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Niu, L.

Publications and source records attributed to Niu, L..

At least 19 recordsLinked to original sources

Explainable t-SNE for Single-Cell RNA-seq Data Analysis: A Cell-DrivenInformation Fusion Framework

Single-cell RNA sequencing fundamentally depends on defining cell-to-cell similarity to resolve distinct cell states. However, conventional dimensional-reduction frameworks such as t-SNE and UMAP inherently rely on Euclidean geometry, a construct ill-suited for high-dimensional, sparse count matrices, and produce cluster boundaries that lack biological interpretability. Here, we introduce cell-driven information fusion, an end-to-end framework that constructs cell affinity directly from raw counts by integrating three biological signals: gene detection patterns, expression magnitude of dominant transcripts, and global profile correlation. A sparsity-adaptive operator merges these signals into a unified affinity matrix, while an entry-usage diagnostic traces which biological component governs local cluster boundaries. The framework comprises two complementary implementations: c-TSNE for low-to-moderate sparsity (below 80 percent), which consistently outperforms Euclidean baselines across six benchmarks, and c-UMAP for high-sparsity regimes. Evaluated across 29 datasets and two protocols against 11 baseline methods, c-UMAP achieved the highest mean normalized and adjusted mutual information (NMI and AMI) in every setting, with all improvements remaining significant after Bonferroni correction. Because a single fixed weight vector was applied across all 29 datasets per protocol, these gains reflect intrinsic algorithmic robustness rather than dataset-specific hyperparameter tuning. Furthermore, c-UMAP scales seamlessly to 1.14 million cells, running up to 22-fold faster than the leading baseline. Crucially, by operating directly on raw counts without variance-based gene selection, our approach avoids the median 46.9 percent loss of top differentially expressed genes per cell class, preserving essential lineage markers such as IAPP and FOXP3. Together, these results demonstrate that atlas-scale efficiency, raw-data preservation, and mechanistic interpretability are fully compatible.

bioinformatics↗

NF1 deficiency induces metabolic reprogramming and epithelial-mesenchymal transition in glioblastoma

BackgroundMetabolic reprogramming is a common occurrence in tumor cells, where enhanced glycolysis promotes cell growth, invasion and migration. NF1 is tumor suppressor gene that downregulates the encoded neurofibromin protein. However, the effects of NF1 on energy metabolism and epithelial-mesenchymal transition (EMT) in glioblastoma multiforme (GBM), as well as the underlying molecular mechanisms, remain unclear. MethodsCRISPR/Cas9 gene editing technology was employed to construct GBM cell lines with NF1 gene mutations. Metabolomics was utilized to examine the impact of NF1 on metabolic remodeling in GBM. The Seahorse XF24 extracellular flux analyzer was used to detect the effect of NF1 knockdown on glycolysis and mitochondrial oxidative phosphorylation in GBM cells. Wound healing assay and Transwell chamber assay were utilized to detect the effect of NF1 on GBM cell invasion. Orthotopic tumor model in nude mice was established to explore the role of NF1 in vivo. In addition, Co-IP, western blotting, and immunofluorescence were used to explore the changes of key enzymes in glycolysis and mitochondrial oxidative phosphorylation and the relationship between NF1 and MFN1. ResultsThe expression of NF1 is decreased in glioma tissues and is significantly correlated with patient prognosis. NF1 knockdown may promote the invasion, migration, and EMT of GBM cells. At the same time, the activation of the AKT/mTOR signaling pathway promotes aerobic glycolysis in GBM cells, promotes mitochondrial division through targeted regulation of MFN1, and inhibits mitochondrial oxidative phosphorylation. NF1 deficiency promotes EMT in GBM cells by enhancing aerobic glycolysis and mitochondrial division. ConclusionNF1 deficiency promotes GBM glycolysis by activating the AKT/mTOR signaling pathway and inhibits the mitochondrial oxidative phosphorylation by regulating MFN1; NF1 deletion promotes GBM EMT by remodeling the pattern of energy metabolism.

