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Gupta, D.

Publications and source records attributed to Gupta, D..

At least 37 records · Page 2Linked to original sources

Thrombospondin Encapsulated Dense Particles accelerate wound healing and downregulate fibrotic phenotypes

Extracellular particles (EP) released by cells are heterogenous, with extracellular vesicles (EV) believed to be the major component. To investigate different EV subpopulations, we conducted a panel screen of 15 fluorescent EV markers in 4 adherent cell lines. Nanoflow cytometry identifies TSPAN14 as the best EV marker in 3 of 4 cell lines. Surprisingly, less than 50% of EPs are labelled by the top 2 EV markers in half the cell lines. The EV marker negative EPs are detergent resistant, non-lipophilic, dense and have Thrombospondin shells by dSTORM; and were thus named Thrombospondin Encapsulated Dense particles (ThrEDs). ThrEDs are ubiquitous, contain extracellular matrix regulators and are released following cell stress. ThrEDs accelerate scratch-wound closure and downregulate the fibrotic phenotype in Dupuytrens disease patient myofibroblasts. The TSP-1 C-terminus is exposed on the surface of ThrEDs, opening engineering applications.

cell biology↗

Genus-specific remodeling of carbon and energy metabolism facilitates acetoclastic methanogenesis in Methanosarcina spp. and Methanothrix spp.

Methanogenic archaea (methanogens) are microorganisms that obligately produce methane as a byproduct of their energy metabolism. While most methanogens grow on CO2+H2, isolates of the Genus Methanosarcina and Methanothrix can use acetate as the sole substrate for methanogenesis. Methanogenic growth on acetate, i.e., acetoclastic methanogenesis, is hypothesized to require two distinct genetic modules: one for the activation of acetate to acetyl-CoA and the other for producing a chemiosmotic gradient using electrons derived from ferredoxin. In Methanosarcina spp., the activation of acetate to acetyl-CoA is mediated by acetate kinase (Ack) and phosphotransacetylase (Pta) whereas Methanothrix spp. encode AMP-forming acetyl-CoA synthetases (Acs). The Rhodobacter nitrogen fixation complex (Rnf) or Energy converting hydrogenase (Ech) are critical for energy conservation in Methanosarcina spp. during growth on acetate, and a F420:phenazine oxidoreductase-like complex (Fpo) likely plays an analogous role in Methanothrix spp. Here, we tested the proposed modularity of these pathways to facilitate acetoclastic methanogenesis. First, we surveyed over a hundred genomes within the Class Methanosarcinia to show that the genomic potential for acetoclastic methanogenesis using distinct combinations of modules is widespread. We then used the genetically tractable strain, Methanosarcina acetivorans, to build all modular combinations for acetoclastic methanogenesis. Our results indicate that Acs, while functional, cannot replace Ack+Pta to rescue acetate growth in M. acetivorans. Similarly, the Fpo bioenergetic complex cannot replace Rnf. As such, our work suggests that, in addition to horizontal gene transfer of core catabolic modules, acetoclastic metabolism in methanogens requires changes in energetic modules too. IMPORTANCEA large fraction of biogenic methane is derived from acetate, yet acetoclastic methanogens, i.e., methanogens that grow on acetate, remain poorly characterized due to their slow growth. Two groups of methanogens, Methanosarcina spp. and Methanothrix spp., perform acetoclastic methanogenesis using distinct sets of genes for acetate activation and energy conservation. It is widely hypothesized that these genetic modules from Methanosarcina spp. and Methanothrix spp. are functionally analogous and would thus be interchangeable. To test this hypothesis, we engineered different combinations of modules for acetoclastic growth in Methanosarcina acetivorans. Our results challenge this hypothesized paradigm of modularity, and we posit that other changes to the carbon and electron transfer pathways were crucial for the emergence of acetoclastic methanogenesis.

microbiology↗

Systemic Inflammation Modulates Clearance and drives Extra-Hepatic Distribution of Extracellular Vesicles

