scholarly journals Glutathione Restores Hg-Induced Morpho-Physiological Retardations by Inducing Phytochelatin and Oxidative Defense in Alfalfa

Biology ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 364
Author(s):  
Md Atikur Rahman ◽  
Ahmad Humayan Kabir ◽  
Abul Mandal ◽  
Swapan Kumar Roy ◽  
Yowook Song ◽  
...  
Keyword(s):  
Cell Wall ◽  
Bioinformatics Analysis ◽  
In Silico Analysis ◽  
Phytochelatin Synthase ◽  
Forage Crop ◽  
Oxidative Defense ◽  
Forage Plants ◽  
Silico Analysis ◽  
Root Cell Wall

Mercury (Hg) is toxic to plants, but the effect of glutathione in Hg alleviation was never studied in alfalfa, an important forage crop. In this study, Hg toxicity showed morphological retardation, chlorophyll reduction, and PSII inefficiency, which was restored due to GSH supplementation in alfalfa plants treated with Hg. Results showed a significant increase of Hg, but Fe and S concentrations substantially decreased in root and shoot accompanied by the downregulation of Fe (MsIRT1) and S (MsSultr1;2 and MsSultr1;3) transporters in roots of Hg-toxic alfalfa. However, GSH caused a significant decrease of Hg in the shoot, while the root Hg level substantially increased, accompanied by the restoration of Fe and S status, relative to Hg-stressed alfalfa. The subcellular analysis showed a substantial deposition of Hg in the root cell wall accompanied by the increased GSH and PC and the upregulation of MsPCS1 and MsGSH1 genes in roots. It suggests the involvement of GSH in triggering PC accumulation, causing excess Hg bound to the cell wall of the root, thereby reducing Hg translocation in alfalfa. Bioinformatics analysis showed that the MsPCS1 protein demonstrated one common conserved motif linked to the phytochelatin synthase domain (CL0125) with MtPCS1 and AtMCS1 homologs. These in silico analysis further confirmed the detoxification role of MsPCS1 induced by GSH in Hg-toxic alfalfa. Additionally, GSH induces GSH and GR activity to counteract oxidative injuries provoked by Hg-induced H2O2 and lipid peroxidation. These findings may provide valuable knowledge to popularize GSH-derived fertilizer or to develop Hg-free alfalfa or other forage plants.

scholarly journals Intracellular Na+ Modulates Pacemaking Activity in Murine Sinoatrial Node Myocytes: An In Silico Analysis

2021 ◽  
Vol 22 (11) ◽  
pp. 5645
Author(s):  
Stefano Morotti ◽  
Haibo Ni ◽  
Colin H. Peters ◽  
Christian Rickert ◽  
Ameneh Asgari-Targhi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Membrane Potential ◽  
In Silico ◽  
Sinoatrial Node ◽  
In Silico Analysis ◽  
Ankyrin B ◽  
Deficient Mice ◽  
Silico Analysis ◽  
Bursting Activity

Background: The mechanisms underlying dysfunction in the sinoatrial node (SAN), the heart’s primary pacemaker, are incompletely understood. Electrical and Ca2+-handling remodeling have been implicated in SAN dysfunction associated with heart failure, aging, and diabetes. Cardiomyocyte [Na+]i is also elevated in these diseases, where it contributes to arrhythmogenesis. Here, we sought to investigate the largely unexplored role of Na+ homeostasis in SAN pacemaking and test whether [Na+]i dysregulation may contribute to SAN dysfunction. Methods: We developed a dataset-specific computational model of the murine SAN myocyte and simulated alterations in the major processes of Na+ entry (Na+/Ca2+ exchanger, NCX) and removal (Na+/K+ ATPase, NKA). Results: We found that changes in intracellular Na+ homeostatic processes dynamically regulate SAN electrophysiology. Mild reductions in NKA and NCX function increase myocyte firing rate, whereas a stronger reduction causes bursting activity and loss of automaticity. These pathologic phenotypes mimic those observed experimentally in NCX- and ankyrin-B-deficient mice due to altered feedback between the Ca2+ and membrane potential clocks underlying SAN firing. Conclusions: Our study generates new testable predictions and insight linking Na+ homeostasis to Ca2+ handling and membrane potential dynamics in SAN myocytes that may advance our understanding of SAN (dys)function.

