Serum glycopattern and Maackia amurensis lectin-II binding glycoproteins in autism spectrum disorder

Qin, Yannan; Chen, Yanni; Yang, Juan; Wu, Fei; Zhao, Lingyu; Yang, Fuquan; Xue, Peng; Shi, Zhuoyue; Song, Taek Lyul; Huang, Chen

doi:10.1038/srep46041

Cited by 24 publications

(22 citation statements)

References 57 publications

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“…These principles are consistent with previous research. These criteria are in keeping with previous report 20.…”

supporting

confidence: 76%

“…The structures of epoxy-coated, hydroxyl-functionalized magnetic particles and GMPCs were determined by using infrared spectroscopy (FT-IR-spectrometer; Nicolet 5700, Thermo electron Corporation). [18][19][20]…”

Section: Preparation Of Gmpcsmentioning

confidence: 99%

“…The GlcBPs were quantitated by BCA and identified by 10% SDS-PAGE. Then the obtained proteins (about 150 μg) were digested by trypsin and PNGase F as described previously [18][19][20]. 2.5 | Identification of peptides by LC-MS/MS…”

mentioning

confidence: 99%

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Characterization of glucose‐binding proteins isolated from health volunteers and human type 2 diabetes mellitus patients

et al. 2021

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Glucose is one of the most important monosaccharides. Although hyperglycemia in type 2 diabetes mellitus (T2DM) lead to a series of changes; however, little is known about the alterations of serum proteins in T2DM, especially those proteins with glucose affinity. In this study, the glucose-binding proteins (GlcBPs) of serum were isolated from 30 health volunteer (HV) and 30 T2DM patients by glucosemagnetic particle conjugates (GMPC) and identified by mass spectrum analysis.Gene ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) indicated the main gene annotations and pathways of this GlcBPs, while Motif-X webtool provided the potential glucose-binding domains.Further docking analysis and glycan microarray were used to understand the interaction between the glucose and glucose-binding domains. A total of 149 and 119 GlcBPs were identified from HV and T2DM cases. Four hundred and sixty-eight GO annotations in 165 identified GlcBPs were available, while the majority involved in cellular processes and binding function. A short peptide, EGDEEITCLNGFWLE, which was derived from the Motif-X analysis, presented a high-binding ability to the glucose from both docking analysis and glycan analysis. GMPC provides a powerful tool for GlcBPs isolation and indicates the alteration of GlcBPs in T2DM. K E Y W O R D S glucose, glycan-binding proteins, LC-MS/MS, molecular docking, T2DM 1 | INTRODUCTION Diabetes mellitus is a chronic metabolic disease with hyperglycemia caused by the fault in the insulin production. 1 Over 90% of patients are diagnosed with type 2 diabetes mellitus (T2DM), which in many cases can be prevented by adopting a healthy lifestyle 2,3 . As the hyperglycemia associated with a series of complications and glucose levels can affect the pathways leading to abnormal glycosylation or un-enzymatic glycation, numerous studies have investigated the effect of T2DM from a glycomic prospective. Testa and colleagues found that α (1,6)-linked arm mono galactosylated and core-fucosylated biantennary N-glycans were significantly reduced in T2DM compared to healthy controls in serum N-glycome. 4 Lim et al reported a total of 20 up-regulated and 6 down-regulated proteins and the structures of their attached complex N-and O-glycans under the insulin-resistant conditions. These data also supported that the O-GlcNAc modification involved in the regulation of adipocytokine secretion upon the induction of insulin resistance in human adipocytes. 5 Itoh et al analyzed the serum N-glycans by exoglycosidase digestion and mass spectrometry, they found the increase in 1,6-fucosylation is a striking change in the serum N-glycans of the db/db mice model, whereas the change in the

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“…These principles are consistent with previous research. These criteria are in keeping with previous report 20.…”

supporting

confidence: 76%

Section: Preparation Of Gmpcsmentioning

confidence: 99%

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Characterization of glucose‐binding proteins isolated from health volunteers and human type 2 diabetes mellitus patients

et al. 2021

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“…Thereinto, OSTC, MAN1B1 and MGAT5, translating to key enzymes for N-linked glycosylation, were signi cantly down-regulated in ASD. In our previous study, we found a signi cant decrease of STL binding glycans or glycoproteins that contain trimers and tetramers of GlcNAc (core structure of N-glycans) in ASD versus in TD (fold change = 0.54, p = 0.0057) [10]. In all, no matter at the gene level, the transcription level, or the level of translation and post-translation modi cation, abnormalities of glycosylation and carbohydrate metabolism might be an important molecular mechanism of ASD.…”

