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Palecek, S. P.

Publications and source records attributed to Palecek, S. P..

17 recordsLinked to original sources

Coupling a developmental promoter to CRISPR interference for Wnt pathway regulation in human pluripotent stem cells

While directed differentiation of human pluripotent stem cells commonly relies on the timed delivery of extracellular factors, these uniform treatments often yield heterogeneous responses across cell populations. Linking intracellular gene regulation directly to an emerging developmental state offers a complementary strategy to coordinate these differentiation signals from within the cell. Here, we explored this approach by coupling a T/Brachyury promoter to CRISPR interference targeting CTNNB1, which encodes the canonical Wnt signaling mediator {beta}-catenin. A T-promoter EGFP reporter line exhibited transiently increased activity during early differentiation, supporting the use of this promoter as a developmentally responsive input. We then combined the promoter with dCas9-KRAB and a CTNNB1-targeting guide RNA. Cas9-mediated integration was accompanied by indels at the CTNNB1 target site, whereas a Cas12a-mediated integration strategy yielded clones with no indels detected by ICE analysis. During differentiation, the selected T-dCas9 CTNNB1 clone showed reduced CTNNB1 expression and attenuated induction of Wnt associated genes. Together, these findings provide a proof of concept for combining a developmental promoter with a programmable intracellular regulator and identify a strategy for separating circuit integration from unintended target-site editing. This modular approach provides a foundation for developing genetic interventions whose expression is linked to developmental state.

synthetic biology↗

Forward Programming Identifies Inducers of Blood-Brain Barrier Properties in Human Pluripotent Stem Cell-Derived Endothelial Cells

Brain microvascular endothelial cells (BMECs) forming the blood-brain barrier (BBB) maintain brain homeostasis through specialized properties such as tight junctions, efflux transporters, and low levels of transcytosis. However, mechanisms governing induction of BBB properties during development remain poorly understood. We mined single-cell RNA sequencing datasets to identify transcription factors (TFs) critical for BBB development. Forty-four TFs were overexpressed in human pluripotent stem cell-derived endothelial cells cultured in the presence of the Wnt pathway agonist CHIR99021 to identify TFs capable of directing acquisition of BBB properties via forward programming. Individual TFs, including KLF2, KLF4, FOXF1, FOXF2, ZIC2, ZIC3, NR4A1, NR4A2, FOXC1, and FOXQ1, induced distinct BBB-like gene expression patterns. Combinations of these TFs induced many canonical BBB genes, yielding ECs with reduced endocytosis, increased efflux activity, and improved barrier function. The resultant forward programmed CNS-like ECs (fpCECs) offer promising tools for modeling human BBB development and neurovascular disease and for drug screening.

cell biology↗

Early multi-omic signatures and machine learning models predict cardiomyocyte differentiation efficiency and enable robust hPSC differentiation to cardiomyocytes

Protocols for generating cardiomyocytes (CMs) from human pluripotent stem cells (hPSCs) have existed for nearly two decades, yet manufacturing variability in terminal cell identity continues to limit clinical translation. To uncover the origin of fate divergence during hPSC-CM differentiation, we performed temporal transcriptomics, proteomics, and metabolomics of high and low efficiency differentiations. We identified significant early multi-omic divergence between differentiation batches and key pathways underlying fate divergence at critical differentiation stages included Wnt, MAPK, and glucose metabolism. Machine learning models trained on early candidate gene markers predicted hPSC-CM purity better than models using canonical cardiac development markers. Lastly, multi-omic insights informed perturbations, including Wnt and MAPK inhibition, which produced higher CM purities and yields. Our results showcase multi-omic analysis coupled with machine learning models as a powerful tool to identify cell fate determinants and enable robust manufacturing of complex cell products such as hPSC-derived cell therapies. TeaserMulti-omic analysis of hPSC-CM differentiation efficiency reveals early predictive features and enables robust differentiation.

cell biology↗

Human Plasma-Like Medium Promotes Maturation of Human Pluripotent Stem Cell-Derived Cardiomyocytes

