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Biology subjects

Yuan, T.

Publications and source records attributed to Yuan, T..

At least 19 recordsLinked to original sources

Musical Aesthetic Experience Reveals Differential Effects of Professional Vocal Training on Female College Students' Brain Function

Musical aesthetic experience can reveal students' cognitive, aesthetic, and emotional responses to music. However, how professional vocal training alters brain functions in female college students with varying levels of musicianship to promote these is unknown. Here we applied fMRI, psychological measures and Goldsmiths musical sophistication index (Gold-MSI) assessments to study 27 non-music major female college students consisting of instrument group (normal pitch accuracy with instrumental training), general group (normal pitch accuracy without instrumental training) and poor-pitch group (poor pitch accuracy and without instrumental training). After 1 year of one-on-one instructional practice, we found that professional vocal training enhanced information processing related to musical cognition and pleasure during musical aesthetic experiences across all three groups, involving improvements in motor control of vocalization, auditory feedback processing, musical memory and attention together with musical pleasure. Specifically, instrument group showed activation of reward circuits, general group exhibited activation of laryngeal motor control circuits, and poor-pitch group displayed activation of sensory/sensorimotor/motor control circuits. Both pre- and post-training, the instrument group exhibited higher connectivity than the other two groups in the left amygdala-dorsal anterior cingulate cortex (dACC) and the right posterior superior temporal gyrus (pSTG)-left insula pathway. After professional vocal training, the general group showed higher connectivity in the left amygdala-dACC, whereas the poor-pitch group demonstrated increased connectivity in the right pSTG-left insula and dACC-nucleus accumbens pathways. Surprisingly, professional vocal training activated the bed nucleus of the stria terminalis (BNST), a subcortical emotion center, and connectivity with the medial prefrontal cortex associated with musical information processing. Thus, vocal training can significantly improve musical cognition and aesthetic pleasure, and facilitates neural modulation in the brain's emotional centers.

scientific communication and education↗

De novo design of functional RNAs through higher-order interactions

Designing RNA sequences that reliably adopt functional three-dimensional structures remains a central challenge in RNA engineering because folding depends on cooperative interactions beyond canonical base pairing. Here we present DS3dRNA, an interaction-based framework for de novo RNA sequence design that combines a three-body statistical potential with physics-guided sequence sampling and supports design against multiple conformations. Across the evaluated benchmarks, DS3dRNA outperformed representative RNA inverse-design methods in native-sequence recovery and agreement between predicted and target structures. Energy-sequence-quality analyses further showed that lower design energies generally accompanied higher sequence recovery and macro-averaged F1 scores (MacroF1). Experimentally tested Mango II designs retained high-affinity fluorogenic activity, and five twister ribozyme designs yielded mean endpoint cleavage fractions of 37.7-50.6%, compared with 23.5% for the wild type. These results establish explicit higher-order interaction scoring as a complementary approach to emerging data-driven RNA design methods and provide a framework for designing functional RNAs from experimental or predicted structural ensembles.

biophysics↗

Image-Derived 3D Blood-Brain Mechanics: Cerebral Haemodynamics, Brain Motion and In Vivo Benchmarking

Cerebrovascular pulsatility drives measurable brain tissue deformation and has been associated with ageing and a range of neurological disorders. Yet how pulsatile haemodynamic forces are transmitted through deformable cerebral arteries into the surrounding brain remains poorly understood, particularly in anatomically realistic vascular geometries. Existing computational approaches have largely treated cerebral fluid and tissue mechanics separately or relied on idealised geometries, limiting our ability to determine how vascular anatomy simultaneously governs intraluminal haemodynamics and extravascular mechanical loading. Here, we develop an image-derived three-dimensional computational framework that jointly resolves pulsatile blood flow, arterial wall deformation and surrounding brain tissue motion in representative cerebral arteries. Four arterial segments, including the middle cerebral artery, middle cerebral artery bifurcation, basilar artery and internal carotid artery, are reconstructed from high-field (5 Tesla) magnetic resonance imaging data of a healthy subject. A finite-deformation fluid-structure interaction model is established by coupling non-Newtonian blood flow, hyperelastic arterial wall and hyper-viscoelastic brain tissue. The predicted tissue response is benchmarked against in vivo magnetic resonance elastography measurements of cardiac-induced volumetric strain over a cardiac cycle. Results reveal spatially localised arterial and tissue deformation whose magnitude and distribution are strongly governed by vascular geometry and wall thickness. Among the segments examined, the internal carotid artery exhibits the largest deformation response, while reduced wall thickness increases strain transmission into the surrounding tissue. Geometrically complex regions also exhibit greater spatial heterogeneity in near-wall haemodynamic metrics. These findings demonstrate that cerebral vascular anatomy simultaneously shapes intraluminal haemodynamics and extravascular mechanical loading. By integrating image-derived vascular anatomy, coupled blood-vessel-brain mechanics and in vivo benchmarking within a unified framework, this study provides a mechanically consistent reference for healthy cerebral pulsatility and establishes a foundation for quantifying how blood-vessel-brain interactions are altered under pathological conditions.

