scholarly journals Candidate microRNA Biomarkers in Lupus Nephritis: A Meta-Analysis of Profiling Studies in Kidney, Blood and Urine Samples

2022 ◽  
Author(s):  
Amir Roointan ◽  
Alieh Gholaminejad ◽  
Behrokh Shojaie ◽  
Kelly Hudkins ◽  
Yousof Gheisari
Keyword(s):  
Lupus Nephritis ◽  
Expression Profiles ◽  
Meta Analysis ◽  
Kidney Tissue ◽  
Functional Enrichment ◽  
Urine Samples ◽  
P Value ◽  
Altered Expression ◽  
Network Construction ◽  
Blood And Urine Samples

Abstract Lupus nephritis (LN) is a kidney disease caused by systemic lupus erythematosus in which kidneys are attacked by the immune system. MiRNAs participate in the pathogenesis of LN as modulatory effectors in immune responses and nephrogenesis pathways. Despite the large number of miRNAs that are expressed deferentially, identifying the most suitable biomarker candidate for LN is challenging. The aim of this study was to introduce a consensus panel of potential miRNA biomarkers by performing a meta-analysis of miRNA profiles in the kidney, blood, and urine samples of LN patients. A comprehensive literature review approach was considered to find LN-related miRNA expression profiles. After including the 41 eligible studies and performing the data extraction, meta-analysis was done based on the vote-counting rank strategy and as well as meta-analysis of p-value. The result of the meta-analysis was three lists of consensus miRNAs with altered expression profiles in the various tissue samples of LN patients. Of the 13 studies on kidney tissue, the meta-miRNAs were let-7a, miR-198, let-7e, miR-145, and miR-26a. In addition, meta-miRNAs of miR-199a, miR-21, miR-423, miR-1260b, miR-589, miR-150, miR-155, miR-146a, and miR-183 from 21 studies on blood samples, and miR-146a, miR-204, miR-30c, miR-3201, and miR-1273e from 11 studies on urine samples can be considered as non-invasive biomarker panels for LN. The meta-miRNAs and their related genes were subjected to functional enrichment analyses and network construction. Functional enrichment analysis confirmed the involvement of their target genes in nephropathy-related signaling pathways. Network construction showed miR-145-5p in blood and miR-155-5p in kidney, the best hob miRNAs as candidate drug targets. In conclusion using a meta-analysis approach, our study proposes three meta-miRNA panels that could be the target of further research to assess their potential as biomarkers / therapeutic targets in LN disease.

Correlation Between Serological Makers and Immunofluorescence Deposits i n Kidney Tissue of Patients with Lupus Nephritis

2019 ◽  
Vol 9 (02) ◽  
Author(s):  
Haider S Al-Hadad ◽  
Aqeel Abbas Matrood ◽  
Maha Abdalrasool Almukhtar ◽  
Haider Jabur Kehiosh ◽  
Riyadh Muhi Al-Saegh
Keyword(s):  
Lupus Nephritis ◽  
Lupus Erythematosus ◽  
Kidney Biopsy ◽  
Pearson Correlation ◽  
Standard Procedure ◽  
Kidney Tissue ◽  
P Value ◽  
American College Of Rheumatology ◽  
Immune Deposits ◽  
Number Of Patients

Background: Systemic lupus erythematosus (SLE) is an autoimmune disease. Few biomarkers for SLE have been validated and widely accepted for the laboratory follow-up of inflammatory activity. In SLE patients, with lupus nephritis (LN), complement activation leads to fluctuation of serum C3 and C4 that are frequently used as clinicalm biomarker of disease activity in SLE. Patients and Methods: In this study the number of patients were 37, seven patients were excluded for incomplete data collection, 28 were females ,2 were males. The duration of the study is two years from 2015 to 2017. Patients were considered to have SLE and LN according to American College of Rheumatology (ACR) criteria, and International Society of Nephrology/ Renal Pathology Society (ISN/RPS). All patients were evaluated withm clinical presentation, laboratory investigations. Our patients underwent kidney biopsy according to standard procedure by Kerstin Amann, and their tissue specimens were studied in the laboratory with light microscope (LM) and immunofluorescence microscope reagents. The relationship between the serological markers and immunofluorescence deposits in kidney biopsy of all patients were studied using the statistical analysis of Pearson correlation and single table student's T test. A P value 0.05 was considered statistically significant. Results: The granular pattern of IF deposits was present in all LN patients, and in more than two third of patients these IF deposits presented in glomerular, tubular, and mesangium sites. While less than one third of patients had IF deposits in the mesangium only. There was no statistically significant correlation between serum ANA, anti-dsDNA, and IF deposits of different types. There was significant correlation between serum C3 and C4 hypocomplementemia and IgG immune deposits in kidney biopsy, and there was significant relationship between serum C3 hypocomplementemia and full house immunofluorescence (FHIF) deposits inm kidney biopsy.Conclusions:Immunofluorescence deposits is mainly granular pattern in LN patients. There was no significant association between serum ANA, anti-dsDNA, and immune deposits in kidney tissue. Immunofluorescence deposits of IgG type correlates significantly with serum C3 and C4 hypocomplemetemia, and these immune deposits in association with low complement levels correlates with LN flare. There was significant correlation between C3 hypocomplementemia and FHIF.

