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Biology subjects

Cheng, D.

Publications and source records attributed to Cheng, D..

At least 19 recordsLinked to original sources

Multiscale mapping of venous remodelling in idiopathic pulmonary fibrosis

The integrity of the pulmonary vasculature is a key determinant of lung health, yet challenges in visualisation and quantification have hindered interrogation of its pathophysiological role in chronic lung disease. Here, we align recent advances in microscale image acquisition with novel computer vision-based vessel segmentation models to demonstrate expansion of the bronchial and pulmonary veins across varying severities of tissue remodelling in idiopathic pulmonary fibrosis (IPF). Relating these imaging findings to molecular data in control, mild, and severe fibrosis, we show that bronchial venous endothelial cells expand beyond their physiological peribronchial niche even in mild disease, acquiring persistent angiogenic, inflammatory, and matrix-remodelling programmes that define a specialised fibrovascular-immune interface. Finally, we relate these microscale and molecular observations to clinical CT imaging, demonstrating that intrapulmonary vein enlargement independently associates with worsened survival across three IPF cohorts. Collectively, our multimodal, multiscale approach connects previously unresolved three-dimensional venous architecture to its molecular endothelial correlate, establishing venous enlargement as a prognostically significant and clinically relevant feature of IPF. Our analytical approach also demonstrates how biological discoveries made in intact ex vivo human organs can translate into measurable phenotypes in living patients, providing a template for other organs and diseases.

pathology↗

Differential Sensitivity of HSV-1 and PRV to IFN-{lambda} Reveals a Neuron-Specific Antiviral Role for RSAD2

Alpha herpesviruses (-HV) initially infect mucosal epithelial cells and subsequently establish lifelong latency in the peripheral nervous system (PNS). Herpes simplex virus-1 (HSV-1), a human pathogen persisting in the majority of the adult population, shares neuroinvasive properties with Pseudorabies virus (PRV), a swine -HV, commonly used as a model -HV. Utilizing primary peripheral neuronal cultures, we previously showed that IFN-{lambda} pre-treatment significantly reduced PRV yield. In this paper, we further characterized the early and late neuronal responses to IFN-{lambda} by RNA-seq, and the antiviral potential of this response against HSV-1. Notably, HSV-1 exhibited neuron-specific resistance to IFN-{lambda} mediated antiviral responses both in murine primary neurons and human neuronal cells. An ICP34.5-deficient HSV-1 ({Delta}34.5) mutant showed IFN-{lambda} sensitivity in neurons, while replicating normally in untreated neurons showing that ICP34.5 is responsible for the neuron specific IFN-{lambda} resistance of HSV-1. Our results further demonstrate that RSAD2 is strongly induced by IFN-{lambda} in neurons, localizing to ER-associated membranes, and effectively restricting -HV protein synthesis in the absence of ICP34.5. siRNA-mediated RSAD2 knockdown in IFN-{lambda}-primed primary neurons largely restored replication of {Delta}34.5 HSV-1, highlighting the role of this IFN-{lambda} induced host factor in neuronal infections. Together, neuronal IFN-{lambda}-induced RSAD2 and HSV-1 ICP34.5 define a neuron-specific antagonistic mechanism that collectively determines the replication efficiency of HSV-1 in the PNS.

microbiology↗

STARMAP: A 3D-informed framework for mapping functional regions in proteins to regulatory and cellular phenotypes

Artificial Intelligence (AI) has transformed biology by revealing patterns in large-scale datasets and predicting regulatory relationships. Yet even the most advanced models often fail to identify biologically meaningful mechanisms from statistical associations. This limitation arises not from algorithmic capacity but from the lack of mechanistically grounded input features. Our structure-informed framework Structure-based Topological Analysis of Regulatory and Molecular Activity Patterns (STARMAP) embeds protein three-dimensional structure and population-scale functional genomics data into a unified representation for mechanistic inference. By mapping over 1.5 million naturally occurring variants across [~]1,700 cancer cell lines onto protein structures, STARMAP was able to identify spatial clusters of variation associated with shifts in transcriptional regulatory networks and drug response phenotypes. This approach transforms natural genetic variation into a large-scale, structure-informed screen, enabling systematic discovery of regulatory relationships across the proteome and providing interpretable and testable models of cellular regulation.

genomics↗

REST-AKT-SOX2 axis controls neuronal lineage state and Midkine-mediated communication in SHH-medulloblastoma.