bioengineering↗

Sleep reactivation of positive self-evaluation reveals neural-evaluative alignment that varies with depressive symptoms

Positive self-evaluation underpins resilience and mental health, yet how to enhance positive self-evaluation and the underlying neurocognitive mechanisms remain poorly understood. Existing data mostly examined self-evaluative processing of the wakeful minds, with the role of sleep remain unexplored. Here, we demonstrated that reactivation of positive self-evaluation during sleep revealed fine-grained neural-evaluative alignment that varies with depressive symptoms. We found that targeted reactivation of positive personality traits during non-rapid eye movement (NREM) sleep enhanced positive self-evaluation, but this benefit diminished with elevated depressive symptoms. Moreover, cueing positive traits during NREM sleep elicited trait-specific, 11-16 Hz EEG sigma power-based neural representations that aligned with post-sleep positive self-evaluative representational structures, as revealed by representational similarity analyses. Notably, individuals with elevated depressive symptoms exhibited weaker neural-evaluative representational alignments, identifying a maladaptive self-evaluative processing that bridges across sleep and wakefulness states. These findings provide mechanistic insights on how fine-grained neural-evaluative alignment can substantiate positive self-evaluation, and why it was disrupted as depressive symptoms increased. HighlightsO_LIPositive-trait reactivation during NREM sleep enhances positive self-evaluation C_LIO_LIThis behavioral benefit decreases as depressive symptoms increase C_LIO_LISleep cueing evokes trait-specific sigma-band neural representations C_LIO_LINeural-evaluative alignment weakens as depressive symptoms increase C_LI

neuroscience↗

cf-Cabernet: Nick Repair Prior to End Repair Preserves Endogenous DNA Methylation Information in Cell-Free DNA Methylation Sequencing

Cell-free DNA (cfDNA) methylation profiling holds great promise for non-invasive cancer detection, yet accurate methylome analysis is compromised by DNA damage inherent to cfDNA. Standard library preparation workflows involve an end-repair step during which DNA polymerases can initiate synthesis from single-strand breaks (nicks), replacing endogenous methylated nucleotides with unmethylated nucleotides in the 3' direction and systematically erasing methylation information. This artifact is distinct from the terminal jagged-end effect and disproportionately affects cfDNA and FFPE DNA, which harbor abundant nicks. Here, we developed cf-Cabernet, which builds upon the Cabernet framework (Cao et al., 2023) -- an enzymatic methylation sequencing method featuring carrier DNA-assisted sample recovery and amplification-friendly post-conversion processing -- with the addition of a Taq DNA ligase-mediated nick repair step prior to end repair. Using matched cfDNA samples, we compared cf-Cabernet against standard EM-seq and WGBS. cf-Cabernet and EM-seq both substantially outperformed WGBS in alignment rate. Critically, while standard EM-seq exhibited globally reduced methylation levels compared to WGBS, cf-Cabernet yielded methylation levels concordant with WGBS. M-bias analysis revealed that EM-seq libraries showed persistently depressed methylation across the entire read length, whereas cf-Cabernet methylation recovered to the WGBS baseline beyond the terminal [~]40 bp jagged-end region. Nick-induced methylation erasure during end repair is a significant but previously underappreciated source of error in cfDNA methylation sequencing. cf-Cabernet effectively mitigates this artifact through pre-emptive nick ligation, enabling accurate methylome profiling from damaged DNA templates. This method is broadly applicable to cfDNA, FFPE DNA, and other clinical specimens where DNA integrity is compromised, providing a robust foundation for methylation-based liquid biopsy applications.

