ◽  
The Media

Abstract Oxidative stress is considered a major mechanism causing sperm damage during cryopreservation and storage, and underlies male factor infertility. Currently, oxidative stress is no longer believed to be caused only by the overproduction of reactive oxygen species, but rather by the deregulation of redox signaling and control mechanisms. With this concept in mind, here, we describe for the first time the presence of the soluble carrier family 7 member 11 (SLC7A11) antiporter, which exchanges extracellular cystine (Cyss) for intracellular glutamate, in stallion spermatozoa, as well as its impact on sperm function using the specific inhibitor sulfasalazine. Spermatozoa incubated with Cyss exhibited an increased intracellular GSH content compared with controls (P < 0.01): 50% in fresh extended stallion spermatozoa and 30% in frozen-thawed spermatozoa. This effect was prevented by the addition of sulfasalazine to the media. Cystine supplementation also reduced the oxidation–reduction potential of spermatozoa, with sulfasalazine only preventing this effect on fresh spermatozoa that were incubated for 3 h at 37°C, but not in frozen-thawed spermatozoa. While sulfasalazine reduced the motility of frozen-thawed spermatozoa, it increased motility in fresh samples. The present findings provide new and relevant data on the mechanism regulating the redox status of spermatozoa and suggest that a different redox regulatory mechanism exists in cryopreserved spermatozoa, thus providing new clues to improve current cryopreservation technologies and treat male factor infertility.

scholarly journals Positive feedback between ROS and cis-axis of PIASxα/p38α-SUMOylation/MK2 facilitates gastric cancer metastasis

2021 ◽  
Vol 12 (11) ◽  
Author(s):  
Qian Wang ◽  
Ci Xu ◽  
Qiang Fan ◽  
Haihua Yuan ◽  
Xin Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gastric Cancer ◽  
Reactive Oxygen Species ◽  
Stress Response ◽  
Cancer Cells ◽  
Regulatory Mechanism ◽  
Reactive Oxygen ◽  
Oxidative Stress Response ◽  
Oxygen Species ◽  
Gastric Cancer Cells

AbstractMAPK/p38 is an important mammalian signaling cascade that responds to a variety of intracellular or extracellular stimuli, such as reactive oxygen species (ROS), and participates in numerous physiological and pathological processes. However, the biological function of p38 in different tumors, and even at different stages of the same tumor, remains elusive. To further understand the regulatory mechanism of p38 and oxidative stress in the occurrence and development of gastric cancer, we report SUMOylation as a novel post-translational modification occurring on lysine 152 of MAPK14/p38α through immunoprecipitation and series of pull-down assays in vitro and in vivo. Importantly, we determine that p38α-SUMOylation functions as an authentic sensor and accelerator of reactive oxygen species generation via interaction with and activation of MK2 in the nucleus, and the ROS accumulation, in turn, promotes the SUMOylation of p38α by stabilizing the PIASxα protein. This precise regulatory mechanism is exploited by gastric cancer cells to create an internal environment for survival and, ultimately, metastasis. This study reveals novel insights into p38α-SUMOylation and its association with the intracellular oxidative stress response, which is closely related to the processes of gastric cancer. Furthermore, the PIASxα/p38α-SUMOylation/MK2 cis-axis may serve as a desirable therapeutic target in gastric cancer as targeting PIASxα, MK2, or a specific peptide region of p38α may reconcile the aberrant oxidative stress response in gastric cancer cells.

scholarly journals LncRNA MALAT1 Suppression Protects Endothelium against oxLDL-Induced Inflammation via Inhibiting Expression of MiR-181b Target Gene TOX

2019 ◽  
Vol 2019 ◽  
pp. 1-11
Author(s):  
Liuqing Wang ◽  
Yinliang Qi ◽  
Yi Wang ◽  
Haitao Tang ◽  
Zhenzhen Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Target Gene ◽  
Regulatory Mechanism ◽  
High Mobility ◽  
Signal Pathways ◽  
Lncrna Malat1 ◽  
Luciferase Activity Assay ◽  
And Oxidative Stress

Rare studies have been conducted to investigate the exact interactions between lung adenocarcinoma transcript 1 (MALAT1), thymocyte selection-associated high mobility group box (TOX), and miRNAs in the pathogenesis of atherosclerosis (AS). We aim to investigate the crosstalk between MALAT1 and TOX and evaluate whether the regulatory mechanism was associated with the miRNA network. AS tissues were collected to determine the level of MALAT1 expression in AS patients, together with determination of miR-181b expression. Cultured endothelial cells were utilized to analyze the expressions of MALAT1, miR-181b, and TOX in the presence of oxLDL. Luciferase activity assay was conducted to evaluate the potential target sites of miR-181b on MALAT1 and TOX. In this study, we demonstrated that MALAT1 was upregulated in patients with AS. MALAT1 silencing significantly downregulated the expression of the miR-181b target gene TOX via reversing the effect of miR181b. Importantly, positive modulation of miR181b and inhibition of MALAT1 and TOX significantly attenuated oxLDL-induced endothelial inflammation and oxidative stress. Moreover, the MAPK signal pathways in endothelial cells were also inhibited through regulation of above endogenous RNAs. In summary, MALAT1 suppression protects the endothelium from oxLDL-induced inflammation and oxidative stress in endothelial cells by upregulation of miR-181b and downregulation of TOX.

scholarly journals Melatonin and its-Remodeled Fecal Microbiota Improve Gut Health Through Inhibiting Oxidative Stress, Autophagy and Inflammation

2021 ◽  
Author(s):  
Yingqian Wang ◽  
Weike Shaoyong ◽  
Rui Cai ◽  
Xudong Yi ◽  
Wenlong Yong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Regulatory Mechanism ◽  
Fecal Microbiota Transplantation ◽  
Short Chain Fatty Acids ◽  
Fecal Microbiota ◽  
Control Group ◽  
Intestinal Epithelial ◽  
Gut Health ◽  
Intestinal Villus ◽  
Villus Height

Abstract Background Gut health is involved in the nutrition absorption, reproduction and lactation in antenatal, perinatal and early weaned mammals. Recent literatures have demonstrated that melatonin functions in aging, cancer and obesity, but to date, few investigations toward exploring whether melatonin-reprogrammed fecal microbiota transplantation (FMT) and foster care (FC) affect gut health have been performed. Results Here, compared with the control group, melatonin and FMT increased intestinal villus height/crypt depth (V/C), inhibited gut oxidative stress, autophagy and inflammation in antenatal and perinatal rats. Likewise, not only melatonin and FMT, but also FC enhanced intestinal V/C through above parallel ways with decreasing intestinal permeability in early weaned rats. Mechanically, melatonin directly strengthened antioxidation, attenuated autophagy and apoptosis in H2O2-induced IEC6 intestinal epithelial cells. Furthermore, melatonin, FMT and FC reprogrammed intestinal microbiota in which more beneficial microbiota, including Allobaculum, Bifidobacterium and Faecalibaculum produced more metabolic short-chain fatty acids (SCFAs) including acetic acid and butyric acid to protect gut health. Most interestingly, compared with the control group, early weaned rats may get above probiotics via eating or licking the dung of the co-cage rats treated with melatonin in the FC group. Conclusions Overall, melatonin, FMT and FC improved gut health and the potential regulatory mechanism was associated with strengthening antioxidation, suppressing autophagy, inflammatory and apoptosis, as well as producing more SCFAs from reprogrammed gut microbiota. These findings suggest that melatonin, FMT and FC may be novel and effective methods to ameliorate gut health in antenatal, perinatal and weaned mammals.

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