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Huang, Y.

Publications and source records attributed to Huang, Y..

At least 847 records · Page 47Linked to original sources

Reduction of neuronal activity mediated by blood-vessel regression in the brain

The brain vasculature supplies neurons with glucose and oxygen, but little is known about how vascular plasticity contributes to brain function. Using longitudinal in vivo imaging, we reported that a substantial proportion of blood vessels in the adult brain sporadically occluded and regressed. Their regression proceeded through sequential stages of blood-flow occlusion, endothelial cell collapse, relocation or loss of pericytes, and retraction of glial endfeet. Regressing vessels were found to be widespread in mouse, monkey and human brains. Both brief occlusions of the middle cerebral artery and lipopolysaccharide-mediated inflammation induced an increase of vessel regression. Blockage of leukocyte adhesion to endothelial cells alleviated LPS-induced vessel regression. We further revealed that blood vessel regression caused a reduction of neuronal activity due to a dysfunction in mitochondrial metabolism and glutamate production. Our results elucidate the mechanism of vessel regression and its role in neuronal function in the adult brain.

neuroscience↗

Myogenic Vasoconstriction Requires Canonical Gq/11 Signaling of Angiotensin II Type 1a Receptor in Murine Vasculature

BackgroundThe myogenic response is an inherent vasoconstrictive property of resistance arteries to keep blood flow constant in response to increases in intravascular pressure. Angiotensin II (Ang II) type 1 receptors (AT1R) are broadly distributed, mechanoactivated receptors, which have been proposed to transduce myogenic vasoconstriction. However, the AT1R subtype(s) involved and their downstream G protein- and {beta}-arrestin-mediated signaling pathways are still elusive. ObjectiveTo characterize the function of AT1aR and AT1bR in the regulation of the myogenic response of resistance size arteries and possible downstream signaling cascades mediated by Gq/11 and/or {beta}-arrestins. MethodsWe used Agtr1a-/-, Agtr1b-/- and tamoxifen-inducible smooth muscle-specific AT1aR knockout mice (SM-Agtr1a mice). FR900359, [Sar1, Ile4, Ile8] Ang II (SII) and TRV120055 were used as selective Gq/11 protein inhibitor and biased agonists to activate non-canonical {beta}-arrestin and canonical Gq/11 signaling of the AT1R, respectively. ResultsMyogenic and Ang II-induced vasoconstrictions were diminished in the perfused renal vasculature of Agtr1a-/- and SM-Agtr1a mice. Similar results were observed in isolated pressurized mesenteric and cerebral arteries. Myogenic tone and Ang II-induced vasoconstrictions were normal in arteries from Agtr1b-/- mice. The Gq/11 blocker FR900359 decreased myogenic tone and Ang II vasoconstrictions while selective biased targeting of AT1R {beta}-arrestin signaling pathways had no effects. ConclusionThe present study demonstrates that myogenic arterial constriction requires Gq/11-dependent signaling pathways of mechanoactivated AT1aR but not G protein-independent, noncanonical alternative signaling pathways in the murine mesenteric, cerebral and renal circulation.

physiology↗

CancerSiamese: one-shot learning for primary and metastatic tumor classification

We consider cancer classification based on one single gene expression profile. We proposed CancerSiamese, a new one-shot learning model, to predict the cancer type of a query primary or metastatic tumor sample based on a support set that contains only one known sample for each cancer type. CancerSiamese receives pairs of gene expression profiles and learns a representation of similar or dissimilar cancer types through two parallel Convolutional Neural Networks joined by a similarity function. We trained CancerSiamese for both primary and metastatic cancer type predictions using samples from TCGA and MET500. Test results for different N-way predictions yielded an average accuracy improvement of 8% and 4% over the benchmark 1-Nearest Neighbor (1-NN) classifier for primary and metastatic tumors, respectively. Moreover, we applied the guided gradient saliency map and feature selection to CancerSiamese to identify and analyze the marker-gene candidates for primary and metastatic cancers. Our work demonstrated, for the first time, the feasibility of applying one-shot learning for expression-based cancer type prediction when gene expression data of cancer types are limited and could inspire new and ingenious applications of one-shot and few-shot learning solutions for improving cancer diagnosis, treatment planning, and our understanding of cancer.

