scholarly journals Effect of 8-Day Fasting on Leukocytes Expression of Genes and Proteins Involved in Iron Metabolism in Healthy Men

2021 ◽  
Vol 22 (6) ◽  
pp. 3248
Author(s):  
Andżelika Borkowska ◽  
Maja Tomczyk ◽  
Małgorzata Żychowska ◽  
Wiesław Pilis ◽  
Michał Zych ◽  
...  
Keyword(s):  
Exercise Capacity ◽  
Molecular Mechanisms ◽  
Iron Acquisition ◽  
Quantitative Polymerase Chain Reaction ◽  
Essential Element ◽  
The Body ◽  
Iron Storage ◽  
Healthy Men ◽  
Protein Levels ◽  
Expression Of Genes

The popularity of fasting and restricted food intake is increasing. While the body’s adaptability to dietary insufficiency is crucial for health, molecular mechanisms of adaptive changes are not well understood. Here, we compared the effects of fasting and exercise on the expression of leukocyte genes and proteins involved in the storage, export, and acquisition of iron, an essential element with physiological roles. Healthy men participated in the study (age, 30–70 years; body weight, 60–100 kg; body mass index, 20–29.9 kg/m2). The participants performed an exercise test with a gradually increasing intensity until the individual maximum exercise capacity was reached, before and after 8-d fast. Blood samples were collected before, immediately after, and 3 h after exercise. Gene expression was analyzed by reverse-transcription quantitative polymerase chain reaction and protein levels were analyzed by immunobloting. Eight days of total starvation diet affected the body composition and decreased exercise capacity. Further, fasting decreased the expression of genes associated with iron storage and export, and increased the expression of genes involved in iron acquisition. Conversely, only PCBP2 protein increased after fasting; however, an upward trend was apparent for all proteins. In conclusion, the body adapts to starvation by adjusting iron economy.

Environmentally Relevant Level of Aflatoxin B1 Dysregulates Human Dendritic Cells Through Signaling on Key Toll-Like Receptors

2014 ◽  
Vol 33 (3) ◽  
pp. 175-186 ◽  
Author(s):  
Azam Mohammadi ◽  
Jalil Mehrzad ◽  
Mahmoud Mahmoudi ◽  
Marion Schneider
Keyword(s):  
Dendritic Cells ◽  
Messenger Rna ◽  
Molecular Mechanisms ◽  
Quantitative Polymerase Chain Reaction ◽  
Immune Surveillance ◽  
Toll Like Receptors ◽  
Myeloid Dendritic Cells ◽  
Protein Levels ◽  
Tlr4 Mrna ◽  
Relevant Level

Aflatoxins (AFs) are highly hazardous fungal biometabolites usually present in feeds and foods. Aflatoxin B1 (AFB1) is the most toxic and a known carcinogen. Toll-like receptors (TLRs), highly expressed by myeloid dendritic cells (DC), are key innate immune-surveillance molecules. Toll-like receptors not only sense pathogen-associated molecular patterns but also contribute to infections and cancer. To assess AFB1–TLR interactions on human myeloid DC, pure CD11c+ DC were generated from monocytes isolated from healthy individuals and then exposed to relevant level of AFB1 for 2 hours. Both quantitative polymerase chain reaction and flow cytometric assays were used to quantify, respectively, expression of TLR2 and TLR4 at the messenger RNA (mRNA) and protein levels in these DC. Levels of interleukin (IL) 1β, IL-6, and IL-10 were also analyzed in AFB1- and mock-treated DC. Compared to nontreated CD11c+ DC, expression levels of both TLR2 and TLR4 mRNA and proteins were significantly upregulated in AFB1-treated cells. Further, although IL-10 levels in AFB1-treated DC were similar to those in the mock-treated DC, the AFB1-exposed DC secreted higher amounts of IL-1β and IL-6. Dendritic cells are sensitive to environmentally relevant level of AFB1, and TLR2 and TLR4 are involved in sensing AFB1. Considering the broad roles of TLR2, TLR4, and DC in immunity and infections, our novel findings open a new door to understanding the molecular mechanisms and functional consequences of AFB1 in inducing immunodysregulation, immunotoxicity, and thus (non)infectious diseases in humans.

scholarly journals Mechanisms and heterogeneity of mineral use by natural colonies of the cyanobacterium Trichodesmium