scholarly journals Aripiprazole as a candidate treatment of COVID-19 identified through genomic analysis

2020 ◽  
Author(s):  
Benedicto Crespo-Facorro ◽  
Miguel Ruiz-Veguilla ◽  
Javier Vazquez-Bourgon ◽  
Ana C. Sanchez-Hidalgo ◽  
Nathalia Garrido-Torres ◽  
...  
Keyword(s):  
Expression Profiles ◽  
Phase 1 ◽  
Gene Expression Profiles ◽  
Genomic Analysis ◽  
Cell Receptor ◽  
Therapeutic Drug ◽  
P Value ◽  
Immunological Parameters ◽  
Altered Expression ◽  
Exact Test

Background: Antipsychotics suppress expression of inflammatory cytokines and inducible inflammatory enzymes. Elopiprazole (a phenylpiperazine antipsychotic drug in phase 1) has been characterized as a therapeutic drug to treat SARS-CoV-2 infection in a repurposing study. We aim to investigate the potential effects of aripiprazole (an FDA approved phenylpiperazine) on COVID19-related immunological parameters. Methods: Differential gene expression profiles of non-COVID versus COVID RNA-Seq samples (CRA002390 project in GSA database) and drug-naive patients with psychosis at baseline and after three months of aripiprazole treatment was identified. An integrative analysis between COVID and aripiprazole immunomodulatory antagonist effects was performed. Findings: 82 out the 377 genes (21.7%) with expression significantly altered by aripiprazole have also their expression altered in COVID-19 patients and in 93.9% of these genes their expression is reverted by aripiprazole. The number of common genes with expression altered in both analyses is significantly higher than expected (Fisher's Exact Test, two tail; P value=3.2e-11). 11 KEGG pathways were significantly enriched with genes with altered expression both in COVID-19 patients and aripiprazole medicated schizophrenia patients (P adj<0.05). The most significant pathways were associated to the immune system such as the inflammatory bowel disease (IBD) (the most significant pathway with a P adj of 0.00021), Th1 and Th2 cell differentiation and B cell receptor signaling pathway, all three related to the defense against infections. Interpretation: This exploratory investigation may provide further support to the notion that protective effect is exerted by phenylpiperazine by modulating the immunological dysregulation associated to COVID-19. Along with many ongoing studies and clinical trials, repurposing available medications could be of use in countering SARS-CoV-2 infection, but require further studies and trials.

scholarly journals Computational Analysis Revealed miRNAs Produced by Chikungunya Virus Target Genes Associated with Cellular Proliferation and Cell Cycle Regulation

2020 ◽  
Author(s):  
Md. Sajedul Islam ◽  
Md. Abdullah-Al-Kamran Khan
Keyword(s):  
Cell Cycle ◽  
Chikungunya Virus ◽  
Target Genes ◽  
Cellular Proliferation ◽  
Enrichment Analysis ◽  
Microarray Dataset ◽  
Functional Enrichment ◽  
P Value ◽  
Altered Expression ◽  
Regulatory Pathways