bioinformatics↗

Single-cell RNA-seq reveals early heterogeneity during ageing in yeast

The budding yeast Saccharomyces cerevisiae has relatively short lifespan and is genetically tractable, making it a widely used model organism in ageing research. Here, we carried out a systematic and quantitative investigation of yeast ageing with single-cell resolution through transcriptomic sequencing. We optimized a single-cell RNA sequencing (scRNA-seq) protocol to quantitatively study the whole transcriptome profiles of single yeast cells at different ages, finding increased cell-to-cell transcriptional variability during ageing. The single-cell transcriptome analysis also highlighted key biological processes or cellular components, including oxidation-reduction process, oxidative stress response (OSR), translation, ribosome biogenesis and mitochondrion that underlie ageing in yeast. Remarkably, we uncovered a molecular marker, FIT3, that was linked to mitochondrial DNA loss and indicated the early heterogeneity during ageing in yeast. We also analyzed the regulation of transcription factors and further characterized the distinctive temporal regulation of the OSR by YAP1 and proteasome activity by RPN4 during ageing in yeast. Overall, our data profoundly reveal early heterogeneity during ageing in yeast and shed light on the ageing dynamics at the single cell level.

genomics↗

A simplified cell-based assay to identify coronavirus 3CL protease inhibitors

We describe a mammalian cell-based assay capable of identifying coronavirus 3CL protease (3CLpro) inhibitors without requiring the use of live virus. By enabling the facile testing of compounds across a range of coronavirus 3CLpro enzymes, including the one from SARS-CoV-2, we are able to quickly identify compounds with broad or narrow spectra of activity. We further demonstrate the utility of our approach by performing a curated compound screen along with structure-activity profiling of a series of small molecules to identify compounds with antiviral activity. Throughout these studies, we observed concordance between data emerging from this assay and from live virus assays. By democratizing the testing of 3CL inhibitors to enable screening in the majority of laboratories rather than the few with extensive biosafety infrastructure, we hope to expedite the search for coronavirus 3CL protease inhibitors, to address the current epidemic and future ones that will inevitably arise.

microbiology↗

Profiles of Expression pattern and tissue distribution of host defense peptides genes in different chicken (Gallus gallus) breeds related to body weight

Host defense peptides (HDPs) are an important first line of defense with antimicrobial and immunomodulatory properties. Selection for increased body weight is suggested to be related to reduced immune response. We studied the relationships among body weight, age, and the HDP expression patterns in intestine and immune organs. We used chickens with marked differences of body sizes. The non-selected Daweishan mini chickens showed the highest indexes of immune organs and the lowest concentrations of the plasma immune parameters C3, C4, IgA, and IgY, while the commercial Avian broiler showed the opposite results. The Daweishan mini chickens showed the highest mRNA expressions of HDP genes in small intestine followed by the semi-selected Wuding chickens. Compared with local breeds, broiler chickens showed higher mRNA expression of HDP genes in spleen, thymus, and bursa. Body weight and HDP expression levels were negatively correlated in the intestine and positively in the immune organs. These results indicated that the HDP immune regulatory roles in small intestine acted as first line of defense in innate immunity in local breeds, and as an adaptive immunity in broiler chickens. Selection was associated with the expression profiles of HDP genes in a chicken, age, and organ-specific manner.

immunology↗

N6-methyladenine DNA demethylase ALKBH1 regulates mammalian axon regeneration

Recent studies have shown that DNA N6-methyladenine (N6-mA) modification is emerging to be a novel and important epigenetic regulator of mammalian gene transcription. Several studies demonstrated DNA N6-mA in human or rodents was regulated by methyltransferase N6AMT1 and demethylase ALKBH1. Moreover, studies in mouse brain or human glioblastoma cells showed that reduced level of N6-mA or higher level of ALKBH1 was correlated with up regulated levels of genes associated with neuronal development. We thus investigated the functional roles of ALKBH1 in sensory axon regeneration. Our results showed that ALKBH1 regulated the level of N6-mA in sensory neurons, and upon peripheral nerve injury ALKBH1 was up regulated in mouse sensory neurons. Functionally, knocking down ALKBH1 in sensory neurons resulted in reduced axon regeneration in vitro and in vivo, which could be rescued by simultaneously knocking down N6AMT1. Moreover, knocking down ALKBH1 led to decreased levels of many neurodevelopment regulatory genes, including neuritin that is well known to enhance axon growth and regeneration. Our study not only revealed a novel physiological function of DNA N6-mA, but also identified a new epigenetic mechanism regulating mammalian axon regeneration. Significance StatementThe study demonstrated that DNA N6-methyladenine (N6-mA) modification played important roles in regulation of sensory axon regeneration, likely through controlling the expression of neurodevelopmental associated genes. The results will add new evidence about the physiological function of DNA N6-mA and its regulatory demethylase ALKBH1 in neurons.