Cancer Biology↗

Glycolytic Specialization Shapes Neuronal Physiology and Function in vivo

Neurons perform diverse functions that impose distinct energetic demands, but how energy-metabolic pathways are matched to these functions in vivo remains unknown. Here we show that two functionally divergent sister chemosensory neurons in C. elegans, ASEL and ASER, exhibit asymmetric glycolytic flux, with ASER exhibiting high and ASEL having low levels of glycolysis. Metabolic imaging, metabolic network modeling, and electrophysiology measurements reveal that ASERs elevated glycolysis supports a hyperpolarized resting potential, low input resistance, and rapid repolarization that enable a distinct functional role compared to ASEL. Impairing glycolysis collapses these electrophysiological specializations without abolishing neuronal excitability, and selectively disrupts ASERs calcium responses while leaving ASEL largely unaffected. These findings demonstrate that neuron-specific glycolytic programs shape core biophysical properties and are required for functional identity in vivo, establishing metabolism as an active determinant of neuronal physiology.

neuroscience↗

Microglial Lag3 Drives α-Synuclein--induced Neurotoxic Activated (A1) Astrocytes and Neurodegeneration

BackgroundNeuroinflammation and pathologic -synuclein (-syn) aggregation cooperate to drive dopaminergic neurodegeneration in Parkinsons disease, but the glial receptors that couple extracellular -syn to inflammatory cascades remain incompletely defined. Microglia express higher levels of lymphocyte activation gene 3 (Lag3) than neurons, yet the contribution of microglial Lag3 to -syn recognition, glial crosstalk, and neurodegeneration is unknown. MethodsBiochemical binding assays, live-cell imaging, cytokine profiling, and neuron-microglia-astrocyte co-culture paradigms were used to define Lag3-dependent -syn preformed fibril (PFF) binding, uptake, and microglial activation. To interrogate in vivo function, microglia-specific Lag3 conditional knockout mice (Lag3L/L-Cx3cr1CreER) and littermate controls received unilateral intrastriatal -syn PFF injections, followed by histological, biochemical, and behavioral assessments of -syn pathology, gliosis, nigrostriatal integrity, and motor performance. Results-syn PFFs bound microglial Lag3 with high specificity and nanomolar affinity and required Lag3 for efficient fibril internalization and induction of proinflammatory cytokines. Microglial Lag3 deficiency markedly blunted -syn PFF-evoked microglial activation, prevented cytokine-driven conversion of astrocytes into neurotoxic reactive A1 astrocytes, and abolished astrocyte-dependent neuronal death in vitro. In vivo, microglia-specific Lag3 deletion reduced cortical, striatal, and substantia nigra pS129 -syn pathology, suppressed microgliosis and A1 astrocyte induction, preserved substantia nigra dopaminergic neurons and striatal dopamine transporter/tyrosine hydroxylase expression, and ameliorated -syn PFF-induced motor deficits. ConclusionsThis study identifies microglial Lag3 as a key receptor linking extracellular -syn PFF recognition to inflammatory amplification, neurotoxic reactive A1 astrocyte conversion, and dopaminergic neurodegeneration. Together with prior work on neuronal Lag3, these findings support a cell-type-specific dual-axis model in which neuronal Lag3 mediates -syn propagation while microglial Lag3 drives glia-dependent neurotoxicity, positioning Lag3 as a promising precision therapeutic target in -synucleinopathies.

neuroscience↗

A scaffold attachment factor PHM-2 regulates synaptic transmission through SLO-2 potassium channel in C. elegans

Scaffold attachment factor B (SAFB) proteins are evolutionarily conserved DNA/RNA binding proteins that are involved in multiple processes of gene expression. These proteins are broadly expressed with particular high expression observed in the nervous system. However, their physiological roles in neurons are largely unclear. Here we show that PHM-2, the sole SAFB ortholog in C. elegans, regulates synaptic transmission at the neuromuscular junctions through an effect on SLO-2 potassium channel. We found that phm-2 knockout suppresses a sluggish phenotype of worms expressing a hyperactive SLO-2 channel, greatly reduces SLO-2-mediated neuronal whole-cell currents, and enhances neuromuscular synaptic transmission. In addition, we found that PHM-2 genetically interacts with another DNA/RNA binding protein, HRPU-2/hnRNP U, to control SLO-2 expression through a posttranscriptional mechanism. These results reveal a novel function of a SAFB protein in regulating neuronal activity, and may help understand the physiological roles of SAFB proteins in the nervous system of other species. Author SummaryProteins in the SAFB family are found in many species, and they help control how genes are expressed in cells. These proteins are commonly present in the nervous system, but their exact roles in nerve cells are not well understood. In this study, we examined the single SAFB-like protein called PHM-2 in the nematode C. elegans to learn how it affects the nervous system. We discovered that PHM-2 plays an important role in communication between nerve cells and muscles. Worms lacking PHM-2 were able to counteract the sluggish movement caused by a hyperactive potassium channel called SLO-2. Without PHM-2, nerve cells had much smaller electrical currents mediated by SLO-2 and a stronger signaling from nerves to muscles. We also found that PHM-2 works together with another genetic regulator, HRPU-2, to control the amount of SLO-2 protein made in nerve cells. These findings reveal a new role for SAFB proteins in shaping neuronal activity by regulating potassium channels. Understanding this process in worms may provide clues about how these proteins contribute to brain function in humans.