Extracellular vesicles (EVs) are promising vehicles for targeted therapeutic delivery, capable of encapsulating and transporting biomolecules to specific cells and tissues. Given that inflammation is central to many acute and chronic diseases, understanding EV biodistribution under inflammatory conditions is essential for therapeutic optimization. This study examines how acute systemic inflammation influences EV biodistribution, clearance, and plasma half-life, with a focus on the role of macrophages and their polarization states. Using a lipopolysaccharide (LPS)-induced inflammation model in wild-type mice and bioluminescent and fluorescent labelling of EVs, we observed that inflammation extends the plasma half-life of EVs by over 600-fold within 2 hours and 900-fold at 24 hours post-administration, leading to significant enrichment in inflamed organs, particularly the liver and spleen. Enhanced accumulation in specific tissues translated to increased targeting of immune- and epithelial cells within those organs, with notable uptake by hepatocytes in the liver. This prolonged half-life was attributed to the altered EV protein corona in inflamed tissues, which facilitates cellular association. These findings underscore the complex dynamics between EVs and immune cells under inflammatory conditions and provide critical insights for advancing EV-based therapies in chronic inflammatory diseases.

bioengineering↗

KODAMA enables self-guided weakly supervised learning in spatial transcriptomics

Spatial transcriptomics provides researchers with a powerful tool to investigate gene expression patterns within their native positional context in tissues, revealing intricate cellular relationships. However, analyzing spatial transcriptomics data presents unique challenges due to their high dimensionality and complexity. Several competitive tools have emerged, each aiming to integrate spatial dependencies into their workflow. Yet, the overall performance of these approaches remains constrained by limitations in prediction accuracy and compatibility with specific data types. Here, we introduce the third version of the KODAMA algorithm, specifically tailored for spatial transcriptomics analysis. This upgraded version incorporates a novel approach that effectively reduces data dimensionality while preserving spatial information. At its core, the KODAMA algorithm employs parallel iterations that enforce spatial constraints throughout an embedded clustering process. Our method provides the flexibility to simultaneously analyze multiple samples, streamlining analysis workflows. Additionally, it extends beyond traditional 2D analysis to accommodate multidimensional datasets, including 3D spatial information. KODAMA seamlessly integrates into various pipelines, such as Seurat and Giotto. Extensive evaluations of KODAMA on 10x Visium, Visium HD, and image-based 3D datasets demonstrate its high accuracy in spatial domain prediction. Comparative analyses against alternative dimensionality reduction techniques and spatial analysis tools consistently validate and highlight KODAMAs superior performance in unraveling the spatial organization of cellular components across both single and integrated tissue samples.

bioinformatics↗

Differential expression of mitochondria-associated genes in clinical samples of Plasmodium falciparum showing severe manifestations

The malaria parasite mitochondrial proteins are critical targets for antimalarial drugs, however, the emergence of drug resistance against the existing protein targets necessitates novel therapeutic approaches. In this study,we profiled mitochondrial sense and natural antisense transcripts (NATs) in 22 Plasmodium falciparum clinical isolates, classified into three disease groups - uncomplicated malaria (UNC, n=6), cerebral malaria (CM, n=4), and hepatic dysfunction (HD, n=12), using a custom, strand-aware 60K microarray, and validated the transcriptome using pooled, strand-specific RNA-seq (uncomplicated pool and complicated pool). Differential gene expression in the CM and HD cohort was obtained by comparing with uncomplicated malaria (UNC) as the control cohort. The analysis revealed distinct disease-specific sense and NATs, encoded by the mitochondrial genome, along with those encoded in the nucleus and targeted to the parasite mitochondria. Although mitochondrial activity is known to be reduced in blood-stage malaria, upregulation of genes linked to tricarboxylic-acid-cycle and electron-transport in the CM cluster indicates disrupted mitochondrial bioenergetics in severe disease. Profiling of sense and antisense mitochondrial transcripts reveal a correlated expression of sense-antisense transcript pairs in both the disease manifestations, indicating a potential regulatory role of NATs in mitochondrial function. These data provide direct evidence of NATs originating from the parasite mitochondrial genome and nominate key NATs against core mitochondrial functions as potential non-conventional antimalarial targets.

genomics↗

COP9 signalosome and PRMT5 methylosome complexes are essential regulators of Lis1-dynein based transport