Stem/progenitor-like cells are known drivers of tumor progression, chemoresistance, and relapse in Sonic-Hedgehog medulloblastoma (SHH-MB), yet the regulatory mechanisms that sustain these resilient cellular states remain incompletely defined. Here, we identify the RE1-silencing transcription factor (REST) as a key transcriptional regulator that preserves the progenitor compartment in SHH-MB through stabilization of the stemness factor SOX2. Mechanistically, REST activates AKT signaling, which in turn enhances SOX2 protein stability, revealing a REST-AKT-SOX2 axis that supports stem/progenitor identity and ongoing tumor maintenance. Beyond maintaining intrinsic stem-like programs, REST also orchestrates the extrinsic communication network of SHH-MB tumors. Single cell transcriptomic profiling and ligand-receptor interaction mapping highlight Midkine (MDK)-mediated signaling as one of the most upregulated intercellular communication routes in MB. We demonstrate that REST drives this signaling cascade through its control of SOX2. Perturbation of REST or SOX2 results in reduced MDK and its receptor, SDC2 expression, and chromatin immunoprecipitation assays show that SOX2 directly binds and regulates MDK/SDC2 expression, establishing and reinforcing a REST/SOX2 centered transcriptional mechanism that coordinates both progenitor maintenance and cell-cell communication in the malignant compartment. Together, these findings position REST as an integrator of intrinsic progenitor cell programs and extrinsic MDK-mediated signaling in SHH-MB. By linking stemness, communication and potential for therapeutic resistance, the REST-AKT-SOX2-MDK signaling axis emerges as a targetable vulnerability to suppress stem/progenitor driven tumor program in REST-driven SHH-MBs.

cancer biology↗

Syndecan is critical for Drosophila CNS and PNS glia function

Glia are irreplaceable components for the nervous system development and function. However, the cellular mechanisms each glial layer utilizes to communicate with each other and the extracellular environment is not well characterized. Here, we investigated the role of a heparan-sulfate proteoglycan, Syndecan (Sdc), in regulating glial cell function and development in the Drosophila nervous system. Sdc is expressed throughout multiple glial layers and loss of Sdc in all glia resulted in disruption of both central and peripheral glia. Within the CNS loss of Sdc in all glia lead to reduced brain lobes and disruption of neuroblast proliferation. In the PNS, loss of Sdc in different glial layers resulted in impaired ensheathment in wrapping glia and abnormal septate junction morphology in subperineurial glia. We focused on the outer layer of perineurial glia and found ensheathment defects and a reduction in glial numbers with Sdc loss. These phenotypes mirror those previously observed with the loss of integrins and a mutation in the integrin {beta}-subunit enhanced the phenotypes observed with loss of Sdc within the perineurial. Thus, our results indicate Sdc has multiple roles in Drosophila nervous system development including as an integral component in regulating glial cell morphology, maintaining neuroblast populations within the optic lobe and in mediating glial-ECM interactions.

neuroscience↗

Systematic mapping of emergent transcriptional states in interacting single-cell dyads by Cell-Cell-seq