neuroscience↗

Aβ-induced NOX2 activation underlies oxidative stress leading to brain hypometabolism and hyperactivity in Alzheimer's disease

A predominant trigger and driver of sporadic Alzheimers disease (AD) is the synergy of brain oxidative stress and glucose hypometabolism starting at early preclinical stages. Oxidative stress damages macromolecules, while glucose hypometabolism impairs cellular energy supply and antioxidant defense. However, the exact cause of AD-associated glucose hypometabolism and its network consequences has remained unknown. Here we report NADPH oxidase 2 (NOX2) activation as the main initiating mechanism behind A{beta}1-42-related glucose hypometabolism and network dysfunction. We utilize a combination of electrophysiology with real-time recordings of metabolic transients both ex- and in-vivo to show that A{beta}1-42 induces oxidative stress and acutely reduces cellular glucose consumption followed by long-lasting network hyperactivity and abnormalities in the animal behavioral profile. Critically, all of these pathological changes were prevented by the novel bioavailable NOX2 antagonist GSK2795039. Our data provide the first direct experimental evidence for causes and consequences of AD-related brain glucose hypometabolism, and suggest that targeting NOX2-mediated oxidative stress is a promising approach to both the prevention and treatment of AD. Single sentence summaryBeta-amyloid induces brain hypometabolism, network hyperactivity, and behavioral changes via NADPH oxidase-mediated oxidative stress, suggesting a novel therapeutic target for Alzheimers disease treatment.

neuroscience↗

Membrane Nanoparticles Derived from ACE2-rich Cells Block SARS-CoV-2 Infection

The ongoing COVID-19 epidemic worldwide necessitates the development of novel effective agents against SARS-CoV-2. ACE2 is the main receptor of SARS-CoV-2 S1 protein and mediates viral entry into host cells. Herein, the membrane nanoparticles prepared from ACE2-rich cells are discovered with potent capacity to block SARS-CoV-2 infection. The membrane of human embryonic kidney-239T cell highly expressing ACE2 is screened to prepare nanoparticles. The nanomaterial termed HEK-293T-hACE2 NPs contains 265.1 ng mg-1 of ACE2 on the surface and acts as a bait to trap SARS-CoV-2 S1 in a dose-dependent manner, resulting in reduced recruitment of the viral ligand to host cells. Interestingly, SARS-CoV-2 S1 can translocate to the cytoplasm and affect the cell metabolism, which is also inhibited by HEK-293T-hACE2 NPs. Further studies reveal that HEK-293T-hACE2 NPs can efficiently suppress SARS-CoV-2 S pseudovirions entry into human proximal tubular cells and block viral infection with a low half maximal inhibitory concentration. Additionally, this biocompatible membrane nanomaterial is sufficient to block the adherence of SARS-CoV-2 D614G-S1 mutant to sensitive cells. Our study demonstrates a easy-to-acheive memrbane nano-antagonist for curbing SARS-CoV-2, which enriches the existing antiviral arsenal and provides new possibilities to treat COVID-19. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=182 SRC="FIGDIR/small/247338v1_ufig1.gif" ALT="Figure 1"> View larger version (81K): org.highwire.dtl.DTLVardef@4086baorg.highwire.dtl.DTLVardef@4d239eorg.highwire.dtl.DTLVardef@5d8b76org.highwire.dtl.DTLVardef@16f2581_HPS_FORMAT_FIGEXP M_FIG Graphical Table of Contents C_FIG

microbiology↗

TRIM28 regulates SARS-CoV-2 cell entry by targeting ACE2

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of coronavirus disease 2019 (COVID-19), it binds to angiotensin-converting enzyme 2 (ACE2) to enter into human cells. The expression level of ACE2 potentially determine the susceptibility and severity of COVID-19, it is thus of importance to understand the regulatory mechanism of ACE2 expression. Tripartite motif containing 28 (TRIM28) is known to be involved in multiple processes including antiviral restriction, endogenous retrovirus latency and immune response, it is recently reported to be co-expressed with SARS-CoV-2 receptor in type II pneumocytes; however, the roles of TRIM28 in ACE2 expression and SARS-CoV-2 cell entry remain unclear. This study showed that knockdown of TRIM28 induces ACE2 expression and increases pseudotyped SARS-CoV-2 cell entry of A549 cells and primary pulmonary alveolar epithelial cells (PAEpiCs). In a co-culture model of NK cells and lung epithelial cells, our results demonstrated that NK cells inhibit TRIM28 and promote ACE2 expression in lung epithelial cells, which was partially reversed by depletion of interleukin-2 and blocking of granzyme B in the co-culture medium. Furthermore, TRIM28 knockdown enhanced interferon-{gamma} (IFN-{gamma})-induced ACE2 expression through a mechanism involving upregulating IFN-{gamma} receptor 2 (IFNGR2) in both A549 and PAEpiCs. Importantly, the upregulated ACE2 induced by TRIM28 knockdown and co-culture of NK cells was partially reversed by dexamethasone in A549 cells but not PAEpiCs. Our study identified TRIM28 as a novel regulator of ACE2 expression and SARS-CoV-2 cell entry.