genetics↗

Instantaneous Phase-Shifting Optothermal Microscopy for Live-cell Metabolic Monitoring

Cellular metabolic activities can be studied using label-free vibrational spectroscopic imaging to leverage the endogenous contrast of biomolecules. However, fast live-cell imaging over large fields-of-view remains challenging due to the need for raster scanning and despite advances in wide-field modalities, imaging rapid cellular activities across large cell populations remains challenging. Here, we introduce a mid-infrared optothermal microscopy method termed Instantaneous Phase-Shifting Optothermal Microscopy (IPSOM). IPSOM circumvents conventional mechanical phase-shifting methods, achieved single-frame imaging speed 588-fold increase compared to the sequential approach, under field-of-view of 300x350 {micro}m. For multi-wavelength hyperspectral imaging, IPSOM achieves an 8-fold speed improvement. IPSOM is used here to monitor lipid remodelling in adipocytes during lipolysis, demonstrating its potential for studying rapid cellular metabolism.

bioengineering↗

Closed-loop auditory stimulation during sleep shapes cortical responses and memory consolidation depending on spindle timing

Sleep spindles contribute to memory consolidation, and acoustic stimulation during sleep can modulate spindle activity. However, it remains unclear whether these effects depend on the timing of stimulation relative to the spindle cycle. Using closed-loop spindle detection, we delivered four variants of pink noise either during ongoing spindles or shortly after spindle offset. In Experiment 1, stimulation delivered during a spindle prolonged its duration, whereas stimulation applied shortly after spindle offset, i.e., within the refractory period, delayed the onset of the subsequent spindle. This pattern was consistent across all sound variants, indicating that the stimulation timing, rather than acoustic properties, drove the observed effects. Experiment 2 examined whether post-spindle stimulation influences memory consolidation. Relative to a no-stimulation nap, post-spindle stimulation reduced post-nap deterioration in motor sequence accuracy but did not significantly affect word-pair recall. EEG analyses revealed that stimulation elicited widespread slow oscillation activity without triggering new spindles, demonstrating that cortical processing of external input persists even during the refractory period. Notably, the motor benefit was greatest in participants with lower spindle density during the baseline adaptation nap. Together, these findings challenge the notion that the post-spindle refractory period is a functionally silent interval. Instead, this period remains receptive to external input, capable of eliciting cortical activity and supporting motor memory consolidation even in the absence of new spindle generation.

neuroscience↗

Human heart organoids reveal a regenerative strategy for mitochondrial disease

The human heart is among the most complex tissues to replicate in vitro, with vascular, neuronal, and immune elements shaping its development and function. Here we describe cardiomorphs, self-organising human cardiac organoids that recapitulate the cellular diversity, structural organisation, vascularisation, and innervation of the myocardium and mature along a developmental trajectory from early cardiogenesis to adult tissue. Using patient-derived cardiomorphs, we establish the first three-dimensional human tissue model of Kearns-Sayre syndrome (KSS), a rare mitochondrial disorder characterised by large-scale mtDNA deletions. KSS-cardiomorphs faithfully reproduce disease-associated metabolic, contractile, and ultrastructural hallmarks. Leveraging this platform, we identify Betaxolol, an FDA-approved selective {beta}1-adrenergic antagonist, as a modulator of mitochondrial quality control. Betaxolol increases intracellular oxygenation, selectively eliminates dysfunctional mitochondria via mitophagy, and promotes biogenesis of functional organelles, restoring contractility in KSS tissues. This dual-action, mutation-agnostic mechanism suggests a therapeutic principle with broad relevance to mitochondrial disease, cardiac pathology, and age-associated decline.

cell biology↗

A gap-free telomere-to-telomere pig reference genome provides insight in centromere evolution and breed-specific selection