Cytoplasmic dynein is a minus-end directed microtubule motor essential for retrograde transport in cells. Dynein is tightly regulated by Lis1 where it is reported to stall dynein movement as well as promote formation of active dynein in different model systems. However, the mechanism behind these contrasting functions of Lis1 in regulating dynein is unknown. Here, we identified COP9 Signalosome (CSN) and PRMT5 complexes as critical regulators of Lis1 dependent dynein function. We demonstrated that Lis1 recruits CSN on dynein to facilitate its deneddylation. We show that neddylation of dynein (DIC1 at K42 residue) is essential for assembly of an active dynein complex and subsequent transport of cargoes in cells. Conversely, PRMT5 is recruited to the Lis1-dynein complex where it methylates Lis1. Methylation of Lis1 at R238 position alters its interaction dynamics, leading to dislodging of CSN from dynein resulting in dynein neddylation and activation. In conclusion, we unravel an interplay between CSN, and PRMT5 that provides a sophisticated regulatory mechanism for Lis1s opposing modes of regulating the dynamics of dynein.

cell biology↗

Soleus H-reflex size versus stimulation rate in the presence of background muscle activity: A methodological study

IntroductionHoffmann reflex (HR) operant conditioning has emerged as an important intervention in neurorehabilitation. During conditioning, the HR is elicited at low rates ([~]0.2 Hz) to avoid the initial reduction in HR size that can occur over repeated stimulation, i.e., rate-dependent depression (RDD), thereby maintaining reflex size. This study investigated the impact of higher stimulation rates on HR size, where a stable, low-level, background electromyographic (EMG) signal is maintained over 225 conditioning trials in each of 30 sessions. A higher rate could shorten session length and/or number. MethodsFifteen healthy participants maintained low background soleus EMG (5-18 {micro}V, [~]1-3% of the maximum stimulation evoked direct muscle (M-wave) EMG response (Mmax) while standing. Soleus HR and M-wave recruitment curves were obtained at rates of 0.2, 1, and 2 Hz, from which Mmax and Hmax were calculated. Seventy-five HR trials (HRT) were collected for each stimulation rate at a target M-wave size ([~]10-20% of Mmax). ResultsThere was no evidence of RDD at higher stimulation rates. In addition, the mean HR over trials was reliable across participants and rates. The Intraclass Correlation Coefficient (ICC) was 0.965 (95%CI:0.915, 0.987). DiscussionThis study shows that H-reflex conditioning might be performed at rates up to 2 Hz with no RDD and with consistent HR values. A faster rate could increase the number of conditioning trials per session, reduce session duration, and/or reduce the number of sessions. It could thereby accelerate the conditioning process and make the process less demanding for participants. SupportNIH Grant P41 EB018783 (Wolpaw), NYS Spinal Cord Injury Research Board C37714GG (Gupta) and C38338GG (Wolpaw), VA SPiRE NCT05880251(Brangaccio), Stratton Veterans Affairs Medical Center.

neuroscience↗

AmpC β-lactamases: A Key to Antibiotic Resistance in ESKAPE Pathogens

AmpC {beta}-lactamases (blaAmpC) are one of the important drivers for a high incidence of antimicrobial resistance (AMR) within ESKAPE pathogens, which are a group of bacteria that are the leading cause of hospital-acquired infections. Investigating the presence and characteristics of the blaAmpC is essential for understanding the molecular mechanism of resistance and developing effective strategies to combat AMR. We have investigated the presence of blaAmpC, distribution on plasmids/chromosomes, copy number, amino acid identities/variabilities, and evolutionary characteristics in ESKAPE pathogens. Our analysis indicates 1790 AmpC enzymes in 4713 completely assembled genomes, subdivided into nine different enzyme groups. AmpC is more common in A. baumannii, followed by P. aeruginosa, K. pneumoniae, and Enterobacter spp., but absent in E. faecium and S. aureus. Among the nine AmpC enzyme groups, ACC, ACT, CMH, and MIR are exclusively found in Enterobacter spp., while the largest enzyme group ADC is only present in A. baumannii; PDC and PIB are found only in P. aeruginosa. Phylogenetic analysis revealed significant divergence amongst few enzyme groups and closer evolutionary relationships within others. Functional motif analysis identified conserved catalytic residues across all enzyme groups, except PIB, which demonstrates structural and functional divergence. Because of these variations, PIBs ability to bind cephalosporins decreases while enhancing its activity against carbapenems, hence, we have excluded PIB from further analysis. This is the first detailed report on AmpC in ESKAPE pathogens, which also re-emphasizes the wise use of antibiotics to reduce the rise of AmpC cephalosporins resistance, a significant public health concern. HighlightsO_LIFirst detailed report on ESKAPE blaAmpC localization in chromosomes and plasmids C_LIO_LIblaAmpC is absent in E. faecium & S. aureus but prevalent in other four pathogens C_LIO_LIMost blaAmpC belong to ADC, exclusively present in A. baumannii chromosomes C_LIO_LIInterspecies gene exchange in K. pneumoniae, P. aeruginosa & Enterobacter spp. C_LIO_LIEvolutionary analysis shows recent divergence & possible horizontal gene transfer C_LI