Abstract Chikungunya virus (CHIKV) that causes chikungunya fever, is an alphavirus that belongs to the Togaviridae family containing a single-stranded RNA genome. Mosquitoes of the Aedes species act as the vectors for this virus and can be found in the blood, which can be passed from an infected person to a mosquito through mosquito bites. CHIKV has drawn much attention recently because of its potential of causing an epidemic. As the detailed mechanism of its pathogenesis inside the host system is still lacking, in this in silico research we have hypothesized that CHIKV might create miRNAs, which would target the genes associated with host cellular regulatory pathways, thereby providing the virus with prolonged refuge. Using bioinformatics approaches we found several putative miRNAs produced by CHIKV. Then we predicted the genes of the host targeted by these miRNAs. Functional enrichment analysis of these targeted genes shows the involvement of several biological pathways regulating cellular proliferation and cell cycle, thereby provide themselves with prolonged refuge and facilitate their pathogenesis, which in turn may lead to disease conditions. Finally, we analyzed a publicly available microarray dataset (GSE49985) to determine the altered expression levels of the targeted genes and found four genes (FLNA, GATA6, HES6, and TP53) associated with transcription factor binding, which have significant (Adjusted p-value <0.05) altered expression level. Our finding presents novel miRNAs and their targeted genes, which upon experimental validation could facilitate in developing new therapeutics to combat CHIKV infection and minimize CHIKV mediated diseases.

scholarly journals Meta-analysis of Transcriptomic Data Reveals Pathophysiological Modules Involved with Atrial Fibrillation

2020 ◽  
Author(s):  
Rodrigo Haas Bueno ◽  
Mariana Recamonde-Mendoza
Keyword(s):  
Atrial Fibrillation ◽  
Differentially Expressed Genes ◽  
Complex Disease ◽  
Meta Analysis ◽  
Differential Expression Analysis ◽  
Interaction Network ◽  
Enrichment Analysis ◽  
Functional Enrichment ◽  
Differentially Expressed ◽  
P Value

Atrial fibrillation (AF) is a complex disease and affects millions of people around the world. The biological mechanisms that are involved with AF are complex and still need to be fully elucidated. Therefore, we performed a meta-analysis of transcriptome data related to AF to explore these mechanisms aiming at more sensitive and reliable results. Public transcriptomic datasets were downloaded, analyzed for quality control, and individually pre-processed. Differential expression analysis was carried out for each individual dataset, and the results were meta-analytically aggregated using the r-th ordered p-value method. We analyzed the final list of differentially expressed genes through network analysis, namely topological and modularity analysis, and functional enrichment analysis. The meta-analysis of transcriptomes resulted in 589 differentially expressed genes, whose protein-protein interaction network presented 11 hubs-bottlenecks and four main identified functional modules. These modules were enriched for, respectively, 23, 54, 33, and 53 biological pathways involved with the pathophysiology of AF, especially with the disease's structural and electrical remodeling processes. Stress of the endoplasmic reticulum, protein catabolism, oxidative stress, and inflammation are some of the enriched processes. Among hubs-bottlenecks genes, which are highly connected and probably have a key role in regulating these processes, we found HSPA5, ANK2, CTNNB1, and VWF. Further experimental investigation of our findings may shed light on the pathophysiology of the disease and contribute to the identification of new therapeutic targets and treatments.

scholarly journals POS0788 CIRCULATING EXOSOMES PROMOTE LUPUS NEPHRITIS IN MRL-LPR MICE

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 646.3-647
Author(s):  
X. Sha ◽  
X. Ge ◽  
Y. Jin ◽  
T. Chen ◽  
X. Ni ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Nephritis ◽  
Western Blot ◽  
Lupus Erythematosus ◽  
Expression Profiles ◽  
Meta Analysis ◽  
Differentially Expressed ◽  
Systemic Lupus ◽  
Exosomal Mirnas