Cell-cell interactions drive rapid and heterogeneous changes in gene expression, yet most transcriptomic methods either dissociate cells, losing pair identity and interaction timing, or infer communication indirectly from ligand-receptor co-expression. Here we present Cell-Cell-seq, a scalable workflow for profiling defined cell pairs ("dyads") with single-cell transcriptomic resolution. Cell-Cell-seq uses cavity-containing hydrogel microparticles (Nanovials) to confine two cells, synchronize contact onset, protect fragile conjugates during handling and sorting, and interface directly with droplet-based RNA sequencing. Using antigen-matched prostate tumor cells and engineered T cells as a model system, Cell-Cell-seq captured thousands of tumor-T cell dyads and revealed broad functional and transcriptional heterogeneity across interactions. Dyads unmasked transient activation programs that were obscured in standard well-plate co-culture, consistent with asynchronous contact in bulk assays. To distinguish interaction-induced programs from the composite nature of dyad transcriptomes, we developed a pseudo-mixing framework that generates in silico pseudo-dyads to construct an empirical null distribution under "no interaction," enabling statistically robust identification of emergent genes and partner-resolved attribution of responses. Dyad-resolved analysis further revealed coordinated cross-cell programs, including coupled chemokine expression consistent with bidirectional paracrine signaling and inverse coupling between tumor immunoregulatory programs and T cell activation. Finally, we introduce ccRepair to correct compositional dilution in mixed transcriptomes, improving interpretability while preserving genuine cross-cell coordination. Together, Cell-Cell-seq provides a generalizable platform for dissecting immune synapse biology and mapping interaction-dependent programs across heterogeneous cell populations, with applications in profiling tumor-immune communication and functionally screening immunotherapies.

bioengineering↗

Characterize Oral-to-Blood Microbial DNA Translocation in Individuals with Cocaine Use Disorder

BackgroundCocaine disrupts gut barriers in animal models, potentially enabling microbial translocation and inflammation in the periphery and central nervous system (CNS), but its direct role in inducing inflammation remains controversial. This study aimed to determine if the oral cavity is a source of circulating microbial DNA translocation in individuals with current cocaine use disorder (CUD). ResultsA cross-sectional case-control study was conducted, comparing CUD and demographically matched non-drug controls. Ten CUD (via smoking or vaping) and 24 controls provided paired saliva and blood samples. Microbial 16S rRNA V4 region was sequenced in isolated microbial DNA from saliva and plasma. Single-cell RNA sequencing (scRNAseq) was analyzed in human peripheral blood mononuclear cells. Saliva from CUD, but not plasma, exhibited reduced alpha diversity and altered beta diversity, characterized by enriched Streptococcus and depleted Fusobacterium, Neisseria, and other taxa relative to controls. Controls exhibited low to undetectable microbial translocation in plasma. By contrast, plasma displayed CUD-specific oral enrichment of several Streptococcal species and evidence of translocation into the bloodstream. S. parasanguinis, but not cocaine alone, induced IL-1{beta} and TNF- production in human primary monocytes in vitro. scRNAseq further revealed innate immune activation, impaired T cell function, and heightened susceptibility to infection in CUD. ConclusionsThis pilot study demonstrating that CUD via smoking or snorting exhibited oral microbial dysbiosis and selective oral-to-blood microbial translocation in vivo. These findings suggest that a compromised oral-to-blood barrier, rather than cocaine itself, promotes immune perturbations in CUD.

microbiology↗

MDFIC2 is a sensory neuron-specific PIEZO channel auxiliary subunit

PIEZO channels are critical for sensory mechanotransduction. While MyoD-family inhibitor proteins were identified as PIEZO1 auxiliary subunits, their broader regulatory roles, particularly in sensory cells, remained unclear. Here we demonstrate native MDFIC and MDFI regulate endogenous PIEZO channel currents in various non-sensory cell types. However, neither MDFIC nor MDFI are expressed in primary sensory neurons. In these cell types we identified an uncharacterised member of this family, Mdfic2/Gm765, that shares the ability to physically bind to PIEZO1 and PIEZO2. MDFIC2 is selectively expressed in subsets of mechanosensitive neurons, including dorsal root ganglia, trigeminal ganglia, and vagal sensory neurons. Like its paralogues, MDFIC2 alters PIEZO1/2 mechanosensitivity and inactivation kinetics, converting them into high-threshold slowly inactivating mechanoreceptors. Extensive cryo-EM reveals a conserved binding pocket for these auxiliary subunits in the pore modules of both PIEZO1 and PIEZO2 mediated by the post-translationally modified distal C-termini of MyoD-family inhibitor proteins. This provides a comprehensive structural and functional characterisation of MyoD-family inhibitor proteins as PIEZO1/2 channel regulators and offers new insights into sensory physiology and mechanical pain mechanisms.