bioinformatics↗

Targeted BDNF upregulation via upstream open reading frame disruption

To understand the relative contributions of 5' UTR elements to translation, we performed a comprehensive analysis of upstream open reading frames (uORFs) across a representative 5' UTR. We selected the neurotrophin BDNF (Brain derived neurotrophic factor) as an exemplar as upregulation of this protein is a potential therapeutic approach for a plethora of neurodevelopmental, neurodegenerative, and neuropsychiatric disorder indications. Predicted uORFs were identified in 14 out of 17 BDNF RefSeq transcript isoforms, and experimentally confirmed to be exerting translation repression effects for five of these transcripts. These findings suggest that uORF elements play an important role in shaping the protein output from this locus. We explored several approaches to disrupt BDNF uORF function. Deletion of a 5' UTR exon in BDNF v11 (containing eight predicted uORFs), in order to simulate an exon skipping outcome, resulted in pronounced upregulation in a reporter construct system. This effect was found to be partially uORF-dependent, but was also dependent on the disruption of an RNA secondary structure element. However, this transcript variant was found to not be expressed in human brain. Conversely, direct disruption of a single uORF start codon in the widely expressed BDNF v4 transcript variant using an adenine base editing approach resulted in a [~]1.8-fold upregulation of endogenous BDNF protein expression in cell culture. This study describes novel BDNF regulatory mechanisms, and potential uORF-targeted modalities for therapeutic gene activation.

molecular biology↗

Robust Prediction of Patient-Specific Cancer Hallmarks Using Neural Multi-Task Learning: a model development and validation study