Background:Systemic Lupus Erythematosus (SLE) is a prototypic autoimmune disease that characterized by the loss of self-tolerance and the production of autoantibodies (autoAbs) [1, 2]. Lupus nephritis (LN), the severe organ-threatening manifestations of SLE, could cause massive damage to patients[3, 4]. Currently, some exosomal microRNAs (miRNAs) are considered as potential biomarkers in SLE. However, the role of exosomal miRNAs in Lupus Nephritis (LN) remains unclear.Objectives:The purpose of this study was to investigate molecular mechanism of plasma exosomal miRNAs in the development of Lupus Nephritis.Methods:Circulating exosomes were isolated from plasma of patients with LN, SLE without LN (NLN). Plasma exosomes were authenticated by Western Blot, Nanosight Tracking Analysis (NTA) and transmission electron microscopy (TEM). Fluorescence microscopy of co-cultured plasma exosomes and podocytes demonstrated that exosomes were uptaken into podocytes. Moreover, cell apoptosis and the inflammation factors was assessed using Western Blot. We analyzed the expression profiles of miRNAs in LN and NLN exosomes and the expression profiles of mRNAs of podocytes stimulated with LN and NLN exosomes with the help of next generation sequencing (NGS).Results:We demonstrate that exosomes derived from LN plasma could be taken by neighboring podocytes and promote the apoptosis of podocytes and the expression of inflammation factors. In addition, the sequencing found that miRNAs were differentially expressed in LN and NLN exosomes and mRNAs were differentially expressed in podocytes stimulated with LN and NLN exosomes.Conclusion:LN plasma exosomes have a potency to stimulate the apoptosis of podocytes and the expression of inflammation factors. Moreover, differentially expressed miRNAs in exosomes play a potential role in the development of LN.References:[1]T. Colasanti, A. Maselli, F. Conti, M. Sanchez, C. Alessandri, C. Barbati, D. Vacirca, A. Tinari, F. Chiarotti, A. Giovannetti, F. Franconi, G. Valesini, W. Malorni, M. Pierdominici, E. Ortona, Autoantibodies to estrogen receptor α interfere with T lymphocyte homeostasis and are associated with disease activity in systemic lupus erythematosus, Arthritis and rheumatism, 64 (2012) 778-787.[2]H.A. Al-Shobaili, A.A. Al Robaee, A.A. Alzolibani, Z. Rasheed, Antibodies against 4-hydroxy-2-nonenal modified epitopes recognized chromatin and its oxidized forms: role of chromatin, oxidized forms of chromatin and 4-hydroxy-2-nonenal modified epitopes in the etiopathogenesis of SLE, Disease markers, 33 (2012) 19-34.[3]A. Kaul, C. Gordon, M.K. Crow, Z. Touma, M.B. Urowitz, R. van Vollenhoven, G. Ruiz-Irastorza, G. Hughes, Systemic lupus erythematosus, Nat Rev Dis Primers, 2 (2016) 16039.[4]M.G. Tektonidou, A. Dasgupta, M.M. Ward, Risk of End-Stage Renal Disease in Patients With Lupus Nephritis, 1971-2015: A Systematic Review and Bayesian Meta-Analysis, Arthritis & rheumatology (Hoboken, N.J.), 68 (2016) 1432-1441.Disclosure of Interests:None declared

scholarly journals Transcriptomic metaanalyses of autistic brains reveals shared gene expression and biological pathway abnormalities with cancer

2018 ◽  
Author(s):  
Jaume Forés-Martos ◽  
Ferrán Catalá-López ◽  
Jon Sánchez-Valle ◽  
Kristina Ibáñez ◽  
Héctor Tejero ◽  
...  
Keyword(s):  
Gene Expression ◽  
Differential Expression ◽  
Expression Profiles ◽  
Meta Analysis ◽  
Gene Expression Profiles ◽  
Atp Synthesis ◽  
Autism Spectrum ◽  
Functional Enrichment ◽  
Biological Processes ◽  
Cancer Types

AbstractEpidemiological and clinical evidence points to cancer as a comorbidity in people with autism spectrum disorders (ASD). A significant overlap of genes and biological processes between both diseases has also been reported. Here, for the first time, we compared the gene expression profiles of ASD frontal cortex tissues and 22 cancer types obtained by differential expression meta-analysis. Four cancer types (brain, thyroid, kidney, and pancreatic cancers) presented a significant overlap in gene expression deregulations in the same direction as ASD whereas two cancer types (lung and prostate cancers) showed differential expression profiles significantly deregulated in the opposite direction from ASD. Functional enrichment and LINCS L1000 based drug set enrichment analyses revealed the implication of several biological processes and pathways that were affected jointly in both diseases, including impairments of the immune system, and impairments in oxidative phosphorylation and ATP synthesis among others. Our data also suggest that brain and kidney cancer have patterns of transcriptomic dysregulation in the PI3K/AKT/MTOR axis that are similar to those found in ASD. These shared transcriptomic alterations could help explain epidemiological observations suggesting direct and inverse comorbid associations between ASD and particular cancer types.