The domestic pig is a key agricultural species and biomedical model, yet its reference genome has remained incomplete. Using PacBio HiFi, Oxford Nanopore reads, and Hi-C sequencing, we assembled the first telomere-to-telomere (T2T), gap-free pig genome (T2T-Sscrofa). Importantly, this assembly derives from the same individual pig that provided the original reference genome, thereby completing the long-standing foundation of pig genomics. This assembly resolves 274.8 Mb of previously unassembled sequence, including centromeres, segmental duplications, and ribosomal DNA arrays, and identifies 255 new protein-coding genes. Comparative analyses reveal a Robertsonian translocation in the western European wild boar and extensive structural variation across global pig populations. T2T-Sscrofa provides a comprehensive genomic foundation for agricultural, evolutionary, and biomedical research.

zoology↗

A Common PD-Risk GBA1 Variant Disrupts LIMP2 Interaction, Impairs Glucocerebrosidase Function, and Drives Lysosomal and Mitochondrial Dysfunction

Variants in GBA1 cause Gaucher disease (GD), a lysosomal storage disorder, and represent the most common genetic risk factor for Parkinsons disease (PD). While some GBA1 variants are associated with both GD and PD, several coding mutations, including E326K, specifically confer risk for developing PD. It is established that GD-linked variants in {beta}-glucocerebrosidase (GCase), the enzyme encoded by GBA1, are loss-of-function, but it remains unclear whether variants solely associated with PD similarly reduce GCase activity. The mechanisms by which some of these variants impact GCase activity and PD-associated pathways, including lysosomal and mitochondrial function, are also poorly defined. Here, we show that the PD-linked E326K variant significantly reduces lysosomal GCase activity by impairing its delivery to lysosomes via altered interactions with its receptor, LIMP2. Biophysical and structural characterization of this variant, both alone and in complex with LIMP2, reveals a dimeric organization that appears to result from the loss of a key salt bridge between E326 and R329. Restoration of this salt bridge through the introduction of a negatively charged side chain at position 329 promotes monomeric organization and interaction with LIMP2 in cells. GBA1-p.E326K cell models show greater deficits in PD-linked pathways compared to more severe loss of GCase function, including secondary lysosomal lipid storage and mitochondrial dysfunction. We confirm the E326K variant impacts GCase pathway activity in relevant CNS cell types, including iPSC-derived microglia, and in biofluids from heterozygous GBA1-p.E326K variant carriers. Together, our data provide key insights into the nature of GCase dysfunction in GBA1-PD and can inform the development of GCase-targeted therapeutic strategies to treat PD.

cell biology↗

Single-cell Characterization of DNA Hydroxymethylation of the Mouse Brain During Aging

DNA methylation dynamics, including 5-hydroxymethylcytosine (5hmC) and 5-methylcytosine (5mC), critically regulate brain function, yet conventional methods cannot distinguish these modifications, obscuring their distinct roles in gene regulation and aging. We present Joint- Cabernet, a bisulfite-free single-cell platform enabling simultaneous profiling of 5hmC, 5mC, and transcriptomes. Applying Joint-Cabernet to 84,071 nuclei from adult and aged mouse brains, we resolved cell-type-specific DNA hydroxymethylation landscapes, revealing elevated 5hmCG and 5hmCH levels in transcriptionally active genes across neuronal subtypes and spatial gradients in cortical layers. During aging, 5hmCG accumulates globally but is selectively enriched at open chromatin loci, aligning with the upregulation of cell-type-specific genes in distinct brain cell types. This single-cell DNA methylation brain cell atlas provides a framework for studying methylation- driven mechanisms in brain aging and neurodegenerative diseases.

genetics↗

In vivo MRI measurement of microstructural constraints for direct delivery of therapeutics within the brain

Brain tissue microstructure influences the efficient delivery of therapeutics within the brain. Diffusion Tensor Imaging (DTI) enables the depiction of tissue properties in vivo, and thus is potentially relevant for planning convection-enhanced delivery (CED) within the brain. We report on the quantitative assessment of the distribution of a Gadolinium solution infused by CED within the brain of a live ovine model. Infusate distributions were measured at multiple timepoints and compared to microstructural properties as depicted by DTI, thus demonstrating the impact of tissue features and catheter positioning on drug distribution in vivo. This study contributed to the clinical translation of the CED for flow-based therapy to ultimately provide new therapeutic approaches for several brain diseases, by providing essential tools and results used to develop a better prediction model and a delivery platform to reach the therapeutic target more precisely and non-invasively.