neuroscience↗

Targeted α-Synuclein mRNA Degradation by PMO-Based RNA-Degrading Chimeras

-Synucleinopathies are devastating neurodegenerative diseases characterized by pathological accumulation of a neuronal protein, -synuclein (Syn). Lowering soluble Syn levels is a promising therapeutic strategy to limit aggregation and neurotoxicity, but directly targeting this protein is hindered by its intrinsically disordered structure and other factors, such as its conformational heterogeneity and intracellular drug delivery barriers. Consequently, increasing attention has been directed toward targeting the SNCA transcript, which encodes Syn. Here, we developed phosphorodiamidate morpholino oligonucleotide (PMO)-based RNA-degrading chimeras (RDCs) that selectively bind the 5' untranslated region of SNCA mRNA and recruit RNase L for targeted RNA degradation. Through the systematic evaluation of 10 RDCs, we identified and optimized 4-D1, which effectively reduced SNCA mRNA and Syn protein expression in HEK293T cells in an RNase L-dependent manner. 4-D1 lowered SNCA transcript and Syn protein levels in both primary cortical neurons from humanized SNCA mice and in human induced pluripotent stem cell-derived cortical neurons. This reduction prevented prion-like seeding induced by patient-derived Syn fibrils and protected neurons from fibril-induced cytotoxicity. Finally, in vivo studies confirmed the efficacy of 4-D1 in reducing Syn mRNA expression in humanized SNCA mice. These findings indicate that PMO-based RDCs may represent a promising therapeutic modality for -synucleinopathies. Significance StatementAbnormal aggregation of the neuronal protein -synuclein is central to Parkinsons disease and related disorders, yet therapeutic candidates that directly target this protein have yet to demonstrate efficacy. in clinical trials. We developed a new strategy that lowers -synuclein production at the RNA level using phosphorodiamidate morpholino oligonucleotide (PMO)-based RNA-degrading chimeras (RDCs). These molecules recruit a natural RNA-degrading enzyme to selectively destroy the RNA transcript encoding -synuclein. Our lead RDC reduced -synuclein levels in cultured cells, humanized mouse and human neurons, blocked -synuclein pathological aggregation, and protected neurons from toxicity. This study establishes RDCs as a promising therapeutic platform for Parkinsons disease and other neurodegenerative diseases driven by -synuclein.

biochemistry↗

Neuronal LAG3 facilitates pathogenic α-synuclein neuron-to-neuron propagation

Lymphocyte activation gene 3 (LAG3) is a key receptor involved in the propagation of pathological proteins in Parkinsons disease (PD). This study investigates the role of neuronal LAG3 in mediating the binding, uptake, and propagation of -synuclein (Syn) preformed fibrils (PFFs). Using neuronal LAG3 conditional knockout mice and human induced pluripotent stem cells-derived dopaminergic (DA) neurons, we demonstrate that LAG3 expression is critical for pathogenic Syn propagation. Our results show that the absence of neuronal LAG3 significantly reduces Syn pathology, alleviates motor dysfunction, and inhibits neurodegeneration in vivo. Electrophysiological recordings revealed that Syn PFFs induce pronounced neuronal hyperactivity in wild-type (WT) neurons, increasing firing rates in cell-attached and whole-cell configurations, and reducing miniature excitatory postsynaptic currents. In contrast, neurons lacking LAG3 resisted these electrophysiological effects. Moreover, treatment with an anti-human LAG3 antibody in human DA neurons inhibited Syn PFFs binding and uptake, preventing pathology propagation. These findings confirm the essential function of neuronal LAG3 in mediating Syn propagation and associated disruptions, identifying LAG3 as a potential therapeutic target for PD and related -synucleinopathies.