molecular biology↗

Evaluation of Fecal Immunoassays for Canine Echinococcus Infection in China

Human echinococcosis is present worldwide but it is in China that prevalence is the highest. Western China and in particular the Tibetan plateau is the region where the burden of echinococcosis is the most important. Dogs are a major carrier of echinococcosis and monitoring the presence of Echinococcus worms in dogs is therefore essential for efficiently controlling the disease. Detection kits based on three different technologies, i.e. sandwich ELISA, ELISA and gold immunodiffusion are currently marketed and used in China. The objective of this work was to assess the efficacy of these kits, in particular with respect to sensitivity and specificity. Four fecal antigen detection kits for canine echinococcosis covering the three technologies were obtained from companies and tested in parallel on 220 fecal samples. The results indicate that the performance is lower than expected, in particular in terms of sensitivity. The best results were obtained with the sandwich ELISA technology. The gold immunofiltration yielded the poorest results. In all cases, further development is needed to improve the performance of these kits, which represent a key element for the control of echinococcosis. Author summaryAlthough present worldwide, human echinococcosis is at its highest prevalence in Western China and particularly on the Tibetan plateau. Controlling echinococcosis is a national priority and routine monitoring must be established. Dogs are the main carriers of echinococcosis and surveying Echinococcus worms in dogs is therefore a key issue. Commercial detection kits are currently in use in China for monitoring the presence of Echinococcosis in dogs. These kits are based on three different technologies, i.e. sandwich ELISA with two monoclonal antibodies, ELISA, and gold immunodiffusion. National survey programs are essential for the control of echinococcosis and it is thus very important to assess the efficacy of these kits, planned to be used for the national survey programs. The work was thus undertaken to assess this efficacy, in particular with respect to sensitivity and specificity. Four fecal antigen detection kits for canine echinococcosis covering the three technologies were obtained from companies and tested in parallel on 220 fecal samples. The performance was lower than expected, in particular for their sensitivity, which ranged from 51.5% to 83.9% with only two samples displaying a worm burden lower than 100. Three out of four kits showed non-specific cross-reactions with other parasites. The best results were obtained with the sandwich ELISA technology, whereas gold immunofiltration yielded the poorest results. However, in all cases, further development is strongly needed to improve the performance of these kits, which represent a key element for the control of echinococcosis.

zoology↗

Neurofeedback fMRI in the motor system elicits bi-directional changes in activity and white-matter structure in the healthy adult human brain

Neurofeedback can be used to alter brain activity and is therefore an attractive tool for neuromodulation in clinical contexts. Different contexts might call for different patterns of activity modulation. For example, following stroke, alternative therapeutic strategies could involve up or down-regulation of activity in the ipsilateral motor cortex. However, effects of such strategies on activity and brain structure are unknown. In a proof of concept study in healthy individuals, we showed that fMRI neurofeedback can be used to drive activity up or down in ipsilateral motor cortex during hand movement. Given evidence for activity-dependent white matter plasticity, we also tested effects of activity modulation on white matter microstructure using diffusion tensor imaging (DTI). We show rapid opposing changes in corpus callosum microstructure that depend on the direction of activity modulation. Bidirectional modulation of ipsilateral motor cortex activity is therefore possible, and results not only in online changes in activity patterns, but also in changes in microstructure detectable 24 hours later.

neuroscience↗

Continuous Constant pH Molecular Dynamics of Transmembrane Proteins

Many membrane channels, transporters, and receptors utilize a pH gradient or proton coupling to drive functionally relevant conformational transitions. Conventional molecular dynamics simulations employ fixed protonation states, thus neglecting the coupling between protonation and conformational equilibria. Here we describe the membrane-enabled hybrid-solvent continuous constant pH molecular dynamics method for capturing atomic details of proton-coupled conformational dynamics of transmembrane proteins. Example protocols from our recent application studies of proton channels and ion/substrate transporters are discussed.