neuroscience↗

Decoding Brain Interstitial Transport In Vivo: A Fully Validated Bottom-Up Mechanistic Prediction Framework

The transport of fluids and substances within the brain parenchyma (i.e. interstitial transport) is fundamental to maintaining brain health and delivering treatments for neurological disorders. However, accurately predicting these transport processes has remained a formidable challenge due to the intricate and dynamic nature of the brains microenvironment. Here, we report a novel, fully validated bottom-up mechanistic framework that bridges advanced mathematical modelling, ultra-high-resolution imaging, and biomechanical testing to achieve precise, in vivo predictions of interstitial transport. Using this approach, we accurately modelled the transport of MRI tracers in living sheep brains, offering unprecedented insights into the interplay between fluid dynamics and tissue properties. This platform is a transformative step forward, with the potential to revolutionise drug delivery strategies not only in the brain but also in cancer therapy and other soft biological systems. By addressing limitations in modelling complex transport in soft tissue, our work establishes a significant tool with profound implications for biomedical engineering and translational medicine.

biophysics↗

Coarse-grained chromatin dynamics by trackingmultiple similarly labeled gene loci

The "holy grail" of chromatin research would be to follow the chromatin configuration in individual live cells over time. One way to achieve this goal would be to track the positions of multiple loci arranged along the chromatin polymer with fluorescent labels. Use of distinguishable labels would define each locus uniquely in a microscopic image but would restrict the number of loci that could be observed simultaneously, because of experimental limits to the number of distinguishable labels. Use of the same label for all loci circumvents this limitation but requires a (currently lacking) framework for how to establish each observed locus identity, i.e. to which genomic position it corresponds. Here we analyze theoretically, using simulations of Rouse-model polymers, how single-particle-tracking of multiple identically-labeled loci enables determination of loci identity. We show that the probability of correctly assigning observed loci to genomic positions converges exponentially to unity as the number of observed loci configurations increases. The convergence rate depends only weakly on the number of labeled loci, so that even large numbers of loci can be identified with high fidelity by tracking them across about 8 independent chromatin configurations. In the case of two distinct labels that alternate along the chromatin polymer, we find that the probability of the correct assignment converges faster than for same-labeled loci, requiring observation of fewer independent chromatin configurations to establish loci identities. Finally, for a modified Rouse-model polymer, that realizes a population of dynamic loops, we find that the success probability also converges to unity exponentially as the number of observed loci configurations increases, albeit slightly more slowly than for a classical Rouse model polymer. Altogether, these results establish particle tracking of multiple identically- or alternately-labeled loci over time as a feasible way to infer temporal dynamics of the coarse-grained configuration of the chromatin polymer in individual living cells. SIGNIFICANCEIn spite of recent success in elucidating its spatial organization, chromatins time-dependent, dynamical behavior remains far less studied, and correspondingly much less understood. To address the critical need to elucidate chromatin dynamics, this paper proffers a route towards an experimental characterization of coarse-grained chromosomal dynamics, via particle tracking of multiple labeled loci, labeled with just one or two different fluophor colors or intensities. Theoretically, we show that particle tracking of multiple identically labeled loci across only about 8 independent chromatin configurations should be a feasible way to establish the time-dependent, coarse-grained configuration of the chromatin polymer in individual living cells.

biophysics↗

TOGGLE identifies fate and function process within a single type of mature cell through single-cell transcriptomics