2020 ◽  
Author(s):  
Noelle A. Held ◽  
Kevin M. Sutherland ◽  
Eric A. Webb ◽  
Matthew R. McIlvin ◽  
Natalie R. Cohen ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Iron Acquisition ◽  
Dust Particles ◽  
Iron Storage ◽  
Global Impact ◽  
Mineral Particles ◽  
Nickel Copper ◽  
Iron Nickel ◽  
Essential Nutrient ◽  
Iron Storage Protein

AbstractThe keystone marine nitrogen fixer Trichodesmium thrives in high dust environments, and while experimental observations suggest that Trichodesmium colonies can access the essential nutrient iron from dust particles, it is not known the extent to which this occurs in the field. Here we demonstrate that Trichodesmium colonies actively process mineral particles in nature with direct molecular impacts. Microscopy and synchrotron-based imaging demonstrated heterogeneous associations with particles consistent with iron oxide and iron silicate minerals. Metaproteomic analysis of individual colonies revealed enrichment of biogeochemically-relevant proteins including photosynthesis proteins and metalloproteins containing iron, nickel, copper and zinc when particles were present. The iron-storage protein ferritin was particularly enriched implying accumulation of particle-derived iron, and multiple iron acquisition pathways including Fe(II), Fe(III), and Fe-siderophore transporters were engaged, including evidence of superoxide-driven particle dissolution. While the particles clearly provided iron, there was also evidence that the concentrated metals had toxic effects. The molecular mechanisms allowing Trichodesmium to interact with particulate minerals are fundamental to its success and global impact on nitrogen biogeochemistry, and may contribute to the leaching of particulate trace metals with implications for global iron and carbon cycling.

scholarly journals Targeted Genetic Reduction of Mutant Huntingtin Lessens Cardiac Pathology in the BACHD Mouse Model of Huntington's Disease

2021 ◽  
Vol 8 ◽  
Author(s):  
Saemi Park ◽  
Shu Hon Christopher Luk ◽  
Raj S. Bains ◽  
Daniel S. Whittaker ◽  
Emily Chiem ◽  
...  
Keyword(s):  
Mouse Model ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Treatment Strategies ◽  
The Body ◽  
Activity Levels ◽  
Protein Levels ◽  
Pathological Cardiac Hypertrophy ◽  
Expression Of Genes ◽  
Wide Range

Individuals affected by Huntington's disease (HD) present with progressive degeneration that results in a wide range of symptoms, including cardiovascular (CV) dysfunction. The huntingtin gene (HTT) and its product are ubiquitously expressed, hence, the cardiomyopathy could also be driven by defects caused by its mutated form (mHTT) in the cardiomyocytes themselves. In the present study, we sought to determine the contribution of the mHTT expressed in the cardiomyocytes to CV symptoms. We utilized the BACHD mouse model, which exhibits many of the HD core symptoms, including CV dysfunction. This model allows the targeted genetic reduction of mHTT expression in the cardiomyocytes while maintaining the expression of the mHTT in the rest of the body. The BACHD line was crossed with a line of mice in which the expression of Cre recombinase is driven by the cardiac-specific alpha myosin-heavy chain (Myh6) promoter. The offspring of this cross (BMYO mice) exhibited a dramatic reduction in mHTT in the heart but not in the striatum. The BMYO mice were evaluated at 6 months old, as at this age, the BACHD line displays a strong CV phenotype. Echocardiogram measurements found improvement in the ejection fraction in the BMYO line compared to the BACHD, while hypertrophy was observed in both mutant lines. Next, we examined the expression of genes known to be upregulated during pathological cardiac hypertrophy. As measured by qPCR, the BMYO hearts exhibited significantly less expression of collagen1a as well as Gata4, and brain natriuretic peptide compared to the BACHD. Fibrosis in the hearts assessed by Masson's trichrome stain and the protein levels of fibronectin were reduced in the BMYO hearts compared to BACHD. Finally, we examined the performance of the mice on CV-sensitive motor tasks. Both the overall activity levels and grip strength were improved in the BMYO mice. Therefore, we conclude that the reduction of mHtt expression in the heart benefits CV function in the BACHD model, and suggest that cardiomyopathy should be considered in the treatment strategies for HD.

scholarly journals Transcriptomic analysis at organ and time scale reveals gene regulatory networks controlling the sulfate starvation response of Solanum lycopersicum.