Maturing human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) in vitro is critical for advancing drug discovery and cardiotoxicity screening applications of these cells. However, the metabolic compositions of basal media used for hPSC-CM culture typically offer limited relevance to human cardiac physiology. Here, we examined how culture in Human Plasma-Like Medium (HPLM) versus conventional basal media affects the behavior of hPSC-CMs. Starting with Day 16 hPSC-CMs, we cultured cells for two weeks in either HPLM or RPMI-based media and then assessed maturation outcomes at Day 30. Compared to RPMI/B27 media containing either RPMI-defined (11.1 mM) or physiologic glucose levels (5 mM), HPLM/B27 markedly enhanced hPSC-CM maturity as evinced by concerted transcriptomic, structural, functional, and metabolic phenotypes. These effects included a higher extent of myosin heavy chain isoform switching (-MHC to {beta}-MHC), accelerated ventricular-specific myosin light chain isoform switching (MLC2a to MLC2v), elongated sarcomeres, increased multinucleation, enhanced calcium transient kinetics, and coordinated activation of oxidative and glycolytic metabolism. Collectively, these findings demonstrate that medium composition has substantial effects on hPSC-CM biology and also establish HPLM as a tool for driving hPSC-CM maturation in vitro. Translational Impact StatementHPLM was designed to more closely recapitulate the metabolic composition of human plasma and thus provides a physiological platform to promote hPSC-CM maturation. By enhancing structural, functional, and metabolic maturity, HPLM-cultured hPSC-CMs better approximate cardiac physiology, positioning them as improved models for cardiovascular disease research, drug-induced cardiotoxicity screening, and personalized therapeutic testing. This medium can integrate with existing maturation strategies, accelerating the translation of basic cardiac research into clinically predictive tools for the drug development pipeline. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=189 SRC="FIGDIR/small/650456v1_ufig1.gif" ALT="Figure 1"> View larger version (29K): org.highwire.dtl.DTLVardef@a169eforg.highwire.dtl.DTLVardef@131e6f4org.highwire.dtl.DTLVardef@131d52dorg.highwire.dtl.DTLVardef@a2b248_HPS_FORMAT_FIGEXP M_FIG C_FIG

bioengineering↗

Hypoimmunogenic hPSC-derived cardiac organoids for immune evasion and heart repair

Human pluripotent stem cell (hPSC)-derived cardiac therapies hold great promise for heart regeneration but face major translational barriers due to allogeneic immune rejection. Here, we engineered hypoimmunogenic hPSCs using a two-step CRISPR-Cas9 strategy: (1) B2M knockout, eliminating HLA class I surface expression, and (2) knock-in of HLA-E or HLA-G trimer constructs in the AAVS1 safe harbor locus to confer robust immune evasion. Hypoimmunogenic hPSCs maintained pluripotency, efficiently differentiated into cardiac cell types that resisted both T and NK cell-mediated cytotoxicity in vitro, and self-assembled into engineered cardiac organoids. Comprehensive analyses of the hypoimmunogenic cells and organoids revealed preservation of transcriptomic, structural, and functional properties with minimal off-target effects from gene editing. In vivo, hypoimmunogenic cardiac organoids restored contractile function in infarcted rat hearts and demonstrated superior graft retention and immune evasion in humanized mice compared to wild-type counterparts. These findings establish the therapeutic potential of hypoimmunogenic hPSC-CMs in the cardiac organoid platform, laying the foundation for off-the-shelf cardiac cell therapies to treat cardiovascular disease, the leading cause of death worldwide.

bioengineering↗

Severe traumatic brain injury temporally affects cerebral blood flow, endothelial cell phenotype, and cilia