neuroscience↗

α-Synuclein Strain Dynamics Correlate with Cognitive Shifts in Parkinson's Disease

-Synuclein (-syn) strains can serve as discriminators between Parkinsons disease (PD) and related -synucleinopathies. The relationship between -syn strain dynamics and clinical performance as patients transition from normal cognition (NC) to cognitive impairment (CI) is not known. Here, we show that the biophysical properties and neurotoxicity of -syn strains change as PD cognitive status transitions from NC to mild cognitive impairment (PD-MCI) and dementia (PD-D). Both cross-sectional and longitudinal analyses reveal distinct -syn strains in PD patients correlating to their level of cognitive impairment. Machine learning (ML) was employed to achieve high classification accuracy. The combination of thioflavin T (ThT) maximal fluorescence intensity (mfi), max slope of rise curve (forming rate), lag time (tlag), 20% time (t20), and half-time (t50), dynamic light scattering (DLS) (peak number, [1/2] peak size, [1/2] peak intensity) and neurotoxicity together with demographic variables for model training yielded superior performance (89[~]99% accuracy in the 4- and 2- classification schema) compared to individual features alone in classifying cognitive status. For the longitudinal study, DLS peak number emerged as the strongest predictor of cognitive transition (HR = 0.12, P = 0.002), with the optimal predictive model combining DLS peak number, sex, education, DLS peak 1 size, and DLS peak 2 polydispersity achieving high accuracy (C-index of [~]93%). This study presents evidence that individuals with PD have different -syn strains correlating to their cognitive status and highlights the potential of -syn strain dynamics to guide future diagnosis, management, and stratification of PD patients. One Sentence SummaryDistinct features of -syn strains change with cognitive decline in Parkinsons disease and AI-based analysis incorporating these combined characteristics serves as a powerful tool for PD clinical stratification.

neuroscience↗

KLHDC7B, a novel gene associated with age-related hearing loss in humans, is required for the maintenance of hearing in mice.

BackgroundAge-related hearing loss (ARHL) is the most common sensory loss in older adults, but the underlying pathological mechanisms remain unclear. Recent genome wide association studies (GWAS) have linked variation in a large number of genes with increased risk of ARHL for the first time. Amongst the strongest of these associations is variation in KLHDC7B, a gene of unknown function and one not previously linked to hearing. MethodsTo confirm whether KLHDC7B plays a role in hearing we investigated auditory function in two independent knockout mutant mouse models of Klhdc7b: Klhdc7bIMPC-/-and Klhdc7bRegn{Delta}/{Delta} on the C57BL/6N background and the B6.CAST-Cdh23753A>G background respectively. The B6.CAST-Cdh23753A>G background was backcrossed to correct a known age-related hearing loss (ahl) mutation in cadherin 23 present in both the C57BL/6N and C57BL/6J strains. ResultsWe showed that Klhdc7b is expressed exclusively in inner and outer sensory hair cells within the cochlea of mice at the RNA and protein level. Homozygous mutants for both knockout mouse models display a similar early-onset, progressive and severe hearing loss. Histological characterization of the two mouse models suggests that hair cells develop normally and are present in neonates. However, after the onset of hearing there is a progressive loss of outer hair cells in a gradient from base to apex of the cochlea consistent with the hearing deficit in the mice and the pattern of hearing loss in ARHL. Inner hair cells remain intact up to the latest age examined (~8 weeks). ConclusionsOur data suggests KLHDC7B is required for maintenance of auditory function rather than in its development, supporting the novel association with ARHL in humans detected in recent GWAS. To our knowledge, this is the first validation in mouse of an ARHL association in humans detected in a GWAS. Our work also provides two distinct mouse models to further investigate the role of KLHDC7B in auditory function and for use in the development of therapeutic tools to prevent or treat ARHL.

genetics↗

A sensitive red/far-red photoswitch for controllable gene therapy in mouse models of metabolic diseases