2020 ◽  
Author(s):  
Javier Canales ◽  
Felipe Uribe ◽  
Carlos Henríquez-Valencia ◽  
Carlos Lovazzano ◽  
Joaquín Medina ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Regulatory Networks ◽  
Molecular Mechanisms ◽  
Essential Element ◽  
Transcript Level ◽  
Central Component ◽  
Transcriptomic Response ◽  
Starvation Response ◽  
Expression Of Genes ◽  
The Impact

Abstract Background: Sulfur is a major component of biological molecules and thus an essential element for plants. Deficiency of sulfate, the main source of sulfur in soils, negatively influences plant growth and crop yield. The effect of sulfate deficiency on plants has been well characterized at the physiological, transcriptomic and metabolomic levels in Arabidopsis thaliana and a limited number of crop plants. However, we still lack a thorough understanding of the molecular mechanisms and regulatory networks underlying sulfate deficiency in most plants. In this work we analyzed the impact of sulfate starvation on the transcriptome of tomato plants to identify regulatory networks and key transcriptional regulators at a temporal and organ scale. Results: Sulfate starvation reduces the growth of roots and leaves which is accompanied by major changes in the organ transcriptome, with the response being temporally earlier in roots than leaves. Comparative analysis showed that a major part of the Arabidopsis and tomato transcriptomic response to sulfate starvation is conserved between these plants and allowed for the identification of processes specifically regulated in tomato at the transcript level, including the control of internal phosphate levels. Integrative gene network analysis uncovered key transcription factors controlling the temporal expression of genes involved in sulfate assimilation, as well as cell cycle, cell division and photosynthesis during sulfate starvation in tomato roots and leaves. Interestingly, one of these transcription factors presents a high identity with SULFUR LIMITATION1, a central component of the sulfate starvation response in Arabidopsis. Conclusions: Together, our results provide the first comprehensive catalog of sulfate-responsive genes in tomato, as well as novel regulatory targets for future functional analyses in tomato and other crops.

Molecular mechanisms of iron uptake in eukaryotes

1996 ◽  
Vol 76 (1) ◽  
pp. 31-47 ◽  
Author(s):  
D. M. de Silva ◽  
C. C. Askwith ◽  
J. Kaplan
Keyword(s):  
Iron Uptake ◽  
Mammalian Cells ◽  
Iron Homeostasis ◽  
Molecular Mechanisms ◽  
Iron Acquisition ◽  
Genetic Disorders ◽  
Essential Element ◽  
Recent Developments

Iron serves essential functions in both prokaryotes and eukaryotes, and cells have highly specialized mechanisms for acquiring and handling this metal. The primary mechanism by which the concentration of iron in biologic systems is controlled is through the regulation of iron uptake. Although the role of transferrin in mammalian iron homeostasis has been well characterized, the study of genetic disorders of iron metabolism has revealed other, transferrin-independent, mechanisms by which cells can acquire iron. In an attempt to understand how eukaryotic systems take up this essential element, investigators have begun studying the simple eukaryote Saccharomyces cerevisiae. Several genes have been identified and cloned that act in concert to allow iron acquisition from the environment. Some of these genes appear to have functional homologues in human systems. This review focuses on the recent developments in understanding eukaryotic iron uptake with an emphasis on the genetic and molecular characterization of these systems in both cultured mammalian cells and S. cerevisiae. An unexpected connection between iron and copper homeostasis has been revealed by recent genetic studies, which confirm biologic observations made several decades ago.

scholarly journals LuxS Involvement in the Regulation of Genes Coding for Hemin and Iron Acquisition Systems in Porphyromonas gingivalis

2006 ◽  
Vol 74 (7) ◽  
pp. 3834-3844 ◽  
Author(s):  
Chloe E. James ◽  
Yoshiaki Hasegawa ◽  
Yoonsuk Park ◽  
Vincent Yeung ◽  
Gena D. Tribble ◽  
...  
Keyword(s):  
Porphyromonas Gingivalis ◽  
Binding Protein ◽  
Iron Acquisition ◽  
Signal Transduction Pathway ◽  
Periodontal Pathogen ◽  
Wild Type ◽  
Iron Storage ◽  
Altered Expression ◽  
Reverse Transcription Pcr ◽  
Expression Of Genes