Section: Discussionmentioning

confidence: 87%

“…In recent years, blood/serum biomarkers have drawn much attention due to their accessibility, low cost and rapid detection. In our previous study, we identi ed four candidate peptides as biomarkers, namely SerpinA5-A, ApoC1-A, FABP1-A and PF4-A [9], and α2-3-linked sialylation of apolipoprotein D (APOD) [10] as potential biomarkers for ASD. A recent study also showed that SLC25A12, LIMK1, and RARS might serve as potential blood protein biomarkers for ASD [11].…”

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confidence: 99%

Whole-transcriptome analysis of serum neuron-derived exosomes reveals specific signature for autism spectrum disorder in Chinese children

Qin

Cao

Zhang

et al. 2021

Preprint

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BackgroundAutism spectrum disorder (ASD) is a prevalent developmental disorder that appears in early childhood and manifests repetitive behavioral and social deficits. Reported biomarkers for ASD cannot directly and specifically reflect the abnormality of brain neurons which are preferentially affected and correlated with clinical severity of the disease. Neuron-derived exosomes (NDEs), which carry proteins, lipids and nucleic acids can reflect a variety of brain diseases. However, little research has been reported about NDEs in children with ASD. MethodsSerum samples were collected from 100 ASD children and 60 age-matched typically developed (TD) children, and were pooled into 5 ASD groups and 3 TD groups (n=20). NDEs from the pooled sera in each group were isolated using L1CAM antibody mediated immunosorbent assay and characterized by nanoparticle tracking analysis, transmission electron microscopy and western blot. Whole-transcriptome of NDEs was detected by lncRNA microarray and RNA-Sequencing. RNAs expressed differently in NDEs from ASD sera as versus those from TD sera were screened, analyzed, and validated. ResultsSerum NDEs were isolated successfully. A total of 1418 mRNAs, 1745 lncRNAs and 11 miRNAs were identified to be differentially expressed, and most of them were down-regulated in ASD. The differentially expressed RNAs were prone to be distributed on chromosome 17. Target gene prediction and bioinformatic analysis revealed that a large portion of RNAs were involved in neuron- and glycan-related networks implicated in ASD. qRT-PCR identified that the levels of EDNRA, SLC17A6, HTR3A, OSTC, TMEM165, PC-5p-139289_26, and hsa-miR-193a-5p changed significantly in ASD, indicating them as potential biomarkers for the disease. LimitationsThe correlation between the expression of candidate biomarkers and disease severity were not examined. Some of our participants were not medication-free. Samples were mainly from a single hospital. ConclusionsWhole-transcriptome analysis of serum NDEs reveals specific signature for ASD in Chinese children, which may help detect predictive biomarkers and molecular mechanisms of ASD, and provide reference for diagnoses and therapeutic management of the disease.

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The NO Answer for Autism Spectrum Disorder

et al. 2023

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Autism spectrum disorders (ASDs) include a wide range of neurodevelopmental disorders. Several reports showed that mutations in different high-risk ASD genes lead to ASD. However, the underlying molecular mechanisms have not been deciphered. Recently, they reported a dramatic increase in nitric oxide (NO) levels in ASD mouse models. Here, they conducted a multidisciplinary study to investigate the role of NO in ASD. High levels of nitrosative stress biomarkers are found in both the Shank3 and Cntnap2 ASD mouse models. Pharmacological intervention with a neuronal NO synthase (nNOS) inhibitor in both models led to a reversal of the molecular, synaptic, and behavioral ASD-associated phenotypes. Importantly, treating iPSC-derived cortical neurons from patients with SHANK3 mutation with the nNOS inhibitor showed similar therapeutic effects. Clinically, they found a significant increase in nitrosative stress biomarkers in the plasma of low-functioning ASD patients. Bioinformatics of the SNO-proteome revealed that the complement system is enriched in ASD. This novel work reveals, for the first time, that NO plays a significant role in ASD. Their important findings will open novel directions to examine NO in diverse mutations on the spectrum as well as in other neurodevelopmental disorders. Finally, it suggests a novel strategy for effectively treating ASD.

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Serum glycopattern and Maackia amurensis lectin-II binding glycoproteins in autism spectrum disorder

Cited by 24 publications

References 57 publications

Characterization of glucose‐binding proteins isolated from health volunteers and human type 2 diabetes mellitus patients

Characterization of glucose‐binding proteins isolated from health volunteers and human type 2 diabetes mellitus patients

Whole-transcriptome analysis of serum neuron-derived exosomes reveals specific signature for autism spectrum disorder in Chinese children

The NO Answer for Autism Spectrum Disorder

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