BackgroundAccurate quantification of cancer hallmark activity is essential for understanding tumor progression, tailoring treatments, and improving patient outcomes. Traditional methods, such as histopathological grading and immunohistochemistry for protein expression, often overlook the complex interplay between cancer cells and the tumor microenvironment and provide limited insight into hallmark-specific mechanisms. We aimed to develop OncoMark, a high-throughput deep learning-enabled neural multi-task learning framework capable of systematically quantifying integrative hallmarks activities using transcriptomics data from routine tumor biopsies. MethodsIn this study, we acquired single-cell transcriptomics data from 941 tumor samples across 14 tissue types, comprising nearly 3.1 million cells from 56 studies conducted worldwide, to form a large multicenter dataset. Our model employs a supervised neural multi-task learning method designed to predict multiple cancer hallmarks present in the biopsy samples simultaneously. The OncoMark model was developed and tested on 90% of the studies (patients from 51 studies) using repeated five-fold cross-validation performed twice. For further evaluation, the model was assessed on the remaining 10% of the studies (patients from 5 studies) that were excluded from the initial training and testing dataset. Additionally, we included patients from publicly available datasets, including TCGA, GTEx, ANTE, MET500, POG570, CCLE, TARGET, and PCAWG to validate the models performance. The primary objective was to evaluate the performance of the model in identifying cancer hallmarks in cancer datasets and ensure no hallmark predictions were made in normal samples across the four prespecified groups: (i) internal test set, (ii) external test set, (iii) normal samples (real-world), and (iv) cancer samples (real-world). FindingsOncoMark demonstrated exceptional performance in predicting cancer hallmark states, achieving near-perfect accuracy across internal test data and five external test datasets. Internal testing consistently showed accuracy, precision, recall, and F1 scores exceeding 99%, underscoring the models reliability across hallmarks. External test further confirmed these findings, with accuracy, precision, recall, F1 scores, and balanced accuracy consistently exceeding 96{middle dot}6%, and multiple datasets achieving perfect scores, highlighting the models exceptional generalizability and robustness. Specificity tests using GTEx and ANTE datasets accurately classified normal tissues, while sensitivity analysis on TCGA, MET500, CCLE, TARGET, PCAWG, and POG570 datasets effectively identified cancer hallmarks. InterpretationWe developed an AI-based framework that enables accurate, efficient, and cost-effective quantification of cancer hallmark activity directly from transcriptomics data. The framework demonstrated significant potential as an assistive tool for guiding personalized treatment strategies and advancing the clinical management of cancer patients. FundingAshoka University, S.N. Bose National Centre for Basic Sciences, Mphasis F1 Foundation, DST SERB Core Research Grant. Research in ContextO_ST_ABSEvidence before this studyC_ST_ABSWe conducted an extensive literature search using Google Scholar and PubMed without language restrictions, employing search terms such as "(Predicting OR Classifying OR Annotating) and (cancer hallmarks) AND (Deep OR Machine Learning) OR (Artificial Intelligence OR AI)." While there have been advancements in molecular oncology and computational methodologies over the two decades since the concept of cancer hallmarks was first introduced, a comprehensive machine learning or deep learning framework to annotate all cancer hallmarks simultaneously from tumor biopsy samples remains to be developed. Additionally, the scarcity of hallmark-annotated datasets has posed a significant challenge, hindering the development of robust predictive models. Added value of this studyThis study introduces OncoMark, a novel high-throughput neural multi-task learning (N-MTL) framework designed to predict all cancer hallmark activities simultaneously from biopsy samples. OncoMark addresses the lack of annotated hallmark-specific data by generating synthetic biopsy (pseudo-bulk) datasets annotated with hallmark activity, meticulously modeled to reflect real-world tumor biology while maintaining clinical relevance. The framework employs a multi-task learning approach to capture interdependencies among hallmarks, advancing beyond isolated predictions to offer a holistic view of tumor biology. Validation on five independent datasets comprising 95 patient samples demonstrated its generalizability and reproducibility. Further external validation using eight datasets, encompassing over 11,679 cancer and 8348 normal patient samples, reinforced its robustness. To promote clinical integration, a user-friendly web-based tool was developed, enabling seamless access for oncologists and researchers. Implications of all the available evidenceThe OncoMark framework represents a transformative advancement in cancer diagnostics and treatment planning. By enabling accurate and reproducible prediction of all hallmark activities simultaneously from biopsy samples, this model paves the way for precision oncology at scale. Its ability to systematically capture hallmark interdependencies provides deeper insights into tumor behavior, guiding the development of individualized targeted therapies. The incorporation of a web-based interface ensures the accessibility of this innovation to clinicians worldwide, bridging the gap between computational oncology and clinical practice. Following further validation and integration into healthcare workflows, OncoMark has the potential to improve cancer outcomes by delivering timely, cost-effective, and precise tumor analyses, facilitating informed therapeutic decision-making with unparalleled precision. Cancer progression is driven by a set of well-defined biological principles--collectively termed the "hallmarks of cancer"--yet current diagnostic approaches seldom incorporate these distinct molecular features into clinical practice. Despite substantial progress in molecular oncology, traditional methods like histopathological grading and immunohistochemical assays often fail to capture the complex interplay between cancer cells and the tumor microenvironment, emphasizing the need for robust computational frameworks capable of systematically quantifying hallmark-specific activity. Here, we address this gap by developing OncoMark, a high-throughput neural multi-task learning (N-MTL) framework designed to simultaneously quantify hallmark activities in tumor biopsies using transcriptomics data. We show that OncoMark achieves near-perfect accuracy, precision, recall, and F1 scores (>99%) in cross-validation, with external validation consistently exceeding 96.6% on five independent datasets. Further evaluation on eight additional datasets--including large-scale cancer cohorts (TCGA, MET500, CCLE, TARGET, PCAWG, POG570) and normal tissue datasets (GTEx, ANTE)--demonstrated high specificity for normal samples and robust sensitivity for hallmark prediction in cancer. By delivering a comprehensive and cost-effective molecular portrait of tumor biology and providing a user-friendly web platform accessible at https://oncomark-ai.hf.space/, OncoMark has the potential to guide tailored treatment strategies and advance precision oncology. More broadly, this framework signifies a transformative step toward routine hallmark-based diagnostics, promising to improve patient outcomes by facilitating timely and precise tumor profiling.