Red light optogenetic systems are in high demand for the precise control of gene expression for gene- and cell-based therapies. Here, we report a red/far-red light-inducible photoswitch (REDLIP) system based on the chimeric photosensory protein FnBphP (Fn-REDLIP) or PnBphP (Pn-REDLIP) and their interaction partner LDB3, which enables efficient dynamic regulation of gene expression with a timescale of seconds without exogenous administration of a chromophore in mammals. We used the REDLIP system to establish the REDLIP-mediated CRISPR-dCas9 (REDLIPcas) system, enabling optogenetic activation of endogenous target genes in mammalian cells and mice. The REDLIP system is small enough to support packaging into adeno-associated viruses (AAVs), facilitating its therapeutic application. Demonstrating its capacity to treat metabolic diseases, we show that an AAV-delivered Fn-REDLIP system achieved optogenetic control of insulin expression to effectively lower blood glucose levels in type 1 diabetes model mice and control an anti-obesity therapeutic protein (thymic stromal lymphopoietin, TSLP) to reduce body weight in obesity model mice. REDLIP is a compact and sensitive optogenetic tool for reversible and non-invasive control that can facilitate basic biological and biomedical research.

synthetic biology↗

Track-A-Worm 2.0: A Software Suite for Quantifying Properties of C. elegans Locomotion, Bending, Sleep, and Action Potentials

Comparative analyses of locomotor behavior and cellular electrical properties between wild-type and mutant C. elegans are crucial for exploring the gene basis of behaviors and the underlying cellular mechanisms. Although many tools have been developed by research labs and companies, their application is often hindered by implementation difficulties or lack of features specifically suited for C. elegans. Track-A-Worm 2.0 addresses these challenges with three key components: WormTracker, SleepTracker, and Action Potential (AP) Analyzer. WormTracker accurately quantifies a comprehensive set of locomotor and body bending metrics, reliably distinguish between the ventral and dorsal sides, continuously tracks the animal using a motorized stage, and seamlessly integrates external devices, such as a light source for optogenetic stimulation. SleepTracker detects and quantifies sleep-like behavior in freely moving animals. AP Analyzer assesses the resting membrane potential, afterhyperpolarization level, and various AP properties, including threshold, amplitude, mid-peak width, rise and decay times, and maximum and minimum slopes. Importantly, it addresses the challenge of AP threshold quantification posed by the absence of a pre-upstroke inflection point. Track-A-Worm 2.0 is potentially a valuable tool for many C. elegans research labs due to its powerful functionality and ease of implementation.

neuroscience↗

The asymmetric opening of HIV-1 Env by a potent CD4 mimetic enables anti-coreceptor binding site antibodies to mediate ADCC

HIV-1 envelope glycoproteins (Env) from primary HIV-1 isolates typically adopt a pretriggered "closed" conformation that resists to CD4-induced (CD4i) non-neutralizing antibodies (nnAbs) mediating antibody-dependent cellular cytotoxicity (ADCC). CD4-mimetic compounds (CD4mcs) "open-up" Env allowing binding of CD4i nnAbs, thereby sensitizing HIV-1-infected cells to ADCC. Two families of CD4i nnAbs, the anti-cluster A and anti-coreceptor binding site (CoRBS) Abs, are required to mediate ADCC in combination with the indane CD4mc BNM-III-170. Recently, new indoline CD4mcs with improved potency and breadth have been described. Here, we show that the lead indoline CD4mc, CJF-III-288, sensitizes HIV-1-infected cells to ADCC mediated by anti-CoRBS Abs alone, contributing to improved ADCC activity. Structural and conformational analyses reveal that CJF-III-288, in combination with anti-CoRBS Abs, potently stabilizes an asymmetric "open" State-3 Env conformation, This Env conformation orients the anti-CoRBS Ab to improve ADCC activity and therapeutic potential.

microbiology↗

High accuracy methylation identification tools on single molecular level for PacBio HiFi data