BackgroundPrevious clinical work suggested that altered cerebral blood flow (CBF) in severe traumatic brain injury (sTBI) correlates with poor executive function and clinical outcome. However, the molecular consequences of altered CBF on endothelial cells (ECs) and their blood flow-sensor organelle called cilia are not known. MethodsWe performed laser speckle contrast imaging, single cell isolation, and single cell RNA sequencing (scRNAseq) after sTBI in a closed skull, linear impact mouse model. Validation of select ciliary target protein changes was performed using flow cytometry. Additionally, in vitro experiments modeled the post-injury hypoxic environment to evaluate the effect on cilia protein ARL13B in human brain microvascular ECs. ResultsWe detected immediate reductions in CBF that were sustained for at least 100 minutes in both impacted and non-impacted sides of the brain. Our scRNAseq data detected heterogeneity in the brain cortex-derived EC cluster and demonstrated that two of five unique EC sub-clusters changed their relative proportions post-sTBI. Consistent with flow changes, we identified multiple genes associated with the fluid shear stress pathway that were significantly differentially expressed in brain ECs post-injury. Also, ECs displayed activation of ischemic pathway as early as day 1 post-injury, and enrichment of hypoxia pathway at day 7 and 28 post- injury. Arl13b ciliary gene expression was lost on day 1 in ECs cluster and remained lost for the entire course of the injury. We validated the loss of cilia protein ARL13B specifically from brain ECs as early as day 1 post-injury and detected the protein in the peripheral blood of the injured mice. We also determined that hypoxia could induce loss of ARL13B protein from cultured ECs. ConclusionsIn severe TBI, blood flow is disrupted in both impacted and non-impacted regions of the brain, creating a hypoxic environment that may influence ciliary gene and protein expression on ECs.

neuroscience↗

SNRK regulates TGFbeta levels in atria to control cardiac fibrosis

Atrial fibrosis is central to the pathology of heart failure (HF) and atrial fibrillation (AF). Identifying precise mechanisms underlying atrial fibrosis will provide effective strategies for clinical intervention. This study investigates a metabolic serine threonine kinase gene, sucrose non-fermenting related kinase (SNRK), that we previously reported to control cardiac metabolism and function. Conditional knockout of Snrk in mouse cardiomyocytes (Snrk cmcKO) leads to atrial fibrosis and subsequently HF. The precise mechanism underlying cardiomyocyte SNRK-driven repression of fibrosis is not known. Here, using mouse, rat, and human tissues, we demonstrate that SNRK expression is high in atria, especially in atrial cardiomyocytes. SNRK expression correlates with lower levels of pro-fibrotic protein transforming growth factor-beta 1 (TGF{beta}1) in the atrial cardiomyocytes. In HL-1 adult immortalized mouse atrial cells, using siRNA approaches, we show that Snrk knockdown cells show more TGF{beta}1 secretion, which was also observed in heart lysates from Snrk cardiac-specific knockout mice in vivo. These effects were exacerbated upon infusion of Angiotensin II. Results from Snrk knockdown cardiomyocytes co-cultured with cardiac fibroblasts suggest that SNRK represses TGF{beta}1 signaling (Smad 2/3) in atrial CMs and prevents paracrine cardiac fibroblast activation (-SMA marker). In conclusion, high SNRK expression in atria regulates cardiac homeostasis, by preventing the release of TGF{beta}1 secretion to block cardiac fibrosis. These studies will assist in developing heart chamber-specific fibrosis therapy for non-ischemic HF and AF.

cell biology↗

Activity-dependent regulation of vascular cholesterol metabolism acts as a negative feedback mechanism for neurovascular coupling

Brain function is dependent on a continuous supply of bloodborne oxygen and nutrients. Because neurons require a greater supply of oxygen and nutrients when active, there is increased local blood flow following neuronal activity. The underlying mechanisms of this hyperemia are termed neurovascular coupling (NVC). Many complex processes contribute to NVC, and there is still much unknown about how vascular physiology adapts to changes in neuronal activity and blood flow. Here we show that neuronal activity increases brain endothelial expression of genes related to cholesterol synthesis and uptake in vivo, and that shear stress is sufficient for upregulation of these genes in vitro. We previously found that treatment with PLX5622 induces upregulation of the same cassette of cholesterol-related genes in brain endothelial cells. In the present study, we find that increasing brain endothelial cholesterol synthesis and/or uptake, either with PLX5622 or targeted AAV-mediated expression of LDLR, inhibits brain arteriole dilation in response to capillary K+ stimulation, and this deficit is rescued by cholesterol depletion. Together, these data suggest that neuronal activity regulates brain endothelial cholesterol, which in turn blocks endothelial retrograde signaling and vasodilation, thus acting as a negative feedback mechanism for NVC.