biophysics↗

From short-lived to persistent: The significance of extracellular RNA in disinfected drinking water microbiomes

To assure the safe distribution of drinking water, it is critical to identify adaptations that allow microorganisms to thrive in an oligotrophic system under disinfectant stress. Microbial adaptive responses are determined using RNA-based differential transcriptomics which cannot be performed in environmental settings due to lack of a baseline. This study introduces the concept of using extracellular RNA (eRNA) as a reference to determine important adaptive features in disinfected drinking water microbiome. Using this method, we determined energy efficiency, dynamic membrane composition, oxidative stress response, and proper protein folding to be extremely important for survival in drinking water systems. Additionally, multiple antibiotic resistance genes are expressed and upregulated in intracellular RNA fraction, indicating selection pressure. Non-coding RNA and transfer-messenger RNA found in eRNA suggest important regulatory functions. This study advances our understanding of eRNA in drinking water microbiomes and provides a framework for exploration in other environmental systems.

ecology↗

Psoralen Enhances Direct Cardiac Reprogramming via PPARα Activation and Promotion of Mitochondrial Fission

BACKGROUNDCell-based therapy is a promising strategy for heart repair and regeneration. However, its clinical application has been hampered by the low efficiency of cell direct reprogramming and the immature state of the inducing cells. Developing novel strategies to enhance direct reprogramming efficiency and yield mature functional cardiomyocytes remains a critical challenge. METHODSWe evaluated the effect of Psr on cardiac reprogramming using RepSox and Forskolin (RF) as the baseline cocktail. Reprogramming efficiency, cardiomyocyte marker expression, and calcium handling were assessed by RT-qPCR, immunofluorescence. Ultrastructural features were examined by transmission electron microscopy. Metabolic profiles were analyzed using Seahorse assays. Transcriptomic changes were explored by RNA sequencing, followed by pathway and protein-protein interaction analyses. A myocardial infarction (MI) mouse model was used for in vivo validation. RESULTSSupplementation with Psr (10 M) markedly enhanced the induction of induced cardiomyocytes (iCMs), leading to earlier appearance of beating clusters (day 1 vs. day 6-8), improved sarcomere organization, robust calcium transients, and higher energy metabolism. Transcriptomic profiling identified activation of the PPAR signaling pathway, with PPAR, RXRG, and UCP1 as central regulators. Mechanistically, Psr promoted mitochondrial fission, thereby facilitating metabolic remodeling essential for cardiomyocyte maturation. In vivo, RF+Psr treatment significantly improved cardiac function and reduced fibrosis after MI compared to RF alone. CONCLUSIONPsr enhances direct cardiac reprogramming by activating PPAR signaling and promoting mitochondrial fission. These findings provide a novel mechanistic framework and suggest psoralen as a promising natural enhancer for cardiac regeneration strategies. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=193 SRC="FIGDIR/small/681288v1_ufig1.gif" ALT="Figure 1"> View larger version (40K): org.highwire.dtl.DTLVardef@13a5d27org.highwire.dtl.DTLVardef@b9cce5org.highwire.dtl.DTLVardef@3afef8org.highwire.dtl.DTLVardef@1398972_HPS_FORMAT_FIGEXP M_FIG C_FIG