ABSTRACT The periodontal pathogen Porphyromonas gingivalis employs a variety of mechanisms for the uptake of hemin and inorganic iron. Previous work demonstrated that hemin uptake in P. gingivalis may be controlled by LuxS-mediated signaling. In the present study, the expression of genes involved in hemin and iron uptake was determined in parent and luxS mutant strains by quantitative real-time reverse transcription-PCR. Compared to the parental strain, the luxS mutant showed reduced levels of transcription of genes coding for the TonB-linked hemin binding protein Tlr and the lysine-specific protease Kgp, which can degrade host heme-containing proteins. In contrast, there was up-regulation of the genes for another TonB-linked hemin binding protein, HmuR; a hemin binding lipoprotein, FetB; a Fe2+ ion transport protein, FeoB1; and the iron storage protein ferritin. Differential expression of these genes in the luxS mutant was maximal in early-exponential phase, which corresponded with peak expression of luxS and AI-2 signal activity. Complementation of the luxS mutation with wild-type luxS in trans rescued expression of hmuR. Mutation of the GppX two-component signal transduction pathway caused an increase in expression of luxS along with tlr and lower levels of message for hmuR. Moreover, expression of hmuR was repressed, and expression of tlr stimulated, when the luxS mutant was incubated with AI-2 partially purified from the culture supernatant of wild-type cells. A phenotypic outcome of the altered expression of genes involved in hemin uptake was impairment of growth of the luxS mutant in hemin-depleted medium. The results demonstrate a role of LuxS/AI-2 in the regulation of hemin and iron acquisition pathways in P. gingivalis and reveal a novel control pathway for luxS expression.

scholarly journals Brain Protein Expression Profile Confirms the Protective Effect of the ACTH(4–7)PGP Peptide (Semax) in a Rat Model of Cerebral Ischemia–Reperfusion

2021 ◽  
Vol 22 (12) ◽  
pp. 6179
Author(s):  
Olga Yu. Sudarkina ◽  
Ivan B. Filippenkov ◽  
Vasily V. Stavchansky ◽  
Alina E. Denisova ◽  
Vadim V. Yuzhakov ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion ◽  
Artery Occlusion ◽  
Subcortical Structures ◽  
Protein Levels ◽  
Expression Of Genes ◽  
A Genome ◽  
Neurotransmitter Genes

The Semax (Met-Glu-His-Phe-Pro-Gly-Pro) peptide is a synthetic melanocortin derivative that is used in the treatment of ischemic stroke. Previously, studies of the molecular mechanisms underlying the actions of Semax using models of cerebral ischemia in rats showed that the peptide enhanced the transcription of neurotrophins and their receptors and modulated the expression of genes involved in the immune response. A genome-wide RNA-Seq analysis revealed that, in the rat transient middle cerebral artery occlusion (tMCAO) model, Semax suppressed the expression of inflammatory genes and activated the expression of neurotransmitter genes. Here, we aimed to evaluate the effect of Semax in this model via the brain expression profiling of key proteins involved in inflammation and cell death processes (MMP-9, c-Fos, and JNK), as well as neuroprotection and recovery (CREB) in stroke. At 24 h after tMCAO, we observed the upregulation of active CREB in subcortical structures, including the focus of the ischemic damage; downregulation of MMP-9 and c-Fos in the adjacent frontoparietal cortex; and downregulation of active JNK in both tissues under the action of Semax. Moreover, a regulatory network was constructed. In conclusion, the suppression of inflammatory and cell death processes and the activation of recovery may contribute to the neuroprotective action of Semax at both the transcriptome and protein levels.

scholarly journals Transcriptomic analysis at organ and time scale reveals gene regulatory networks controlling the sulfate starvation response of Solanum lycopersicum.

2020 ◽  
Author(s):  
Javier Canales ◽  
Felipe Uribe ◽  
Carlos Henríquez-Valencia ◽  
Carlos Lovazzano ◽  
Joaquín Medina ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Regulatory Networks ◽  
Molecular Mechanisms ◽  
Essential Element ◽  
Transcript Level ◽  
Central Component ◽  
Transcriptomic Response ◽  
Starvation Response ◽  
Expression Of Genes ◽  
The Impact