Cells that appear transcriptionally identical can maintain vastly different functions or fates--an enduring blind spot in single-cell transcriptomics. Here we introduce TOGGLE, a self-supervised graph diffusion framework that delineates fine-grained functional heterogeneity within phenotypically stable cell populations. By combining deep diffusion learning with reinforcement-guided clustering and a BERT-inspired masking strategy, TOGGLE reconstructs hidden trajectories of cell fate without prior labels or temporal information. Applied across multiple single-cell RNA-seq datasets, TOGGLE achieves up to 90 % accuracy in unsupervised fate prediction, surpassing existing trajectory algorithms such as WOT and Cospar. It distinguishes ferroptotic, apoptotic, and intermediate neuronal states in ischemic stroke, with predictions experimentally validated in animal models. In neural stem cells TOGGLE reveals epigenetic memory of metabolic activity, linking local DNA demethylation and chromatin accessibility to mitochondrial RNA expression. We further introduce the Graph Diffusion Functional Map, which isolates subtle RNA functional groupings otherwise obscured by conventional dimensionality reduction. TOGGLE thus establishes a generalizable framework for mapping functional identity and epigenetic dynamics at single-cell resolution, providing new insights into cellular memory, regeneration, and disease mechanisms. Biographical NoteChens guidance comes from Dr. Alex P. Carll. Another mentor is Dr. Lu Cai, one of the contributors to the standardization of autophagy detection methods, whose research on criteria for identifying diabetes induced apoptosis has been included in numerous clinical guidelines. Professor Jinwen Ge is a State Council Special Allowance Expert of China. He has been involved in formulating medical standards for integrated traditional Chinese and Western medicine in China and has participated in developing retrieval/indexing norms for journals in the field of integrated traditional Chinese and Western medicine. Code and Data availabilityThe raw data for the hematopoiesis dataset can be accessed at the Gene Expression Omnibus database with accession number GSE140802, the reprogramming dataset with accession number GSE99915, the e-cigarette aerosol inhalation on mouse cardiac tissue with accession number GSE183614, the rat myocardial infarction dataset with accession number GSE253768, the ischemic stroke dataset with accession number GSE232429, and the adult NSC lineage dataset with accession number GSE209656 and GSE211786. All codes and guide page & analyzed data are full open available at: https://github.com/FullBlackWolf/TOGGLE?tab=readme-ov-file https://fullblackwolf.github.io/TOGGLE/ Key points(1) Previous studies have primarily focused on distinguishing cell types and different cellular subpopulations, whereas our tool is designed to identify subtle functional differences among highly similar cell states. For example, in Test2, it first isolates neurons undergoing cell death, then further differentiates early, intermediate, and late death stages, and separates ferroptosis from apoptosis as two major categories. Notably, ferroptosis and apoptosis share a large number of molecular pathways, making this task highly challenging. In addition, in Test4, our method discriminates fibroblasts with distinct immune-communication patterns, even though they do not show prominent separation or temporal progression on conventional UMAP plots. (2) We developed an innovative Graph Diffusion Functional Map that significantly reduces noise, resulting in clearer visualization of RNA functional groupings and enabling the detection of subtle functional differences in high-dimensional data. This provides a novel tool for pathway discovery. For instance, in Test4, we found that the KEGG inflammatory response pathway was most strongly activated in young mice, suggesting that e-cigarette exposure exerts more severe effects on immature cardiac tissue. (3) We implemented a novel trajectory-tracking strategy capable of distinguishing early, intermediate, and late stages of cellular programming, which we refer to as functional lineage tracing. In Test3, we successfully separated nearly indistinguishable aNSC and qNSC populations and further uncovered their methylation-regulated transcriptional programs, demonstrating that local DNA demethylation activates genes involved in cell proliferation and energy metabolism, thereby regulating the activation of quiescent neurons. (4) In the testing dataset, it was found that local DNA demethylation activates the expression of genes associated with cell proliferation and energy metabolism, thereby regulating the activation of quiescent neurons. Neuronal ferroptosis in ischemic stroke may be linked to the high expression of ferroptosis driver genes such as Ctsb, Mtdh, Ndrg1, Smad7, Cd82, and Acsl1.

bioinformatics↗

Single-Cell RNA-Seq Reveals Adventitial Fibroblast Alterations during Mouse Atherosclerosis

