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Keywords = ATP synthetase β

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15 pages, 2009 KiB  
Article
S-Adenosylmethionine Decreases Bacterial Translocation, Proinflammatory Cytokines, Oxidative Stress and Apoptosis Markers in Hepatic Ischemia-Reperfusion Injury in Wistar Rats
by Sergio Valdés, Sergio D. Paredes, Carmen García Carreras, Pilar Zuluaga, Lisa Rancan, Beatriz Linillos-Pradillo, Javier Arias-Díaz and Elena Vara
Antioxidants 2023, 12(8), 1539; https://doi.org/10.3390/antiox12081539 - 31 Jul 2023
Cited by 9 | Viewed by 1613
Abstract
Hepatic ischemia/reperfusion injury (IRI) can seriously impair liver function. It is initiated by oxidative stress, resulting in inflammation and apoptosis-induced cellular damage. Glutathione (GSH) prevents oxidative stress. S-Adenosylmethionine (SAMet) is a GSH synthesis precursor that avoids the deficit in SAMet-synthetase activity and contributes [...] Read more.
Hepatic ischemia/reperfusion injury (IRI) can seriously impair liver function. It is initiated by oxidative stress, resulting in inflammation and apoptosis-induced cellular damage. Glutathione (GSH) prevents oxidative stress. S-Adenosylmethionine (SAMet) is a GSH synthesis precursor that avoids the deficit in SAMet-synthetase activity and contributes to intracellular ATP repletion. It also acts as a methyl group donor, stabilizing hepatocyte membranes, among other functions. This study investigated the effect of SAMet on bacterial translocation and levels of proinflammatory cytokines, oxidative stress and apoptosis markers in male Wistar rats subjected to hepatic IRI. Animals were randomly divided into six groups: (1) sham operation, (3) animals undergoing 60 min of ischemia of the right lateral lobe for temporary occlusion of the portal vein and hepatic artery plus 10 min of reperfusion, and (5) the same as (3) but with a reperfusion period of 120 min. Groups 2, 4 and 6, respectively, are the same as (1), (3) and (5), except that animals received SAMet (20 mg/kg) 15 min before ischemia. GSH, ATP, lipid peroxidation (LPO), TNF-α, IL-1β, IL-6, total caspase-1 and caspase-9, total and cleaved caspase-3, and phosphatidylcholine were determined in the liver. Endotoxin, TNF-α, IL-1β, IL-6, IL-10 and LPO in vena cava and portal vein blood samples were also measured. Endotoxin and LPO levels as well as proinflammatory cytokines and apoptotic markers increased significantly in animals undergoing IRI, both after 10 and 120 min of reperfusion. IRI produced a significant decrease in GSH, ATP, portal IL-10 and phosphatidylcholine. SAMet treatment prevented these effects significantly and increased survival rate. The study suggests that SAMet exerts protective effects in hepatic IRI. Full article
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17 pages, 5413 KiB  
Article
27-Hydroxycholesterol-Induced Dysregulation of Cholesterol Metabolism Impairs Learning and Memory Ability in ApoE ε4 Transgenic Mice
by Yushan Wang, Ling Hao, Tao Wang, Wen Liu, Lijing Wang, Mengwei Ju, Wenjing Feng and Rong Xiao
Int. J. Mol. Sci. 2022, 23(19), 11639; https://doi.org/10.3390/ijms231911639 - 1 Oct 2022
Cited by 9 | Viewed by 2783
Abstract
Dysregulated brain cholesterol metabolism is one of the characteristics of Alzheimer’s disease (AD). 27-Hydroxycholesterol (27-OHC) is a cholesterol metabolite that plays an essential role in regulating cholesterol metabolism and it is suggested that it contributes to AD-related cognitive deficits. However, the link between [...] Read more.