molecular biology↗

BRD4 regulates Aurora B kinase activity

BRD4, a pleiotropic regulator of chromatin structure and transcription, plays critical roles in cancer and immune responses. Unlike other transcriptional regulators, BRD4 largely remains bound to chromosomes during early mitosis. Here we report that BRD4 also regulates mitosis through its direct interaction with and phosphorylation of Aurora B kinase, an essential regulator of mitosis. BRD4 binding to Aurora B inhibits its kinase activity, preventing autophosphorylation and phosphorylation of the key mitotic targets histone H3 and MCAK, the mitotic centromere associated kinesin. This inhibition is relieved during metaphase when JNK is activated and phosphorylates BRD4, triggering its transient release from chromatin. Importantly, Aurora B activity during mitosis inversely correlates with BRD4 binding and directly correlates with JNK activation and BRD4 release. Our findings thus reveal a regulatory mechanism whereby Aurora B activity is directly controlled by BRD4, which in turn is regulated by JNK. Significance StatementBRD4 has been extensively characterized for its role in regulating chromatin structure and transcription. But its function during mitosis has remained unclear. This study reveals a novel mechanism by which BRD4 directly regulates mitotic progression through its interaction with and inhibition of Aurora B kinase, a central player in chromosome segregation. The timely release of BRD4 from chromatin via JNK-mediated phosphorylation enables Aurora B activation at a critical stage of mitosis. These findings uncover a previously unrecognized BRD4-Aurora B-JNK signaling axis that integrates chromatin dynamics with mitotic control, offering new insights into cell cycle regulation and potential therapeutic targets in cancer.

cell biology↗

TMEM63 proteins act as mechanically-activated cholesterol modulated lipid scramblases contributing to membrane mechano-resilience

OSCA/TMEM63 mechanosensitive ion channels play critical physiological roles in plants and animals. These channels bear structural homology to the dual functional TMEM16 family, and OSCA1.2 was recently shown to form a lipid-lined ion conduction pathway in the open state. This raised the question of whether members of the OSCA/TMEM63 family may also function as mechanically activated lipid scramblases. Using a combination of in vitro and cellular assays with computational techniques, we show that phospholipids can be translocated through the open pores of OSCA1.1/1.2/2.2 and TMEM63A/B proteins, suggesting a dual ion channel and lipid scramblase function for members of this protein family. We characterize the effects of mutating key groove lining residues demonstrating that different residues form bottlenecks for lipids and ions respectively and show that cholesterol inhibits lipid scrambling by stabilizing the closed state and slowing translocation through the open pore. We show that lipid scrambling in TMEM63 proteins can be activated by mechanical forces in the membrane, making these the first identified mechanically activated lipid scramblases. Finally, we demonstrate that this activity is important for the mechanically induced morphological remodeling of biological membranes and the resilience of cells to high mechanical forces.

biophysics↗

Computational Assessment of Circularization Impact on Saxitoxin G-quadruplex Aptamer Performance

Although high-affinity and high-specificity aptamers can be obtained by SELEX (Systematic Evolution of Ligands by Exponential Enrichment), and have good activity in vitro, their performance in vivo is poor. This is mainly because of the degradation of linear nucleic acids by nucleases in body fluids and the difficulty of maintaining stable 3D structures in complex body fluid environments, which seriously hinders the clinical application of aptamers. This makes circular aptamers, which can resist degradation and are more stable in complex body fluid environments, an attractive option. However, the cyclization process may have a considerable impact on the structure of the original linear aptamer, and blind cyclization may lead to a decrease in its affinity. Here, we developed a new method to guide the cyclization of saxitoxin (STX) aptamers based on molecular computation, and verified the activity of circular aptamers through bioactivity experiments to further verify the authenticity and reliability of our methods. Consistent with the computational analysis, although circularization disrupts the G4 structure, circular aptamer not only has a higher affinity than the linear one but also provides certain protection to mice and greatly prolongs their survival, which proves the accuracy and reliability of the circular structure designed by our computational method. Our findings provide important ideas for better guidance in the design of circular aptamers and demonstrate their great potential in therapeutic applications.

biochemistry↗

Identification of Raptor and GLI1 as USP37 substrates highlight its context-specific function in medulloblastoma cells.