neuroscience↗

Wnt signaling mediates acquisition of blood-brain barrier properties in naïve endothelium derived from human pluripotent stem cells

Endothelial cells (ECs) in the central nervous system (CNS) acquire their specialized blood-brain barrier (BBB) properties in response to extrinsic signals, with Wnt/{beta}-catenin signaling coordinating multiple aspects of this process. Our knowledge of CNS EC development has been advanced largely by animal models, and human pluripotent stem cells (hPSCs) offer the opportunity to examine BBB development in an in vitro human system. Here we show that activation of Wnt signaling in hPSC-derived naive endothelial progenitors, but not in matured ECs, leads to robust acquisition of canonical BBB phenotypes including expression of GLUT-1, increased claudin-5, and decreased PLVAP. RNA-seq revealed a transcriptome profile resembling ECs with CNS-like characteristics, including Wnt-upregulated expression of LEF1, APCDD1, and ZIC3. Together, our work defines effects of Wnt activation in naive ECs and establishes an improved hPSC-based model for interrogation of CNS barriergenesis.

neuroscience↗

A comprehensive analysis of gene expression changes in a high replicate and open-source dataset of differentiating hiPSC-derived cardiomyocytes

We performed a comprehensive analysis of the transcriptional changes within and across cell populations during human induced pluripotent stem cell (hiPSC) differentiation to cardiomyocytes. Using the single cell RNA-seq combinatorial barcoding method SPLiT-seq, we sequenced >20,000 single cells from 55 independent samples representing two differentiation protocols and multiple hiPSC lines. Samples included experimental replicates ranging from undifferentiated hiPSCs to mixed populations of cells at D90 post-differentiation. As expected, differentiated cell populations clustered by time point, with differential expression analysis revealing markers of cardiomyocyte differentiation and maturation changing from D12 to D90. We next performed a complementary cluster-independent sparse regression analysis to identify and rank genes that best assigned cells to differentiation time points. The two highest ranked genes between D12 and D24 (MYH7 and MYH6) resulted in an accuracy of 0.84, and the three highest ranked genes between D24 and D90 (A2M, H19, IGF2) resulted in an accuracy of 0.94, revealing that low dimensional gene features can identify differentiation or maturation stages in differentiating cardiomyocytes. Expression levels of select genes were validated using RNA FISH. Finally, we interrogated differences in differentiation population composition and cardiac gene expression resulting from two differentiation protocols, experimental replicates, and three hiPSC lines in the WTC-11 background to identify sources of variation across these experimental variables.

cell biology↗

Cardiac Differentiation of Human Pluripotent Stem Cells Using Defined Extracellular Matrix Proteins Reveals Essential Role of Fibronectin

Research and therapeutic applications using human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) require robust differentiation strategies. Efforts to improve hPSC-CM differentiation have largely overlooked the role of extracellular matrix (ECM). The present study investigates the ability of defined ECM proteins to promote hPSC cardiac differentiation. Fibronectin, laminin-111, and laminin-521 enabled hPSCs to attach and expand; however, fibronectin ECM either endogenously produced or exogenously added promoted, while laminins inhibited, cardiac differentiation in response to growth factors Activin A, BMP4, and bFGF. Inducible shRNA knockdown of fibronectin prevented Brachyury+ mesoderm formation and subsequent hPSC-CM differentiation. Antibodies blocking fibronectin binding to integrin {beta}1, but not 5, inhibited cardiac differentiation. Furthermore, inhibition of integrin-linked kinase blocked cardiac differentiation. These results identify fibronectin, laminin-111 and laminin-521 as defined substrates enabling cardiac differentiation of hPSCs and uncover the essential role of fibronectin and downstream signaling pathways in the early stage of hPSC-CM differentiation.