PacBios Circular Consensus Sequencing (CCS) allows us to obtain highly accurate bases and simultaneously determine the methylation states of individual molecules. However, existing CCS-based methods for 5mC detection have low accuracy (<90% on most datasets) at the single-molecule level and can produce inaccurate methylation patterns. These methods rely on the information from 21 bp contexts surrounding the target CpGs and have over 29% low-confidence (<75% accuracy) calls at CpGs with less distinguishable signals. We hypothesize that incorporating CpG methylation correlation information at the single-molecule level could improve the methylation calls on low-confidence CpGs. Here, we present a novel deep graph convolutional network (hifimeth) that uses 400 bp context in CCS-based 5mC calling and show that its improved performance is mainly due to the inclusion of more neighboring CpGs in contexts. Hifimeth achieves an average single-molecule accuracy of 94.7% and an average F1 score of 94.2%, 5.5% and 5.9% higher than the previous state-of-the-art method, respectively. Hifimeth-based methylation frequency quantification by read counting outperforms previous methods on all human and zebrafish datasets tested. The results also show that hifimeths high-accuracy calls can reveal complex single-molecule methylation patterns, either related to haplotypes or repeat regions, with up to single-motif resolution.

bioinformatics↗

A novel hybrid high speed mass spectrometer allows rapid translation from biomarker candidates to targeted clinical tests using 15N labeled proteins

Recent developments in affinity binder or mass spectrometry (MS)-based plasma proteomics are now producing panels of potential biomarker candidates for diagnosis or prognosis. However, clinical validation and implementation of these biomarkers remain limited by the reliance on dated triple quadrupole MS technology. Here, we evaluate a novel hybrid high-speed mass spectrometer, Stellar MS, which integrates the robustness of triple quadrupoles with the enhanced capabilities of an advanced linear ion trap analyzer. This instrument allows for extremely rapid and sensitive parallel reaction monitoring (PRM) and MS3 targeting. The Stellar MS allowed targeting thousands of peptides originally measured on Orbitrap Astral MS, achieving high reproducibility and low coefficients of variation (CV) as well as sensitivity and specificity sufficient for more than the top 1000 plasma proteins. Furthermore, we developed targeted assays for alcohol-related liver disease (ALD) biomarkers, showcasing the potential of Stellar MS in clinical applications. Absolute quantification is typically a requirement for clinical assays and we explore the use of 15 N labeled protein standards in a rapid, streamlined and generic manner. Our results indicate that Stellar MS can bridge the gap between proteomics discovery and routine clinical testing, enhancing the diagnostic and prognostic utility of protein biomarkers.

biochemistry↗

Optimizing Accuracy and Efficiency in Analyzing Non-UMI Liquid Biopsy Datasets Using the Sentieon ctDNA Pipeline

Sequencing clinical liquid biopsy, especially circulating tumor DNA (ctDNA), provides a valuable method for identifying low allele frequency tumor variants, opening novel clinical applications, particularly in treatment selection for late-stage cancer patients. Despite advancements, challenges in assay development persist, primarily due to limited sample volumes and insufficiency of reads supporting low allele frequency variants. The allele frequencies of clinically significant variants often hover close to the threshold of errors introduced by PCR and sequencing processes. Therefore, more sophisticated analysis methods are crucial to further reduce base error rates, enabling accurate discrimination between background errors and genuine somatic variants. While several ctDNA analysis pipelines have been published and adopted, there is room for improvement in terms of accuracy and run efficiency. In this study, we introduce Sentieons innovative consensus-based ctDNA pipeline - a rapid and precise solution for calling small somatic variants from non-UMI ctDNA sequencing data. The pipeline comprises four core modules: alignment, consensus generation, variant calling, and variant filtering. Through benchmarking with in-vitro and real clinical datasets, we observed that the Sentieon ctDNA pipeline exhibits higher accuracy compared to alternative methods.

bioinformatics↗

Neuroinflammation underlies the development of social stress induced cognitive deficit in sickle cell disease.