cancer biology↗

Interparticle Crosslinked Ion-responsive Microgels for 3D and 4D (Bio)printing Applications

AbstractMicrogels offer unique advantages over bulk hydrogels due to their improved diffusion limits for oxygen and nutrients. Particularly, stimuli-responsive microgels with inherently bioactive and self-supporting properties emerge as highly promising biomaterials. This study unveils the development of interparticle-crosslinked, self-supporting, ion-responsive microgels tailored for 3D and 4D (bio)printing applications. A novel strategy was proposed to develop microgels that enabled interparticle crosslinking, eliminating the need for filler hydrogels and preserving essential microscale void spaces to support cell migration and vascularization. Additionally, these microgels possessed unique, ion-responsive shrinking behavior primarily by the Hofmeister effect, reversible upon the removal of the stimulus. Two types of microgels, spherical ({micro}S) and random-shaped ({micro}R), were fabricated, with {micro}R exhibiting superior mechanical properties and higher packing density. Fabricated microgel-based constructs supported angiogenesis with tunable vessel size based on interstitial void spaces while demonstrating excellent shear-thinning and self-healing properties and high print fidelity. Various bioprinting techniques were employed and validated using these microgels, including extrusion-based, embedded, intraembedded, and aspiration-assisted bioprinting, facilitating the biofabrication of scalable constructs. Multi-material 4D printing was achieved by combining ion-responsive microgels with non-responsive microgels, enabling programmable shape transformations upon exposure to ionic solutions. Utilizing 4D printing, complex, dynamic structures were generated such as coiling filaments, grippers, and folding sheets, providing a foundation for the development of advanced tissue models and devices for regenerative medicine and soft robotics, respectively.

bioengineering↗

Comprehensive Enumeration of Cancer Stem-like Cell Heterogeneity Using Deep Neural Network

Cancer stem cells (CSCs), a distinct subpopulation within tumors, are pivotal in driving treatment resistance and tumor recurrence, posing substantial challenges to conventional therapeutic strategies. Precise quantification and profiling of these cells are essential for improving cancer treatment outcomes. We present ACSCeND, an advanced deep neural network model accompanied by a robust workflow, specifically developed to quantify cellular compositions from bulk RNA-seq data, enabling accurate CSC profiling. By integrating bulk RNA-seq data with insights derived from single-cell RNA-seq datasets, ACSCeND effectively captures the diversity and hierarchical organization of tumor-resident cell states, alongside cell-specific gene expression profiles (GEPs). Compared to current tissue deconvolution models, ACSCeND exhibits superior performance, achieving significantly higher Concordance Correlation Coefficient (CCC) values and lower Root Mean Square Error (RMSE) across various pseudobulk and real-world bulk tissue samples. Application of ACSCeND to TCGA and PRECOG datasets reveals a strong association between CSC abundance and poorer disease-free survival outcomes, underscoring the clinical relevance of CSCs in cancer progression. Furthermore, cell-specific GEPs for distinct CSC states unveil novel molecular signatures and illuminate the origins of CSC-driven tumor heterogeneity. In summary, ACSCeND provides a powerful, scalable platform for high-throughput quantification of cellular compositions and distinct potency states within normal tissues as well as highly heterogeneous tissues, such as tumors.

genomics↗

Targeted DNA ADP-ribosylation triggers templated repair in bacteria and base mutagenesis in eukaryotes