biophysics↗

Characterization of extracellular vesicles and artificial nanoparticles with four orthogonal single-particle analysis platforms

We compared four orthogonal technologies for sizing, counting, and phenotyping of extracellular vesicles (EVs) and synthetic particles. The platforms were: single-particle interferometric reflectance imaging sensing (SP-IRIS) with fluorescence, nanoparticle tracking analysis (NTA) with fluorescence, microfluidic resistive pulse sensing (MRPS), and nanoflow cytometry measurement (NFCM). EVs from the human T lymphocyte line H9 (high CD81, low CD63) and the promonocytic line U937 (low CD81, high CD63) were separated from culture conditioned medium (CCM) by differential ultracentrifugation (dUC) or a combination of ultrafiltration (UF) and size exclusion chromatography (SEC) and characterized by transmission electron microscopy (TEM) and Western blot (WB). Mixtures of synthetic particles (silica and polystyrene spheres) with known sizes and/or concentrations were also tested. MRPS and NFCM returned similar particle counts, while NTA detected counts approximately one order of magnitude lower for EVs, but not for synthetic particles. SP-IRIS events could not be used to estimate particle concentrations. For sizing, SP-IRIS, MRPS, and NFCM returned similar size profiles, with smaller sizes predominating (per power law distribution), but with sensitivity typically dropping off below diameters of 60 nm. NTA detected a population of particles with a mode diameter greater than 100 nm. Additionally, SP-IRIS, MRPS, and NFCM were able to identify at least three of four distinct size populations in a mixture of silica or polystyrene nanoparticles. Finally, for tetraspanin phenotyping, the SP-IRIS platform in fluorescence mode was able to detect at least two markers on the same particle, while NFCM detected either CD81 or CD63. Based on the results of this study, we can draw conclusions about existing single-particle analysis capabilities that may be useful for EV biomarker development and mechanistic studies.

cell biology↗

The human liver microenvironment shapes the homing and function of CD4+ T-cell populations

Background & AimsTissue-resident memory T cells (TRM) are important immune sentinels that provide efficient in situ immunity. Liver-resident CD8+ TRM have been previously described, and contribute to viral control in persistent hepatotropic infections. However, little is known regarding liver CD4+ TRM cells. Here we profiled resident and non-resident intrahepatic CD4+ T cell subsets, assessing their phenotype, function, differential generation requirements and roles in hepatotropic infection. MethodsLiver tissue was obtained from 173 subjects with (n=109) or without (n=64) hepatic pathology. Multiparametric flow cytometry and immunofluorescence imaging examined T cell phenotype, functionality and location. Liver T cell function was determined after stimulation with anti-CD3/CD28 and PMA/Ionomycin. Co-cultures of blood-derived lymphocytes with hepatocyte cell lines, primary biliary epithelial cells, and precision-cut autologous liver slices were used to investigate the acquisition of liver-resident phenotypes. ResultsCD69 expression delineated two distinct subsets in the human liver. CD69HI cells were identified as CD4+ TRM due to exclusion from the circulation, a residency-associated phenotype (CXCR6+CD49a+S1PR1-PD-1+), restriction to specific liver niches, and ability to produce robust type-1 multifunctional cytokine responses. Conversely, CD69INT were an activated T cell population also found in the peripheral circulation, with a distinct homing profile (CX3CR1+CXCR3+CXCR1+), and a bias towards IL-4 production. Frequencies of CD69INT cells correlated with the degree of fibrosis in chronic hepatitis B virus infection. Interaction with hepatic epithelia was sufficient to generate CD69INT cells, while additional signals from the liver microenvironment were required to generate liver-resident CD69HI cells. ConclusionsIntermediate and high CD69 expression demarcates two discrete intrahepatic CD4+ T cell subsets with distinct developmental and functional profiles. Graphical Abstract O_FIG_DISPLAY_L [Figure 1] M_FIG_DISPLAY C_FIG_DISPLAY HighlightsO_LICD69HI (CXCR6+CD49a+S1PR1-PD-1+) are the CD4+ TRM of the human liver C_LIO_LIHepatic CD69INTCD4+ T-cells are distinct, activated, and recirculation-competent C_LIO_LIStimulation evokes respective IFN-{gamma} and IL-4 responses in CD69HI and CD69INT cells C_LIO_LICD69INT cell frequencies correlate with worsening fibrosis in chronic HBV patients C_LIO_LILiver slice cultures allow differentiation of CD69INT and CD69HI cells from blood C_LI Lay summaryTissue-resident memory T cells (TRM) orchestrate regional immune responses, but much of the biology of liver-resident CD4+ TRM remains unknown. We found high expression of cell-surface protein CD69 defined hepatic CD4+ TRM, while simultaneously uncovering a distinct novel recirculatory CD69INT CD4+ T cell subset. Both subsets displayed unique immune receptor profiles, were functionally skewed towards type-1 and type-2 responses respectively, and had distinct generation requirements, highlighting the potential for differential roles in the immunopathology of chronic liver diseases.