In silico analysis of selenoprotein N (Gallus gallus): absence of EF-hand motif and the role of CUGS-helix domain in antioxidant protection

Metallomics ◽  
2021 ◽  
Vol 13 (3) ◽  
Author(s):  
Shi-Yong Zhu ◽  
Li-Li Liu ◽  
Yue-Qiang Huang ◽  
Xiao-Wei Li ◽  
Milton Talukder ◽  
...  
Keyword(s):  
In Silico ◽  
Common Ancestor ◽  
In Silico Analysis ◽  
Antioxidant Protection ◽  
Jnk Pathway ◽  
Downstream Target ◽  
Ef Hand ◽  
Silico Analysis

Abstract Selenoprotein N (SEPN1) is critical to the normal muscular physiology. Mutation of SEPN1 can raise congenital muscular disorder in human. It is also central to maturation and structure of skeletal muscle in chicken. However, human SEPN1 contained an EF-hand motif, which was not found in chicken. And the biochemical and molecular characterization of chicken SEPN1 remains unclear. Hence, protein domains, transcription factors, and interactions of Ca2+ in SEPN1 were analyzed in silico to provide the divergence and homology between chicken and human in this work. The results showed that vertebrates’ SEPN1 evolved from a common ancestor. Human and chicken's SEPN1 shared a conserved CUGS-helix domain with function in antioxidant protection. SEPN1 might be a downstream target of JNK pathway, and it could respond to multiple stresses. Human's SEPN1 might not combine with Ca2+ with a single EF-hand motif in calcium homeostasis, and chicken SEPN1 did not have the EF-hand motif in the prediction, indicating the EF-hand motif malfunctioned in chicken SEPN1.

scholarly journals A new insight into role of phosphoketolase pathway in Synechocystis sp. PCC 6803

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Anushree Bachhar ◽  
Jiri Jablonsky
Keyword(s):  
In Silico Analysis ◽  
Bioinformatic Analysis ◽  
Phosphoglycerate Mutase ◽  
Phosphoketolase Pathway ◽  
Multi Level ◽  
Silico Analysis ◽  
Insight Into ◽  
Synechocystis Sp ◽  
Pcc 6803

AbstractPhosphoketolase (PKET) pathway is predominant in cyanobacteria (around 98%) but current opinion is that it is virtually inactive under autotrophic ambient CO2 condition (AC-auto). This creates an evolutionary paradox due to the existence of PKET pathway in obligatory photoautotrophs. We aim to answer the paradox with the aid of bioinformatic analysis along with metabolic, transcriptomic, fluxomic and mutant data integrated into a multi-level kinetic model. We discussed the problems linked to neglected isozyme, pket2 (sll0529) and inconsistencies towards the explanation of residual flux via PKET pathway in the case of silenced pket1 (slr0453) in Synechocystis sp. PCC 6803. Our in silico analysis showed: (1) 17% flux reduction via RuBisCO for Δpket1 under AC-auto, (2) 11.2–14.3% growth decrease for Δpket2 in turbulent AC-auto, and (3) flux via PKET pathway reaching up to 252% of the flux via phosphoglycerate mutase under AC-auto. All results imply that PKET pathway plays a crucial role under AC-auto by mitigating the decarboxylation occurring in OPP pathway and conversion of pyruvate to acetyl CoA linked to EMP glycolysis under the carbon scarce environment. Finally, our model predicted that PKETs have low affinity to S7P as a substrate.

Identification of differentially expressed microRNAs in outgrowth embryos compared with blastocysts and non-outgrowth embryos in mice

2019 ◽  
Vol 31 (4) ◽  
pp. 645 ◽  
Author(s):  
Jihyun Kim ◽  
Jaewang Lee ◽  
Jin Hyun Jun
Keyword(s):  
Bioinformatics Analysis ◽  
Preimplantation Embryo ◽  
Expression Profiles ◽  
In Silico Analysis ◽  
Differentially Expressed ◽  
Recurrent Implantation Failure ◽  
Preimplantation Embryo Development ◽  
Mirna Expression Profiles ◽  
Differentially Expressed Mirnas ◽  
Silico Analysis

Recurrent implantation failure (RIF) is one of the main causes for the repeated failure of IVF, and the major reason for RIF is thought to be a miscommunication between the embryo and uterus. However, the exact mechanism underlying embryo–uterus cross-talk is not fully understood. The aim of the present study was to identify differentially expressed microRNAs (miRNAs) among blastocysts, non-outgrowth and outgrowth embryos in mice using microarray analysis. A bioinformatics analysis was performed to predict the potential mechanisms of implantation. The miRNA expression profiles differed significantly between non-outgrowth and outgrowth embryos. In all, 3163 miRNAs were detected in blastocysts and outgrowth embryos. Of these, 10 miRNA candidates (let-7b, miR-23a, miR-27a, miR-92a, miR-183, miR-200c, miR-291a, miR-425, miR-429 and miR-652) were identified as significant differentially expressed miRNAs of outgrowth embryos by in silico analysis. The expression of the miRNA candidates was markedly changed during preimplantation embryo development. In particular, let-7b-5p, miR-200c-3p and miR-23a-3p were significantly upregulated in outgrowth embryos compared with non-outgrowth blastocysts. Overall, differentially expressed miRNAs in outgrowth embryos compared with blastocysts and non-outgrowth embryos could be involved in embryo attachment, and interaction between the embryo proper and maternal endometrium during the implantation process.