Base editors create precise genomic edits by directing nucleobase deamination or removal without inducing double-stranded DNA breaks. However, a vast chemical space of other DNA modifications remains to be explored for genome editing. Here, we harness the bacterial anti-phage toxin DarT2 to append ADP-ribosyl moieties to DNA, unlocking distinct editing outcomes in bacteria versus eukaryotes. Fusing an attenuated DarT2 to a Cas9 nickase, we program site-specific ADP-ribosylation of thymines within a target DNA sequence. In tested bacteria, targeting drives efficient homologous recombination in tested bacteria, offering flexible and scar-free genome editing without base replacement nor counterselection. In tested eukaryotes including yeast, plants and human cells, targeting drives substitution of the modified thymine to adenine or a mixture of adenine and cytosine with limited insertions or deletions, offering edits inaccessible to current base editors. Altogether, our approach, called append editing, leverages the addition of a chemical moiety to DNA to expand current modalities for precision gene editing.

synthetic biology↗

A resource for extracellular vesicles from activated CD4 T cells that relay pro-inflammatory signals

CD4 T helper cells (TH cells) play a vital role in coordinating and amplifying the immune response to specific pathogens. They constitutively produce different kinds of extracellular vesicles (EVs), which mediate cell-to cell communication and play diverse roles in immune regulation and inflammatory processes. Here we provide a resource documenting the composition of activated TH cell EVs and demonstrating their ability to instigate pro-inflammatory response in antigen-presenting cells (APCs). EVs were characterized by lipidomics, proteomics, and NanoFCM. The activated TH cells derived EVs (act-EVs) were found to be enriched in TH cell-specific proteins, transmembrane and cytosolic EV marker proteins, and HLA proteins relative to resting CD4 T cells EVs (rest-EVs). The pro-inflammatory effect of act-EVs vs rest-EVs on donor matched APCs were characterized by chemokine and cytokine profiling and flow cytometry analysis. There was no discernible contrast in endotoxin levels between act-EVs and rest-EVs. Functional distinctions were seen to arise from variations in the content and composition of these EVs. Moreover, we validated our findings with an in-vivo investigation in mice, demonstrating the recruitment of monocytes, dendritic cells (DCs), neutrophils, and NK cells in the spleen, accompanied by the release of pro-inflammatory cytokines in the serum after administering act-EVs. In summary, this study sheds light on the role of TH cell released EVs in modulating the immune response during pro-inflammatory responses and this resource provides a foundation for development of novel therapeutics on EV based scaffolds.

immunology↗

RNA binding protein Musashi1 interacts with the viral genomic RNA and restricts SARS-CoV-2 infection by repressing translation

Musashi RNA binding proteins are important post-transcriptional regulators of stem cell homeostasis and are known to be involved in viral infections. However, their role in SARS-CoV-2 infection remains largely unknown. Using computational studies, in vivo RNA immunoprecipitation and biochemical assays, here, we establish that Musashi1 (Msi1) interacts with viral genomic RNA through direct binding to the SARS-CoV-2 3UTR. Importantly, binding of Msi1 to the viral 3UTR results in translational repression mediated by inhibition of Poly (A) binding protein (PABP). Conversely, Msi1 knockout promotes robust viral replication and increased viral protein expression. Using 2D cell cultures, stem cells and 3D organoids, we show that depletion of Msi1 in intestinal cells augments infection. This finding explains why the human intestine serves as a reservoir for the SARS-CoV-2 virus, wherein differentiated enterocytes, which have negligible levels of Msi1, are highly affected. Contrarily, stem cells which are enriched for Msi1 expression, are known to be less permissive to SARS-CoV-2 infection despite expressing the entry receptors. Our findings show how translation repression of SARS-CoV-2 by stem cell RNA binding proteins such as Msi1 could help evasion of infection.

cell biology↗

Effect of high-intensity anaerobic exercise on electrocortical activity in athletes and non-athletes