Transcriptome analysis reveals key signature genes involved in the oncogenesis of lung cancer

2020 ◽  
Vol 29 (4) ◽  
pp. 475-482
Author(s):  
Fanlu Meng ◽  
Linlin Zhang ◽  
Yaoyao Ren ◽  
Qing Ma
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Expression Profiles ◽  
Meta Analysis ◽  
Gene Expression Profiles ◽  
Interaction Network ◽  
Functional Enrichment ◽  
Sequencing Platform ◽  
Signature Genes ◽  
Regulated Expression

Previous studies have suggested potential signature genes for lung cancer, however, due to factors such as sequencing platform, control, data selection and filtration conditions, the results of lung cancer-related gene expression analysis are quite different. Here, we performed a meta-analysis on existing lung cancer gene expression results to identify Meta-signature genes without noise. In this study, functional enrichment, protein-protein interaction network, the DAVID, String, TfactS, and transcription factor binding were performed based on the gene expression profiles of lung adenocarcinoma and non-small cell lung cancer deposited in the GEO database. As a result, a total of 574 differentially expressed genes (DEGs) affecting the pathogenesis of lung cancer were identified (207 up-regulated expression and 367 down-regulated expression in lung cancer tissues). A total of 5,093 interactions existed among the 507 (88.3%) proteins, and 10 Meta-signatures were identified: AURKA, CCNB1, KIF11, CCNA2, TOP2A, CENPF, KIF2C, TPX2, HMMR, and MAD2L1. The potential biological functions of Meta-signature DEGs were revealed. In summary, this study identified key genes involved in the process of lung cancer. Our results would help the developing of novel biomarkers for lung cancer.

scholarly journals Characterisation of transcription factor profiles in polycystic kidney disease (PKD): identification and validation of STAT3 and RUNX1 in the injury/repair response and PKD progression

2019 ◽  
Vol 97 (12) ◽  
pp. 1643-1656 ◽  
Author(s):  
Chiara Formica ◽  
Tareq Malas ◽  
Judit Balog ◽  
Lotte Verburg ◽  
Peter A. C. ‘t Hoen ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Kidney Disease ◽  
Polycystic Kidney Disease ◽  
Molecular Mechanisms ◽  
Expression Profiles ◽  
Meta Analysis ◽  
List Type ◽  
Polycystic Kidney ◽  
Altered Expression ◽  
Injury Repair

Abstract Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic renal disease, caused in the majority of the cases by a mutation in either the PKD1 or the PKD2 gene. ADPKD is characterised by a progressive increase in the number and size of cysts, together with fibrosis and distortion of the renal architecture, over the years. This is accompanied by alterations in a complex network of signalling pathways. However, the underlying molecular mechanisms are not well characterised. Previously, we defined the PKD Signature, a set of genes typically dysregulated in PKD across different disease models from a meta-analysis of expression profiles. Given the importance of transcription factors (TFs) in modulating disease, we focused in this paper on characterising TFs from the PKD Signature. Our results revealed that out of the 1515 genes in the PKD Signature, 92 were TFs with altered expression in PKD, and 32 of those were also implicated in tissue injury/repair mechanisms. Validating the dysregulation of these TFs by qPCR in independent PKD and injury models largely confirmed these findings. STAT3 and RUNX1 displayed the strongest activation in cystic kidneys, as demonstrated by chromatin immunoprecipitation (ChIP) followed by qPCR. Using immunohistochemistry, we showed a dramatic increase of expression after renal injury in mice and cystic renal tissue of mice and humans. Our results suggest a role for STAT3 and RUNX1 and their downstream targets in the aetiology of ADPKD and indicate that the meta-analysis approach is a viable strategy for new target discovery in PKD. Key messages We identified a list of transcription factors (TFs) commonly dysregulated in ADPKD. Out of the 92 TFs identified in the PKD Signature, 35% are also involved in injury/repair processes. STAT3 and RUNX1 are the most significantly dysregulated TFs after injury and during PKD progression. STAT3 and RUNX1 activity is increased in cystic compared to non-cystic mouse kidneys. Increased expression of STAT3 and RUNX1 is observed in the nuclei of renal epithelial cells, also in human ADPKD samples.

scholarly journals Profiling at mRNA, protein, and metabolite levels reveals alterations in renal amino acid handling and glutathione metabolism in kidney tissue ofPept2−/−mice