Cognitive deficit is a debilitating complication of SCD with multifactorial pathobiology. Here we show that neuroinflammation and dysregulation in lipidomics and transcriptomics profiles are major underlying mechanisms of social stress-induced cognitive deficit in SCD. Townes sickle cell (SS) mice and controls (AA) were exposed to social stress using the repeat social defeat (RSD) paradigm concurrently with or without treatment with minocycline. Mice were tested for cognitive deficit using novel object recognition (NOR) and fear conditioning (FC) tests. SS mice exposed to RSD without treatment had worse performance on cognitive tests compared to SS mice exposed to RSD with treatment or to AA controls, irrespective of their RSD or treatment disposition. Additionally, compared to SS mice exposed to RSD with treatment, SS mice exposed to RSD without treatment had significantly more cellular evidence of neuroinflammation coupled with a significant shift in the differentiation of neural progenitor cells towards astrogliogenesis. Additionally, brain tissue from SS mice exposed to RSD was significantly enriched for genes associated with blood-brain barrier dysfunction, neuron excitotoxicity, inflammation, and significant dysregulation in sphingolipids important to neuronal cell processes. We demonstrate in this study that neuroinflammation and lipid dysregulation are potential underlying mechanisms of social stress-related cognitive deficit in SS mice. Key PointsO_LINeuroinflammation and lipid dysfunction are potential underlying mechanisms of social stress-related cognitive deficit in SCD patients. C_LIO_LIMitigating or ameliorating the impact of cognitive deficits in SCD needs to consider the biological changes already created by exposure to social stress. C_LI Novelty of our FindingsWe show for the first time, that neuroinflammation along with changes in the brain lipidome and transcriptome, are underlying biological mechanism contributing to the development and potentially progression of cognitive impairment among sickle cell patients. These findings also provide for the first time, a mechanistic basis for an earlier reported observation of a higher likelihood of having lower intelligence quotient scores among children with sickle cell disease exposed to social stress in the form of low parental socioeconomic status.

neuroscience↗

NGAL contributes to hemostasis and thrombosis by potentiating or suppressing coagulant or anticoagulant factors

Coagulation is related to inflammation, but the key pathways, especially innate immunity inflammatory response-coagulation, hemostasis, and thrombosis regulation is poorly understood and need to be further explored. In the current study, we showed that innate immunity inflammatory mediator neutrophil gelatinase-associated apolipoprotein (NGAL) which was upregulated in plasma of deep vein thrombosis patients interacted with and potentiated thrombin, kallikrein, FXIa, and FVIIa and suppressed antithrombin to induce coagulation, hemostasis, and thrombosis. Furthermore, NGAL can augment thrombin-induced platelet aggregation. In multiple mice hemostasis and thrombosis models, NGAL overexpression or intravenous administration promoted coagulation and hemostasis and aggravated thrombus, whereas NGAL knockout or treatment with anti-NGAL monoclonal antibody significantly prolonged bleeding time and alleviated thrombus formation. Notably, NGAL knockout prolonged both mice tail bleeding time and artery occlusion time to over 40 min, resembling uncontrollable bleeding and clotting disorder seen in Hemophilia mice. Furthermore, anti-NGAL monoclonal antibody treatment markedly reduced the formation of blood clots in a mouse-tail thrombosis model induced by carrageenan, which is linked to inflammation. Collectively, these findings suggest NGAL is a crucial coagulation regulator and mediates the crosstalk between innate immunity inflammation and coagulation, hemostasis, and thrombus, and provide new target and strategy for the development of innovative antithrombotic drugs.

biochemistry↗

Genomics-Driven Discovery of Myxopyromides, a Class of Polyketidic Amides Associated with Predation of Myxococcus sp. SDU36

Myxobacteria are renowned for their genuine prowess to deliver multifarious bioactive natural products. Genome mining of Myxococcus sp. SDU36 identified a hybrid PKS-NRPS BGC (mpd) that presumably specified previously uncharacterized molecules. The expression of mpd was activated by exchanging the innate promoter of core PKS-NRPS genes with our recently characterized strong constitutive promoter BBa_J23104. Comparative metabolic profiling allowed facile isolation of the elicited compounds 1-5 designated myxopyromides A-E, a group of structurally related polyketidic amides. Especially, myxopyromides D was appended with an uncommon pyrrolinone warhead at the carboxylic terminus, whereas myxopyromide C was instead decorated with a rare structural unit of aminobutanone. Although myxopyromides basically follow a textbook modular PKS-NRPS biosynthetic trajectory, an anteriorly unappreciated flexible chain release strategy is adopted to enrich the chemical repertoire of mpd BGC. Interestingly, myxopyromides were associated with the predation of Myxococcus sp. SDU36. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=80 SRC="FIGDIR/small/535179v1_ufig1.gif" ALT="Figure 1"> View larger version (23K): org.highwire.dtl.DTLVardef@29d791org.highwire.dtl.DTLVardef@1079fdcorg.highwire.dtl.DTLVardef@19044d8org.highwire.dtl.DTLVardef@97c7dc_HPS_FORMAT_FIGEXP M_FIG C_FIG

biochemistry↗