scholarly journals Role of nitric oxide synthase in insect cell radioresistance: an in-silico analysis

2008 ◽  
Vol 3 (1) ◽  
pp. 8-13 ◽  
Author(s):  
Shubhankar Suman ◽  
Rakesh Kumar Seth ◽  
Sudhir Chandna
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Insect Cell ◽  
In Silico ◽  
In Silico Analysis ◽  
Oxide Synthase ◽  
Silico Analysis

scholarly journals Cardiac miRNAs were involved in the regulation of pathophysiological mechanisms underlying HF in pediatric patients after ventricular assist device implantation

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
R Ragusa ◽  
A Di Molfetta ◽  
S Del Turco ◽  
G Basta ◽  
M Rizzo ◽  
...  
Keyword(s):  
Cardiac Muscle ◽  
Real Time ◽  
Mirna Expression ◽  
Real Time Pcr ◽  
In Silico ◽  
In Silico Analysis ◽  
Adiponectin Receptors ◽  
Silico Analysis

Abstract Background VAD use in heart failure (HF) children have undergone rapid progress in the last three decades through pump technological innovation and improvement of perioperative care. Studies in HF adults showed that VAD put native heart at rest and lead to molecular changes in cardiac muscle, including at microRNA (miRNA) level. However, little is known on changes induced by VAD implant in cardiac miRNA expression and their putative targets in HF children. Purpose The aims of this study were to evaluate: 1) modification of miRNA expression in cardiac muscle from HF children after VAD support; 2) the putative targets of selected miRNAs by in silico analysis; 2) the role of the identify miRNAs on putative targets by in vitro study. Methods Cardiac biopsies were collected from HF children at the moment of VAD implant [n=8; 20 (7.5–64.5) months, 2 males; 19 (15.75–32.25) LVEF%] and at the time of heart transplant after VAD support [n=5; 32 (5–204) months; 4 males; 13.5 (10–18) LVEF%]. Cardiac miRNA expression was evaluated by NGS. The potential miRNA targets were identified by bioinformatics analyses and their cardiac expression by real-time PCR was evaluated. HL-1 cell line was used for testing the regulatory role of selected miRNA on predicted targets by miRNA mimic transfection study. Results At NGS, 465 miRNA were found on average in each sample and the cardiac expression levels of miR19a-3p, miR-1246 and miR-199b-5p decreased in HF children after VAD support compared to pre-implant (Fig. 1A-B). In silico analysis showed that more than 5000 potential gene targets regulated by miR-19a-3p, miR-1246 and miR-199b-5p. Among them, adiponectin receptors (AdipoR1, AdipoR2, T-CAD) were identified as common targets for 3 miRNAs. Real-time PCR data showed that levels of all adiponectin receptors increased significantly whilst the expression of 3 miRNAs decreased after VAD support (Fig. 1C). Moreover, AdipoR2 and T-CAD were inversely related to miRNA levels (Fig. 1D). In vitro studies confirmed the regulatory role of miR-1246 and miR-199b-5p on AdipoR2 (Fig. 1E-F), whilst only miR-199b-5p reduced the expression of T-CAD (Fig. 1G). Finally, AdipoR1 expression levels are not modified compared to control by miRNAs mimic transfection (data not shown). Conclusion In HF children the use of VAD could modify the expression of several miRNAs potentially involved in the regulation of several pathophysiological mechanisms underlying HF. Specifically, the reductions of miR-1246, mir-19a-3p, miR-199b-5p were associated with an increase of the adiponectin receptors AdipoR2 and T-CAD mRNA, suggesting the existence of a miRNAs related fine tuning of the adiponectin system at cardiac tissue level by VAD implant, able to favour the protective effect of adiponectin in HF cardiac muscle. FUNDunding Acknowledgement Type of funding sources: Public grant(s) – EU funding. Main funding source(s): FP7-ICT-2009 Project, Grant Agreement 24863 Figure 1

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