BackgroundAtherosclerotic cardiovascular disease (ASCVD) remains the leading cause of mortality in the western world despite the success of lipid lowering therapies, highlighting the need for novel lipid-independent therapeutic strategies. Genome-wide association studies (GWAS) have identified numerous genes associated with ASCVD that function in the vessel wall, suggesting that vascular cells mediate ASCVD, and that the genes and pathways essential for this vascular cell function may be novel therapeutic targets for the treatment of ASCVD. Furthermore, some of these implicated genes appear to function in the adventitial layer of the vasculature, suggesting these cells are able to potentiate ASCVD. MethodsTo investigate the role of adventitial cells in atherosclerosis, we conducted single-cell RNA sequencing (scRNA-seq) of the aortic adventitia during atherogenesis in male Ldlr-/- mice via pools of three mice, two samples per condition. We cross-referenced the scRNA-seq data with human ASCVD GWAS to identify regulators of adventitial responses in ASCVD. These regulators were then validated in vitro in human adventitial fibroblasts. ResultsWe identified four adventitial fibroblast populations, all of which displayed shifts in population size and gene expression over the course of atherogenesis. SERPINH1, an ASCVD-linked GWAS gene, was differentially expressed in adventitial fibroblasts during atherogenesis. Knockdown of SERPINH1 in vitro reduced fibroblast migration and altered subcluster marker gene expression. ConclusionsThese findings reveal dynamic changes in adventitial fibroblasts during atherosclerosis and suggest that reduced SERPINH1 expression disrupts adventitial fibroblast function, contributing to ASCVD progression.

genomics↗

HIF1α controls adipose tissue growth through metabolic rechanneling

Excessive expansion of white adipose tissue occurs when energy intake exceeds demand. It creates a state of relative hypoxia that is directly linked to activation of the hypoxia-inducible factor (HIF) in obese human subjects and mouse models of obesity. Whether HIF1 function is important for the development of basal adiposity and diet-induced obesity remains unclear. In the present study, we genetically ablated Hif1 in adipocytes and analyzed the corresponding mice for both basal and diet-induced obesity-associated visceral white adipose tissue mass as well as parameters of systemic glucose homeostasis and peripheral insulin sensitivity. We found that inactivation of Hif1 in mouse adipocytes inhibited basal adiposity and suppressed nutrient-overload-induced adipose tissue growth. These changes in adiposity were associated with improved systemic glucose homeostasis and peripheral insulin sensitivity. Mechanistically, Hif1 mediated effects on adipocyte metabolism by re-routing glycolytic intermediates into the glycerolipid shunt, leading to increased de novo triacylglyceride synthesis in hypertrophic adipocytes. Our results have established key roles for HIif1 in controlling adipocyte growth and metabolism and adipose tissue expansion under basal conditions and in response to a high-fat diet, highlighting the central role of hypoxia and HIF1 in the development of obesity. Article HighlightsO_LIHif1 function is critical for basal adipose tissue mass expansion, and is also required for fat accumulation in response to high fat diet. C_LIO_LICo-option and co-activation of the glycerolipid biosynthetic pathway by glycolysis is an important modulator of visceral adiposity. C_LIO_LIThese findings reveal an important role of Hif1 in the adipose tissue through the coupling of glycolysis and lipid anabolism in response to HFD, which may provide a potential therapeutic target for type 2 diabetes in the future. C_LI

cell biology↗

GABAAR-PPT1 palmitoylation homeostasis controls synaptic transmission and circuitry oscillation in CLN1 disease

CLN1 disease, also called infantile neuronal ceroid lipofuscinosis, is a fatal neurodegenerative disease caused by mutations in the CLN1 gene encoding palmitoyl protein thioesterase 1 (PPT1). To identify depalmitoylation substrate of PPT1 is crucial to understand CLN1 disease. In this study, we found that PPT1 depalmitoylates GABAAR 1 subunit at Cystein-260, while binding to Cystein-165 and -179. Mutations of PPT1 or its GABAAR 1 subunit binding site result in enhanced inhibitory synaptic transmission, strengthened and oscillation but disrupted phase coupling in CA1 region and impaired learning and memory in 1- to 2-months-old PPT1-deficient and Gabra1em1 mice. Our study highlights the critical role of PPT1 in maintaining GABAAR palmitoylation homeostasis and reveals a previously unknown molecular pathway in PPT1 induced diseases.

neuroscience↗