USP37 gene encodes a deubiquitylase (DUB), which catalyzes the proteolytic removal of ubiquitin moieties from proteins to modulate their stability, cellular localization or activity. Its expression is downregulated in a subgroup of medulloblastomas driven by constitutive activation of sonic hedgehog (SHH) signaling. Patients with SHH-driven medulloblastomas with elevated expression of the RE1 silencing transcription factor (REST) and reduced expression of USP37 have poor outcomes. In previous studies, we showed sustained proliferation of SHH-medulloblastoma cells due to blockade of terminal cell cycle exit and neuronal differentiation stemming from a failure in USP37-dependent stabilization of its target, the cyclin-dependent kinase inhibitor (CDKI)-p27. This finding suggested a tumor suppressive function for USP37. Interestingly, the current study also uncovered Raptor, a component of the mTORC1 complex, as a novel target of USP37. Under conditions of low-USP37 expression, reduced Raptor stability and mTORC1 activity caused a decline in phosphorylation of 4E-binding protein 1 (4EBP1) and increased its interaction with eukaryotic elongation factor 4E (eIF4E), which is known to inhibit CAP-dependent translation initiation. Surprisingly, a subset of patients with SHH-driven medulloblastomas with elevated expression of USP37 and the Glioma associated Oncogene 1 (GLI1), also exhibited poor outcomes. Using genetic and biochemical analyses, we showed that USP37-mediated stabilization of GLI1, a terminal effector of SHH signaling, increases pathway activity and upregulates expression of its target oncogene products, NMYC and CCND1, to drive cell proliferation. These data indicate that USP37 elevation in SHH-driven medulloblastomas has the potential to promote non-canonical activation of SHH signaling. Overall, our findings suggest that USP37 may have context-specific oncogenic and tumor suppressive roles in medulloblastoma cells.

cancer biology↗

Enteric Viruses and Free-Living Amoebae: Protozoa as Potential Reservoirs and Transport Vessels for human Norovirus and Adenovirus

Human norovirus (HNoV) and human adenovirus (HAdV) are major causes of acute viral gastroenteritis globally and environmentally transmitted via the faecal-oral route through contaminated food and water. Recent evidence of these enteric viruses residing within environmental free-living amoebae (FLA)--specifically Vermamoeba vermiformis, Acanthamoeba polyphaga, and Willaertia magna--has significant implications for environmental virology and public health. The incorporation of HNoV into the cytoplasm and vacuoles of V. vermiformis and A. polyphaga, as well as the nuclear localization of HAdV within W. magna, was demonstrated using quantitative PCR and fluorescence microscopy. Intact HNoV and HAdV virions persisted inside FLA trophozoites, cysts, and extracellular vesicles for up to 12 days. Moreover, HAdV retained infectivity in buffalo green monkey kidney cells following intracellular persistence, suggesting these viruses can evade amoebal digestion and structural degradation. In the case of HAdV, nuclear incorporation, preservation of capsid integrity, and detection of mRNA associated with adenoviral fiber protein synthesis further suggest the possible initiation of virus-related transcriptional activity within the amoeba host. These findings challenge current assumptions about virus removal rates in sewage treatment, food safety protocols, and drinking water production. The enhanced persistence and protection conferred by FLA may also impact microbial risk assessments for recreational water use, particularly in sewage-impacted rivers and lakes. Recognition of FLA as reservoirs and transport vessels for enteric viruses necessitates a re-evaluation of existing water and sanitation guidelines to better mitigate environmental transmission pathways. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=115 SRC="FIGDIR/small/647535v1_ufig1.gif" ALT="Figure 1"> View larger version (27K): org.highwire.dtl.DTLVardef@5bff70org.highwire.dtl.DTLVardef@1df3d54org.highwire.dtl.DTLVardef@1338905org.highwire.dtl.DTLVardef@68d2f6_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗

High-throughput RNA and Single-cell RNA Sequencing to Identify Sepsis associated Molecular Mechanisms and the Blood Immune Cell Landscape