developmental biology↗

Derivation of Isogenic Mesodermal and Ectomesodermal Chondrocytes from Human Induced Pluripotent Stem Cells for Articular Cartilage Regeneration

Generating phenotypic chondrocytes from human pluripotent stem cells through driving developmental lineage-specific differentiation remains to be of great interest in the field of cartilage regeneration. In this study, we derived chondrocytes from human induced pluripotent stem cells (hiPSCs) along the mesodermal or ectomesodermal lineages to prepare isogenic mesodermal cell-derived chondrocytes (MC-Chs) or neural crest cell-derived chondrocytes (NCC-Chs), respectively, and further evaluated differences in their cellular and molecular characteristics and cartilage repair capabilities. Our results showed that both lineage-derived chondrocytes expressed hyaline cartilage-associated markers and were capable of forming hyaline cartilage-like tissue ectopically and at joint defects. Moreover, NCC-Chs showed the absence of markers of hypertrophic chondrocytes and revealed a closer morphological resemblance to articular chondrocytes and a greater capability of producing glycosaminoglycans and collagen type 2 at cartilage defects compared to MC-Chs. It was found that the profile of global transcript expression of NCC-Chs more closely resembled that of native chondrocytes (NCs) than that of MC-Chs. Induced by additional growth factors identified through the analysis of transcriptome comparison to NCs, both MC-Chs and NCC-Chs showed a further increase in the phenotype of hyaline cartilage chondrocytes. Results of this study reveal differences in cellular and molecular characteristics and cartilage repair capabilities between isogenic hiPSC-derived MC-Chs and NCC-Chs and demonstrate that chondrocytes derived from hiPSCs along the ectomesodermal lineage are a potential cell source for articular cartilage regeneration.

developmental biology↗

Cell states beyond transcriptomics: integrating structural organization and gene expression in hiPSC-derived cardiomyocytes

We present a quantitative co-analysis of RNA abundance and sarcomere organization in single cells and an integrated framework to predict subcellular organization states from gene expression. We used human induced pluripotent stem cell (hiPSC)-derived cardiomyocytes expressing mEGFP-tagged alpha-actinin-2 to develop quantitative image analysis tools for systematic and automated classification of subcellular organization. This captured a wide range of sarcomeric organization states within cell populations that were previously difficult to quantify. We performed RNA FISH targeting genes identified by single cell RNA sequencing to simultaneously assess the relationship between transcript abundance and structural states in single cells. Co-analysis of gene expression and sarcomeric patterns in the same cells revealed biologically meaningful correlations that could be used to predict organizational states. This study establishes a framework for multi-dimensional analysis of single cells to study the relationships between gene expression and subcellular organization and to develop a more nuanced description of cell states. Graphical AbstractTranscriptional profiling and structural classification was performed on human induced pluripotent stem cell-derived cardiomyocytes to characterize the relationship between transcript abundance and subcellular organization. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=199 SRC="FIGDIR/small/081083v1_ufig1.gif" ALT="Figure 1"> View larger version (60K): org.highwire.dtl.DTLVardef@8f89c4org.highwire.dtl.DTLVardef@19dc813org.highwire.dtl.DTLVardef@1ba7c20org.highwire.dtl.DTLVardef@2b3daa_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

Adaptable pulsatile flow generated by quantitative imaging of stem-cell derived cardiomyocytes for disease modeling

Endothelial cells (EC) in vivo are continuously exposed to a mechanical microenvironment from blood flow, and fluidic shear stress plays an important role in EC behavior. New approaches to generate physiologically and pathologically relevant pulsatile flows are needed to understand EC behavior under different shear stress regimes. Here, we demonstrate an adaptable pump (Adapt-Pump) platform for generating pulsatile flows via quantitative imaging of human pluripotent stem cell-derived cardiac spheroids (CS). Pulsatile flows generated from the Adapt-Pump system can recapitulate unique CS contraction characteristics, accurately model responses to clinically relevant drugs, and simulate CS contraction changes in response to fluidic mechanical stimulation. We discovered that ECs differentiated under a long QT syndrome derived pathological pulsatile flow exhibit abnormal EC monolayer organization. This Adapt-Pump platform provides a powerful tool for modeling the cardiovascular system and improving our understanding of EC behavior under different mechanical microenvironments.