Abstract Background: Sulfur is a major component of biological molecules and thus an essential element for plants. Deficiency of sulfate, the main source of sulfur in soils, negatively influences plant growth and crop yield. The effect of sulfate deficiency on plants has been well characterized at the physiological, transcriptomic and metabolomic levels in Arabidopsis thaliana and a limited number of crop plants. However, we still lack a thorough understanding of the molecular mechanisms and regulatory networks underlying sulfate deficiency in most plants. In this work we analyzed the impact of sulfate starvation on the transcriptome of tomato plants to identify regulatory networks and key transcriptional regulators at a temporal and organ scale. Results: Sulfate starvation reduces the growth of roots and leaves which is accompanied by major changes in the organ transcriptome, with the response being temporally earlier in roots than leaves. Comparative analysis showed that a major part of the Arabidopsis and tomato transcriptomic response to sulfate starvation is conserved between these plants and allowed for the identification of processes specifically regulated in tomato at the transcript level, including the control of internal phosphate levels. Integrative gene network analysis uncovered key transcription factors controlling the temporal expression of genes involved in sulfate assimilation, as well as cell cycle, cell division and photosynthesis during sulfate starvation in tomato roots and leaves. Interestingly, one of these transcription factors presents a high identity with SULFUR LIMITATION1, a central component of the sulfate starvation response in Arabidopsis. Conclusions: Together, our results provide the first comprehensive catalog of sulfate-responsive genes in tomato, as well as novel regulatory targets for future functional analyses in tomato and other crops.

scholarly journals Effect of Konjac Glucomannan (KGM) on the Reconstitution of the Dermal Environment against UVB-Induced Condition

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2779
Author(s):  
Kyung Ho Choi ◽  
Sung Tae Kim ◽  
Bum Ho Bin ◽  
Phil June Park
Keyword(s):  
Quantitative Polymerase Chain Reaction ◽  
Human Fibroblasts ◽  
Konjac Glucomannan ◽  
The Body ◽  
Skin Damage ◽  
Related Factors ◽  
Young Cell ◽  
Amorphophallus Konjac ◽  
Protein Levels ◽  
Age Related

Skin layers serve as a barrier against unexpected critical changes in the body due to environmental factors. Excessive ultraviolet (UV) B exposure increases the levels of age-related factors, leading to senescent cells and damaged skin tissues. Widely used as a dietary supplement, konjac (Amorphophallus konjac) glucomannan (KGM) has shown skin regeneration potential in patch or sheet form with anti-inflammatory or immunosuppressive effects. However, the ability of KGM to reconstitute senescent/damaged skin following UV radiation has not been explored. Here, we demonstrate that KGM alleviates skin damage by increasing the proportion of young cell populations in UVB-exposed senescent human epidermal primary melanocytes. Young cell numbers increased depending on KGM dosage, but the senescent cells were not removed. Real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot analysis showed that mRNA and protein levels of age- and pigmentation-related factors decreased in a manner dependent on the rate at which new cells were generated. Moreover, an analysis of mRNA and protein levels indicated that KGM facilitated youth by increasing cell proliferation in UVB-damaged human fibroblasts. Thus, KGM is a highly effective natural agent for maintaining skin homeostasis by promoting the reconstitution of the dermal environment against UVB-induced acute senescence or skin damage.

scholarly journals The Adaptive Mechanism of Plants to Iron Deficiency via Iron Uptake, Transport, and Homeostasis

2019 ◽  
Vol 20 (10) ◽  
pp. 2424 ◽  
Author(s):  
Xinxin Zhang ◽  
Di Zhang ◽  
Wei Sun ◽  
Tianzuo Wang
Keyword(s):  
Iron Deficiency ◽  
Iron Uptake ◽  
Iron Homeostasis ◽  
Iron Acquisition ◽  
Essential Element ◽  
Transport Mechanisms ◽  
Iron Storage ◽  
Iron Deficient ◽  
Dicotyledonous Plants ◽  
Shed Light

Iron is an essential element for plant growth and development. While abundant in soil, the available Fe in soil is limited. In this regard, plants have evolved a series of mechanisms for efficient iron uptake, allowing plants to better adapt to iron deficient conditions. These mechanisms include iron acquisition from soil, iron transport from roots to shoots, and iron storage in cells. The mobilization of Fe in plants often occurs via chelating with phytosiderophores, citrate, nicotianamine, mugineic acid, or in the form of free iron ions. Recent work further elucidates that these genes’ response to iron deficiency are tightly controlled at transcriptional and posttranscriptional levels to maintain iron homeostasis. Moreover, increasing evidences shed light on certain factors that are identified to be interconnected and integrated to adjust iron deficiency. In this review, we highlight the molecular and physiological bases of iron acquisition from soil to plants and transport mechanisms for tolerating iron deficiency in dicotyledonous plants and rice.

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