Dysregulated brain cholesterol metabolism is one of the characteristics of Alzheimer’s disease (AD). 27-Hydroxycholesterol (27-OHC) is a cholesterol metabolite that plays an essential role in regulating cholesterol metabolism and it is suggested that it contributes to AD-related cognitive deficits. However, the link between 27-OHC and cholesterol homeostasis, and how this relationship relates to AD pathogenesis, remain elusive. Here, 12-month-old ApoE ε4 transgenic mice were injected with saline, 27-OHC, 27-OHC synthetase inhibitor (anastrozole, ANS), and 27-OHC+ANS for 21 consecutive days. C57BL/6J mice injected with saline were used as wild-type controls. The indicators of cholesterol metabolism, synaptic structure, amyloid β 1-42 (Aβ1-42), and learning and memory abilities were measured. Compared with the wild-type mice, ApoE ε4 mice had poor memory and dysregulated cholesterol metabolism. Additionally, damaged brain tissue and synaptic structure, cognitive decline, and higher Aβ1-42 levels were observed in the 27-OHC group. Moreover, cholesterol transport proteins such as ATP-binding cassette transporter A1 (ABCA1), apolipoprotein E (ApoE), low-density lipoprotein receptor (LDLR), and low-density lipoprotein receptor-related protein1 (LRP1) were up-regulated in the cortex after the 27-OHC treatment. The levels of cholesterol metabolism-related indicators in the hippocampus were not consistent with those in the cortex. Additionally, higher serum apolipoprotein A1 (ApoA1) levels and lower serum ApoE levels were observed in the 27-OHC group. Notably, ANS partially reversed the effects of 27-OHC. In conclusion, the altered cholesterol metabolism induced by 27-OHC was involved in Aβ1-42 deposition and abnormalities in both the brain tissue and synaptic structure, ultimately leading to memory loss in the ApoE ε4 transgenic mice. Full article
(This article belongs to the Section Molecular Endocrinology and Metabolism)
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15 pages, 1757 KiB  
Article
Proteomic Profiling and Pathway Analysis of Acid Stress-Induced Vasorelaxation of Mesenteric Arteries In Vitro
by Ipsita Mohanty, Sudeshna Banerjee, Arabinda Mahanty, Sasmita Mohanty, Nihar Ranjan Nayak, Subas Chandra Parija and Bimal Prasanna Mohanty
Genes 2022, 13(5), 801; https://doi.org/10.3390/genes13050801 - 29 Apr 2022
Cited by 1 | Viewed by 2760
Abstract
Although metabolic acidosis is associated with numerous pathophysiological conditions and its vasorelaxation effects have been well described in different animal and culture models, the molecular mechanisms of acidosis-induced vasorelaxation are not fully understood. Mesenteric artery models have been used extensively to examine the [...] Read more.
Although metabolic acidosis is associated with numerous pathophysiological conditions and its vasorelaxation effects have been well described in different animal and culture models, the molecular mechanisms of acidosis-induced vasorelaxation are not fully understood. Mesenteric artery models have been used extensively to examine the vascular response to various pathophysiological conditions. Our previous studies and several other reports have suggested the vascular responses of goat mesenteric arteries and human arteries to various stimuli, including acidic stress, are highly similar. In this study, to further identify the signaling molecules responsible for altered vasoreactivity in response to acidic pH, we examined the proteomic profile of acid stress-induced vasorelaxation using a goat mesenteric artery model. The vascular proteomes under acidic pH were compared using 2D-GE with 7 cm IPG strips and mini gels, LC-MS/MS, and MALDI TOF MS. The unique proteins identified by mass spectroscopy were actin, transgelin, WD repeat-containing protein 1, desmin, tropomyosin, ATP synthase β, Hsp27, aldehyde dehydrogenase, pyruvate kinase, and vitamin K epoxide reductase complex subunit 1-like protein. Out of five protein spots identified as actin, three were upregulated > 2-fold. ATP synthase β was also upregulated (2.14-fold) under acid stress. Other actin-associated proteins upregulated were transgelin, desmin, and WD repeat-containing protein 1. Isometric contraction studies revealed that both receptor-mediated (histamine) and non-receptor-mediated (KCl) vasocontraction were attenuated, whereas acetylcholine-induced vasorelaxation was augmented under acidosis. Overall, the altered vasoreactivity under acidosis observed in the functional studies could possibly be attributed to the increase in expression of actin and ATP synthase β. Full article
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15 pages, 2351 KiB  
Article
Characterization of the Gene Encoding S-adenosyl-L-methionine (AdoMet) Synthetase in Penicillium chrysogenum; Role in Secondary Metabolism and Penicillin Production
by Rebeca Domínguez-Santos, Katarina Kosalková, Isabel-Clara Sánchez-Orejas, Carlos Barreiro, Yolanda Pérez-Pertejo, Rosa M. Reguera, Rafael Balaña-Fouce and Carlos García-Estrada
Microorganisms 2022, 10(1), 78; https://doi.org/10.3390/microorganisms10010078 - 30 Dec 2021
Cited by 3 | Viewed by 2843
Abstract
The filamentous fungus Penicillium chrysogenum (recently reidentified as Penicillium rubens) is used in the industrial production of the β-lactam antibiotic penicillin. There are several mechanisms regulating the production of this antibiotic, acting both at the genetic and epigenetic levels, the latter including [...] Read more.