bioengineering↗

Hypoxia-enhanced Blood-Brain Barrier Chip recapitulates human barrier function, drug penetration, and antibody shuttling properties

The highly specialized human brain microvascular endothelium forms a selective blood-brain barrier (BBB) with adjacent pericytes and astrocytes that restricts delivery of many pharmaceuticals and therapeutic antibodies to the central nervous system. Here, we describe an in vitro microfluidic organ-on-a-chip (Organ Chip) model of the BBB lined by induced pluripotent stem cell-derived human brain microvascular endothelium (iPS-BMVEC) interfaced with primary human brain astrocytes and pericytes that recapitulates the high level of barrier function of the in vivo human BBB for at least one week in culture. The endothelium expresses high levels of tight junction proteins, multiple functional efflux pumps, and displays selective transcytosis of peptides and anti-transferrin receptor antibodies previously observed in vivo. This increased level of barrier functionality was accomplished using a developmentally-inspired induction protocol that includes a period of differentiation under hypoxic conditions. This enhanced BBB Chip may therefore represent a new in vitro tool for development and validation of delivery systems that transport drugs and therapeutic antibodies across the human BBB.\n\nThe human blood-brain barrier (BBB) is a unique and selective physiological barrier that controls transport between the blood and the central nervous system (CNS) to maintain homeostasis for optimal brain function. The BBB is composed of brain microvascular endothelial cells (BMVECs) that line the capillaries as well as surrounding extracellular matrix (ECM), pericytes, and astrocytes, which create a microenvironment that is crucial to BBB function1. The brain microvascular endothelium differs from that found in peripheral capillaries based on its complex tight junctions, which restrict paracellular transit and instead, require that transcytosis be used to transport molecules from the blood through the endothelium and into the CNS2. BMVECs also express multiple broad-spectrum efflux pumps on their luminal surface that inhibit uptake of lipophilic molecules, including many drugs, into the brain3,4. The astrocytes and pericytes provide signals that are required for differentiation of the BMVECs5,6, and all three cell types are needed to maintain BBB integrity in vivo as well as in vitro7-9. The BBB is also of major clinical relevance because dysfunction of the BBB associated is observed in many neurological diseases, and the efficacy of drugs designed to treat neurological disorders is often limited by their inability to cross the BBB10. Unfortunately, neither animal models of the BBB nor in vitro cultures of primary or immortalized human BMVECs alone effectively mimic the barrier and transporter functions of the BBB observed in humans11-14. Thus, there is a great need for a human BBB model that could be used to develop new and more effective CNS-targeting therapeutics and delivery technologies as well as advance fundamental and translational research8,9.\n\nDevelopment of human induced pluripotent stem (iPS) cell technology has enabled differentiation of brain-like microvascular endothelial cells (iPS-BMVECs) that exhibit many properties of the human BBB, including well-organized tight junctions, expression of nutrient transporters and polarized efflux transporter activity15,16. The trans-endothelial electrical resistance (TEER) values exhibited by the permeability barrier generated by these human iPS-BMVECs reach physiological levels ([~]3000-5000 {Omega}{middle dot}cm2) within 24-48 h when cultured in Transwell inserts or within a microfluidic organ-on-a-chip (Organ Chip) device15,17-19, a level that is more than an order of magnitude higher than TEER values previously reported in other in vitro human BBB models6,17,20.\n\nHowever, the usefulness of these iPS-BMVEC models for studies on targeted delivery to the CNS is limited because they can only maintain these high TEER levels for [~]2 days, and the expression of efflux pumps in these iPS-BMVECs does not fully mimic those of human brain endothelium in vivo21. Here, we describe the development of an enhanced human BBB model created with microfluidic Organ Chip culture technology22,23 that contains human iPS-BMVECs interfaced with primary human pericytes and astrocytes, and that uses a developmentally-inspired differentiation protocol24-26. The resulting human BBB Chip exhibits physiologically relevant levels of human BBB function for at least one week in vitro, including low barrier permeability and expression of multiple efflux pumps and transporter functions that are required for analysis of drug and therapeutic antibody transport.