AimThe present study aims to verify the information processing in athletes through electroencephalography, analyze cortical areas responsible for cognitive functions related to attentional processing of visual stimuli, and investigate motor activitys influence on cognitive aspects. Material and MethodsThe sample consisted of 29 subjects, divided into an experimental group (n = 13 modern pentathlon athletes) and a control group (n = 16 non-athletes). We collected the electrocortical activity before and after the Wingate Anaerobic Test. During the electrophysiological measures, the volunteers performed a saccadic eye movement paradigm. They also performed cognitive tasks, resting heart rate, and anthropometric measurements. ResultsA mixed ANOVA was applied to analyze the statistical differences between groups (athletes and control) and moments (before and after exercise) for F3, F4, P3, and P4 electrodes during rest one and task (pre-stimulus GO). There was an interaction for the group vs. moment factors in F3 [F = 17,129; p = 0,000; {eta}{superscript 2} = 0.512], F4 [F = 22,774; p = 0,000; {eta}{superscript 2} = 0.510], P3 [F = 11,429; p = 0,001; {eta}{superscript 2} = 0.405], and P4 electrodes [F = 18,651; p = 0,000; {eta}{superscript 2} = 0.379]. We found the main effect for group factors in the frontal and parietal electrodes of the right hemisphere (F4 and P4) and a main effect of the moment factor on the frontal (F3 and F4) and parietal (P3 and P4) electrodes. There was an interaction between the group vs. moment factors for the reaction time. The groups were different in Peak Power (Watts/kg), Average Power (Watts/kg), Fatigue Index (%), and Maximum Power (ms). ConclusionsWe identified chronic effects of exercise training on the cortical activity of modern pentathlon athletes, read-through differences in absolute alpha power, and acute effects of a high-intensity exercise session for athletes and non-athletes for electrocortical and behavioral responses.

neuroscience↗

To integrate or not to integrate: Testing degenerate strategies for solving an accumulation of perceptual evidence decision-making task

A common approach in the study of cognition is to train subjects to perform a task that requires a particular cognitive process to solve. Analysis of the subjects response behavior while they perform these tasks can offer valuable insight into the underlying mechanisms that give rise to cognition. However, if subjects are able to accurately perform such a task by using a strategy that doesnt involve the targeted cognitive process, data from those experiments becomes more difficult to interpret. A number of perceptual decision-making tasks have been designed to study the accumulation of evidence, i.e. how noisy information presented over time is used to form a decision. Recent work, however, has highlighted how a variety of non-integration strategies can by some measures yield strikingly near-optimal performance on such tasks, raising the possibility that past conclusions from these experiments may be incorrect. Here we assemble the largest data set of animals performing one such task - the "Poisson Clicks" task - which is optimally solved by the gradual integration of pulsatile auditory noise. To investigate whether rats are in fact using this strategy, we compiled data from 515 rats performing over 35 million trials. We compare performance of 3 degenerate strategies (that circumvent the need to integrate evidence) to the optimal (integration) strategy. We demonstrate that the pulsatile nature of the stimuli used in the Poisson Clicks Task makes it possible to distinguish which strategy subjects use. Overwhelmingly, we find the rats are using an integration strategy when performing the Poisson Clicks Task.

animal behavior and cognition↗

Attention and working memory investigated through the P300 component in children practicing Karate at different stages of biological maturation

AimTo investigate attention and working memory, comparing children practice Karate and non-Karate practitioners at different stages of biological maturation through the amplitude and latency of the P300 component during the execution of a Go/No-Go paradigm. Material and MethodsThe P300 was analyzed for Fz, Cz, and Pz electrodes in 80 participants separated in two groups: an Karate practitioners group comprising Karate practitioners and comprising non-Karate practitioners. Each group was further subdivided according to the biological maturation range defined by Peak Height Velocity. In addition, the participants performed a Go/No-Go paradigm to measure amplitude and latency. ResultsThe EEG analysis showed Ffr electrodes Pz and Cz, an interaction was found between group and Peak Height Velocity for the amplitude variable (respectively: F = 45.858; d = 0.38; p < 0.001 / F = 10.411; d = 0.17; p = 0.004). For the Fz electrode, a main effect was found between group and Peak Height Velocity (respectively: F = 40.330; d = 0.34; p = 0.010 / F = 36.730; d = 0.30; p = 0.012) for the variable amplitude and latency. main effect between group and Peak Height Velocity (respectively: F = 7.719; d = 0.14; p = 0.012 / F = 38.370; d = 0.31; p = 0.010). ConclusionsIn general, it is possible to conclude that participants in the Karate practitioners group exhibited electrocortical measures corresponding to greater efficiency in decision-making and attention processes, motor planning, working memory, attention allocation, motor execution, and greater attentional engagement. It was also demonstrated that, despite the children being at very close chronological ages, their biological maturation differed.

neuroscience↗