Sepsis, a leading cause of death in intensive care units (ICUs), is a complex systemic inflammatory response to infection with high morbidity and mortality. Its pathogenesis involves dysregulated inflammation, immune dysfunction, and metabolic alterations, particularly in lactate metabolism. This study employed bioinformatics analyses to explore sepsis mechanisms and identify potential therapeutic targets. We analyzed two GEO datasets and found the lactate metabolism pathway significantly enriched in sepsis patients. Seventeen key genes were identified and used to classify sepsis into two subtypes via WGCNA and consensus clustering. These subtypes exhibited distinct clinical and immune profiles. Seven hub genes (BPI, HGF, HP, LCN2, LTF, MMP8, RETN) showed differential expression between subtypes and may serve as diagnostic biomarkers. MMP8 was identified as a critical regulator in lactate metabolism, with associated miRNAs and transcription factors predicted. Single-cell analysis revealed altered immune cell compositions and interactions in sepsis patients. Our findings offer novel insights into sepsis pathogenesis and potential therapeutic strategies targeting lactate metabolism and immune regulation. Keywords: sepsis; lactate metabolism; bioinformatics; immune microenvironment

bioinformatics↗

CompBioAgent: an LLM-powered agent for single-cell RNA-seq data exploration

AO_SCPLOWBSTRACTC_SCPLOWAdvancements in high-throughput biological technologies, particularly single-cell RNA sequencing (scRNA-seq), have generated vast amounts of complex data that offer valuable insights into gene expression, cellular behavior, and disease mechanisms. However, the analysis of such data often requires specialized computational skills and expertise, which can pose a barrier to many researchers. To address this challenge, we developed CompBioAgent, a user-friendly web application designed to democratize access to bioinformatics resources, powered by Large Language Models (LLMs). By integrating with the CellDepot, CompBioAgent allows users to easily query and explore gene expression data related to various diseases, cell types, and experimental conditions. Moreover, the tool employs Cellxgene Visualization In Plugin (Cellxgene VIP) platform to generate a range of intuitive visualizations, including violin plots, UMAP embeddings, heatmaps, etc. With its natural language interface, CompBioAgent automatically converts scientific queries into structured data requests and returns the plot of interest, enabling seamless exploration of biological data without the need for programming expertise. Such integration enhances the ability of researchers to visualize complex biological insights and identify key patterns, making high-level data analysis more accessible and efficient. A demo website and a list of examples are available at https://celldepot.bxgenomics.com/compbioagent, and the source code is released at https://github.com/interactivereport/compbioagent.

bioinformatics↗

Deletion of PIEZO1 in adult cardiomyocytes accelerates cardiac aging and causes premature death

Mechanosensitive PIEZO1 channels have emerged as key transducers of mechanical forces in the cardiovascular system. In cardiomyocytes, we previously showed that PIEZO1 decodes mechanical cues driving pressure-overload induced hypertrophy. However, conflicting reports exist on the influence of PIEZO1 on baseline cardiac function. Here we show that conditional deletion of Piezo1 from cardiomyocytes in adult mice results in premature mortality. The hearts from these mice exhibited signs of accelerated aging, including elevated markers of the senescence associated secretory phenotype, with significant blunting of the normal cardiac hypertrophic response to aging, associated with a reduction in the activation of the pro-hypertrophic Ca2+/calmodulin-dependent protein kinase II (CaMKII). Functionally, aged-Piezo1 KO mice exhibited impaired cardiac relaxation due to altered cellular Ca2+ handling kinetics. Young adult Piezo1 KO mice exhibited a normal resting heart rate but developed significant progressive sinus bradycardia and cardiac fibrotic remodelling with aging, which was most prominent in the right atrium, where Piezo1 expression is highest in the healthy heart. Mechanistically, loss of PIEZO1 was associated with a marked reduction in the anti-fibrotic molecule, atrial natriuretic peptide (ANP). Moreover, in vivo, ANP release instigated by atrial stretch was markedly blunted in conditional Piezo1 KO mice, providing a plausible and long sought-after mechanism for the link between mechanical stretch and ANP release. Taken together, our data show that PIEZO1 is a crucial homeostatic molecule during cardiac aging, enabling adaptation to an aging tissue microenvironment.

biophysics↗