The filamentous fungus Penicillium chrysogenum (recently reidentified as Penicillium rubens) is used in the industrial production of the β-lactam antibiotic penicillin. There are several mechanisms regulating the production of this antibiotic, acting both at the genetic and epigenetic levels, the latter including the modification of chromatin by methyltransferases. S-adenosyl-L-methionine (AdoMet) is the main donor of methyl groups for methyltransferases. In addition, it also acts as a donor of aminopropyl groups during the biosynthesis of polyamines. AdoMet is synthesized from L-methionine and ATP by AdoMet-synthetase. In silico analysis of the P. chrysogenum genome revealed the presence of a single gene (Pc16g04380) encoding a putative protein with high similarity to well-known AdoMet-synthetases. Due to the essential nature of this gene, functional analysis was carried out using RNAi-mediated silencing techniques. Knock-down transformants exhibited a decrease in AdoMet, S-adenosyl-L-homocysteine (AdoHcy), spermidine and benzylpenicillin levels, whereas they accumulated a yellow-orange pigment in submerged cultures. On the other hand, overexpression led to reduced levels of benzylpenicillin, thereby suggesting that the AdoMet synthetase, in addition to participate in primary metabolism, also controls secondary metabolism in P. chrysogenum. Full article
(This article belongs to the Special Issue Secondary Metabolism of Microorganisms)
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15 pages, 4347 KiB  
Article
γ-Aminobutyric Acid Enhances Heat Tolerance Associated with the Change of Proteomic Profiling in Creeping Bentgrass
by Zhou Li, Weihang Zeng, Bizhen Cheng, Ting Huang, Yan Peng and Xinquan Zhang
Molecules 2020, 25(18), 4270; https://doi.org/10.3390/molecules25184270 - 18 Sep 2020
Cited by 18 | Viewed by 3145
Abstract
γ-Aminobutyric acid (GABA) participates in the regulation of adaptability to abiotic stress in plants. The objectives of this study were to investigate the effects of GABA priming on improving thermotolerance in creeping bentgrass (Agrostis stolonifera) based on analyses of physiology and [...] Read more.
γ-Aminobutyric acid (GABA) participates in the regulation of adaptability to abiotic stress in plants. The objectives of this study were to investigate the effects of GABA priming on improving thermotolerance in creeping bentgrass (Agrostis stolonifera) based on analyses of physiology and proteome using iTRAQ technology. GABA-treated plants maintained significantly higher endogenous GABA content, photochemical efficiency, performance index on absorption basis, membrane stability, and osmotic adjustment (OA) than untreated plants during a prolonged period of heat stress (18 days), which indicated beneficial effects of GABA on alleviating heat damage. Protein profiles showed that plants were able to regulate some common metabolic processes including porphyrin and chlorophyll metabolism, glutathione metabolism, pyruvate metabolism, carbon fixation, and amino acid metabolism for heat acclimation. It is noteworthy that the GABA application particularly regulated arachidonic acid metabolism and phenylpropanoid biosynthesis related to better thermotolerance. In response to heat stress, the GABA priming significantly increased the abundances of Cu/ZnSOD and APX4 that were consistent with superoxide dismutase (SOD) and ascorbate peroxidase (APX) activities. The GABA-upregulated proteins in relation to antioxidant defense (Cu/ZnSOD and APX4) for the reactive oxygen species scavenging, heat shock response (HSP90, HSP70, and HSP16.9) for preventing denatured proteins aggregation, stabilizing abnormal proteins, promoting protein maturation and assembly, sugars, and amino acids metabolism (PFK5, ATP-dependent 6-phosphofructokinase 5; FK2, fructokinase 2; BFRUCT, β-fructofuranosidase; RFS2, galactinol-sucrose galactosyltransferase 2; ASN2, asparagine synthetase 2) for OA and energy metabolism, and transcription factor (C2H2 ZNF, C2H2 zinc-finger protein) for the activation of stress-defensive genes could play vital roles in establishing thermotolerance. Current findings provide an illuminating insight into the new function of GABA on enhancing adaptability to heat stress in plants. Full article
(This article belongs to the Special Issue Antioxidants in Plant Sciences)
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13 pages, 2238 KiB  
Article
Wnt10b Participates in Regulating Fatty Acid Synthesis in the Muscle of Zebrafish
by Dongwu Liu, Qiuxiang Pang, Qiang Han, Qilong Shi, Qin Zhang and Hairui Yu
Cells 2019, 8(9), 1011; https://doi.org/10.3390/cells8091011 - 30 Aug 2019
Cited by 13 | Viewed by 4237
Abstract
There are 19 Wnt genes in mammals that belong to 12 subfamilies. Wnt signaling pathways participate in regulating numerous homeostatic and developmental processes in animals. However, the function of Wnt10b in fatty acid synthesis remains unclear in fish species. In the present study, [...] Read more.