bioengineering↗

Preventing S. aureus biofilm formation on titanium surfaces by the release of antimicrobial β-peptides from polyelectrolyte multilayers

Staphylococcus aureus infections represent the major cause of titanium based-orthopaedic implant failure. Current treatments for S. aureus infections involve the systemic delivery of antibiotics and additional surgeries, increasing health-care costs and affecting patients quality of life. As a step toward the development of new strategies that can prevent these infections, we build upon previous work demonstrating that the colonization of catheters by the fungal pathogen Candida albicans can be prevented by coating them with thin polymer multilayers composed of chitosan (CH) and hyaluronic acid (HA) designed to release a {beta}-amino acid-based peptidomimetic of antimicrobial peptides (AMPs). We demonstrate here that this {beta}-peptide is also potent against S. aureus (MIC = 4 {micro}g/mL) and characterize its selectivity toward S. aureus biofilms. We demonstrate further that {beta}-peptide-containing CH/HA thin-films can be fabricated on the surfaces of rough planar titanium substrates in ways that allow mammalian cell attachment and permit the long-term release of {beta}-peptide. {beta}-Peptide loading on CH/HA thin-films was then adjusted to achieve release of {beta}-peptide quantities that selectively prevent S. aureus biofilms on titanium substrates in vitro for up to 24 days and remained antimicrobial after being challenged sequentially five times with S. aureus inocula, while causing no significant MC3T3-E1 preosteoblast cytotoxicity compared to uncoated and film-coated controls lacking {beta}-peptide. We conclude that these {beta}-peptide-containing films offer a novel and promising localized delivery approach for preventing orthopaedic implant infections. The facile fabrication and loading of {beta}-peptide-containing films reported here provides opportunities for coating other medical devices prone to biofilm-associated infections.\n\nSTATEMENT OF SIGNIFICANCETitanium (Ti) and its alloys are used widely in internal fixation devices due to their mechanical strength and long-term biocompatibility. However, these devices are susceptible to bacterial colonization and the subsequent formation of biofilms. Here we report a chitosan and hyaluronic acid polyelectrolyte multilayer-based approach for the localized delivery of helical, cationic, globally amphiphilic {beta}-peptide mimetics of antimicrobial peptides to inhibit S. aureus colonization and biofilm formation. Our results reveal that controlled release of this {beta}-peptide can selectively kill S. aureus cells without exhibiting toxicity toward MC3T3-E1 preosteoblast cells. Further development of this polymer-based coating could result in new strategies for preventing orthopaedic implant-related infections, improving outcomes of these titanium implants.

bioengineering↗

Human pluripotent stem cell-derived brain pericyte-like cells induce blood-brain barrier properties

Brain pericytes play an important role in the formation and maintenance of the neurovascular unit (NVU), and their dysfunction has been implicated in central nervous system (CNS) disorders. While human pluripotent stem cells (hPSCs) have been used to model other components of the NVU including brain microvascular endothelial cells (BMECs), astrocytes, and neurons, cells having brain pericyte-like phenotypes have not been described. In this study, we generated neural crest stem cells (NCSCs), the embryonic precursor to forebrain pericytes, from human pluripotent stem cells (hPSCs) and subsequently differentiated NCSCs to brain pericyte-like cells. The brain pericyte-like cells expressed marker profiles that closely resembled primary human brain pericytes, and they self-assembled with endothelial cells to support vascular tube formation. Importantly, the brain pericyte-like cells induced blood-brain barrier (BBB) properties in BMECs, including barrier enhancement and reduction of transcytosis. Finally, brain pericyte-like cells were incorporated with iPSC-derived BMECs, astrocytes, and neurons to form an isogenic human NVU model that should prove useful for the study of the BBB in CNS health, disease, and therapy.

neuroscience↗