2007 ◽  
Vol 28 (3) ◽  
pp. 301-310 ◽  
Author(s):  
Isabelle M. Frey ◽  
Isabel Rubio-Aliaga ◽  
Anne Siewert ◽  
Daniela Sailer ◽  
Aleksey Drobyshev ◽  
...  
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Kidney Tissue ◽  
Urine Samples ◽  
Differentially Expressed ◽  
Glutathione Metabolism ◽  
Altered Expression ◽  
Urinary Amino Acids ◽  
Urinary Amino

PEPT2 is an integral membrane protein in the apical membrane of renal epithelial cells that operates as a rheogenic transporter for di- and tripeptides and structurally related drugs. Its prime role is thought to be the reabsorption of filtered di- and tripeptides contributing to amino acid homeostasis. To elucidate the role of PEPT2 in renal amino acid metabolism we submitted kidney tissues of wild-type and a Pept2−/−mouse line to a comprehensive transcriptome, proteome and metabolome profiling and analyzed urinary amino acids and dipeptides. cDNA microarray analysis identified 147 differentially expressed transcripts in transporter-deficient animals, and proteome analysis by 2D-PAGE and MALDI-TOF-MS identified 37 differentially expressed proteins. Metabolite profiling by GC-MS revealed predominantly altered concentrations of amino acids and derivatives. Urinary excretion of amino acids demonstrated increased glycine and cysteine/cystine concentrations and dipeptides in urine were assessed by amino acid analysis of urine samples before and after in vitro dipeptidase digestion. Dipeptides constituted a noticeable fraction of urinary amino acids in Pept2−/−animals, only, and dipeptide-bound glycine and cystine were selectively increased in Pept2−/−urine samples. These findings were confirmed by a drastically increased excretion of cysteinyl-glycine (cys-gly). Urinary loss of cys-gly together with lower concentrations of cysteine, glycine, and oxoproline in kidney tissue and altered expression of mRNA and proteins involved in glutathione (GSH) metabolism suggests that PEPT2 is predominantly a system for reabsorption of cys-gly originating from GSH break-down, thus contributing to resynthesis of GSH.

The Oral Intake of Organic Germanium, Ge-132, Elevates α-Tocopherol Levels in the Plas-ma and Modulates Hepatic Gene Expression Profiles to Promote Immune Activation in Mice

2014 ◽  
Vol 84 (3-4) ◽  
pp. 0183-0195 ◽  
Author(s):  
Takashi Nakamura ◽  
Tomoya Takeda ◽  
Yoshihiko Tokuji
Keyword(s):  
Gene Expression ◽  
Immune Activation ◽  
Expression Profiles ◽  
Water Soluble ◽  
Alpha Tocopherol ◽  
Hepatic Gene Expression ◽  
Tocopherol Concentration ◽  
Altered Expression ◽  
Atp Production ◽  
Transfer Protein

The common water-soluble organic germanium compound poly-trans-[(2-carboxyethyl) germasesquioxane] (Ge-132) exhibits activities related to immune responses and antioxidant induction. In this study, we evaluated the antioxidative effect of dietary Ge-132 in the plasma of mice. Male ICR mice (seven mice per group) received an AIN-76 diet with 0.05 % Ge-132; three groups received the Ge-132-containing diet for 0, 1 or 4 days. The plasma alpha-tocopherol (α-tocopherol) concentration increased from 6.85 to 9.60 μg/ml after 4 days of Ge-132 intake (p < 0.05). We evaluated the changes in hepatic gene expression related to antioxidative activity as well as in the entire expression profile after one day of Ge-132 intake, using DNA microarray technology. We identified 1,220 genes with altered expression levels greater than 1.5-fold (increased or decreased) as a result of Ge-132 intake, and α-tocopherol transfer protein (Ttpa) gene expression was increased 1.62-fold. Immune activation was identified as the category with the most changes (containing 60 Gene Ontology (GO) term biological processes (BPs), 41 genes) via functional clustering analysis of altered gene expression. Ge-132 affected genes in clusters related to ATP production (22 GO term BPs, 21 genes), lipid metabolism (4 GO term BPs, 38 genes) and apoptosis (5 GO term BPs). Many GO term BPs containing these categories were significantly affected by the Ge-132 intake. Oral Ge-132 intake may therefore have increased plasma α-tocopherol levels by up-regulating α-tocopherol transfer protein (Ttpa) gene expression.

Sign in / Sign up

Export Citation Format

Share Document