immunology↗

Lead compounds for the development of SARS-CoV-2 3CL protease inhibitors

We report the identification of three structurally diverse compounds - compound 4, GC376, and MAC-5576 - as inhibitors of the SARS-CoV-2 3CL protease. Structures of each of these compounds in complex with the protease revealed strategies for further development, as well as general principles for designing SARS-CoV-2 3CL protease inhibitors. These compounds may therefore serve as leads for the basis of building effective SARS-CoV-2 3CL protease inhibitors.

microbiology↗

TSG Targeting KDM5A affects osteogenic differentiation of bone mesenchymal stem cells induced by bone morphogenetic protein 2

To investigate the effect of 2, 3, 5, 4-tetrahydroxystilbene-2-O-{beta}-D-glucoside (TSG) on osteogenic differentiation of bone marrow mesenchymal stem cells (BMSC) and its molecular mechanism. The effects of TSG on alkaline phosphatase positive cloning and mineralized nodule formation were also detected. Total mRNA and protein were extracted and effects of TSG on the expression levels of osteopontin (OPN), osteocalcin (OCN), Runt-related transcription factor 2 (Runx2), Osterix and Col1a1 were detected by real-time fluorescence quantitative PCR. Western Blotting was used to detect the inhibitory effect of TSG on KDM5A. BMSCs were transfected with Small interfering RNA (siRNA) targeting KDM5A (si-KMD5A) and pcDNA3.1 KMD5A. TSG significantly increased the activity of ALP and the number of alkaline phosphatase clones and calcified nodule formation. The OPN, OCN, Runx2 and Osterix expression levels were significantly increased among the osteoblasts after TSG treatment. The mechanism study showed that the effect of TSG is realized by inhibiting KDM5A. KDM5A signaling may be involved in the regulation of osteogenic differentiation of rBMSC. TSG can promote osteogenic differentiation and maturation of rBMSC at 0.1-50 mol / L. The mechanism of action was realized by inhibiting the expression of KDM5A.

cell biology↗

A Transcriptional Switch Governing Fibroblast Plasticity Underlies Reversibility of Chronic Heart Disease

In diseased organs, stress-activated signaling cascades alter chromatin, triggering broad shifts in transcription and cell state that exacerbate pathology. Fibroblast activation is a common stress response that worsens lung, liver, kidney and heart disease, yet its mechanistic basis remains poorly understood1,2. Pharmacologic inhibition of the BET family of transcriptional coactivators alleviates cardiac dysfunction and associated fibrosis, providing a tool to mechanistically interrogate maladaptive fibroblast states and modulate their plasticity as a potential therapeutic approach3-8. Here, we leverage dynamic single cell transcriptomic and epigenomic interrogation of heart tissue with and without BET inhibition to reveal a reversible transcriptional switch underlying stress-induced fibroblast activation. Transcriptomes of resident cardiac fibroblasts demonstrated robust and rapid toggling between the quiescent fibroblast and activated myofibroblast state in a manner that directly correlated with BET inhibitor exposure and cardiac function. Correlation of single cell chromatin accessibility with cardiac function revealed a novel set of reversibly accessible DNA elements that correlated with disease severity. Among the most dynamic elements was an enhancer regulating the transcription factor MEOX1, which was specifically expressed in activated myofibroblasts, occupied putative regulatory elements of a broad fibrotic gene program, and was required for TGF{beta}-induced myofibroblast activation. CRISPR interference of the most dynamic cis-element within the enhancer, marked by nascent transcription, prevented TGF{beta}-induced activation of Meox1. These findings identify MEOX1 as a central regulator of stress-induced myofibroblast activation associated with cardiac dysfunction. The plasticity and specificity of the BET-dependent regulation of MEOX1 in endogenous tissue fibroblasts provides new trans- and cis- targets for treating fibrotic disease.

molecular biology↗