There are 19 Wnt genes in mammals that belong to 12 subfamilies. Wnt signaling pathways participate in regulating numerous homeostatic and developmental processes in animals. However, the function of Wnt10b in fatty acid synthesis remains unclear in fish species. In the present study, we uncovered the role of the Wnt10b signaling pathway in the regulation of fatty acid synthesis in the muscle of zebrafish. The gene of Wnt10b was overexpressed in the muscle of zebrafish using pEGFP-N1-Wnt10b vector injection, which significantly decreased the expression of glycogen synthase kinase 3β (GSK-3β), but increased the expression of β-catenin, peroxisome proliferators-activated receptor γ (PPARγ), and CCAAT/enhancer binding protein α (C/EBPα). Moreover, the activity and mRNA expression of key lipogenic enzymes ATP-citrate lyase (ACL), acetyl-CoA carboxylase (ACC) and fatty acid synthetase (FAS), and the content of non-esterified fatty acids (NEFA), total cholesterol (TC), and triglyceride (TG) were also significantly decreased. Furthermore, interference of the Wnt10b gene significantly inhibited the expression of β-catenin, PPARγ, and C/EBPα, but significantly induced the expression of GSK-3β, FAS, ACC, and ACL. The content of NEFA, TC, and TG as well as the activity of FAS, ACC, and ACL significantly increased. Thus, our results showed that Wnt10b participates in regulating fatty acid synthesis via β-catenin, C/EBPα and PPARγ in the muscle of zebrafish. Full article
(This article belongs to the Special Issue Wnt Signaling in Health and Diseases)
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30 pages, 5888 KiB  
Article
Computer-Aided Drug Design Applied to Marine Drug Discovery: Meridianins as Alzheimer’s Disease Therapeutic Agents
by Laura Llorach-Pares, Alfons Nonell-Canals, Melchor Sanchez-Martinez and Conxita Avila
Mar. Drugs 2017, 15(12), 366; https://doi.org/10.3390/md15120366 - 27 Nov 2017
Cited by 42 | Viewed by 9991
Abstract
Computer-aided drug discovery/design (CADD) techniques allow the identification of natural products that are capable of modulating protein functions in pathogenesis-related pathways, constituting one of the most promising lines followed in drug discovery. In this paper, we computationally evaluated and reported the inhibitory activity [...] Read more.
Computer-aided drug discovery/design (CADD) techniques allow the identification of natural products that are capable of modulating protein functions in pathogenesis-related pathways, constituting one of the most promising lines followed in drug discovery. In this paper, we computationally evaluated and reported the inhibitory activity found in meridianins A–G, a group of marine indole alkaloids isolated from the marine tunicate Aplidium, against various protein kinases involved in Alzheimer’s disease (AD), a neurodegenerative pathology characterized by the presence of neurofibrillary tangles (NFT). Balance splitting between tau kinase and phosphate activities caused tau hyperphosphorylation and, thereby, its aggregation and NTF formation. Inhibition of specific kinases involved in its phosphorylation pathway could be one of the key strategies to reverse tau hyperphosphorylation and would represent an approach to develop drugs to palliate AD symptoms. Meridianins bind to the adenosine triphosphate (ATP) binding site of certain protein kinases, acting as ATP competitive inhibitors. These compounds show very promising scaffolds to design new drugs against AD, which could act over tau protein kinases Glycogen synthetase kinase-3 Beta (GSK3β) and Casein kinase 1 delta (CK1δ, CK1D or KC1D), and dual specificity kinases as dual specificity tyrosine phosphorylation regulated kinase 1 (DYRK1A) and cdc2-like kinases (CLK1). This work is aimed to highlight the role of CADD techniques in marine drug discovery and to provide precise information regarding the binding mode and strength of meridianins against several protein kinases that could help in the future development of anti-AD drugs. Full article
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