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Gurung, R.

Publications and source records attributed to Gurung, R..

3 recordsLinked to original sources

High throughput single-cell RNA sequencing of intact adult cardiomyocytes and non-myocytes using a split-pool approach

MOTIVATIONAdult cardiomyocytes are difficult to profile by whole-cell single-cell RNA sequencing because of their large size and fragility, which make them poorly compatible with standard workflows. Current approaches for adult cardiomyocyte transcriptomics often require a trade-off between data quality and throughput, thus, studies instead rely heavily on sequencing of nuclei alone. Therefore, we set out to develop a high-quality and scalable workflow for adult heart cells using in-cell ligation and split-pool barcoding strategies to address this methodological gap. This workflow may be further generalisable to other large cell types or samples containing cell populations with highly unequal RNA content. SUMMARYAdult cardiomyocytes are difficult to profile by whole-cell single-cell RNA sequencing (scRNA-seq). Here, we developed a high-quality and scalable workflow for adult heart cells using in-cell ligation and split-pool barcoding. We identified per-cell RNA content as a significant variable that must be accounted for. Separation of cardiomyocytes (large cells) and non-cardiomyocytes (small cells) before library construction, and allocation of deeper sequencing to cardiomyocytes, produced high-quality whole-cell datasets for both compartments. Compared with single-nucleus RNA sequencing, whole-cell cardiomyocyte profiling better recovered metabolic, mitochondrial, cytoplasmic translational, and contractile gene programs. This workflow provides a practical method for scalable, high-quality cardiomyocyte whole-cell scRNA-seq and offers general strategies for other large cell types or samples containing cell populations with highly unequal RNA content.

cell biology↗

Integrated in silico and in vitro approaches identify SNX.2112 as a drug vulnerability in t(7;12) AML stem-like cells

The t(7;12) translocation is a chromosomal rearrangement characteristic of infant Acute Myeloid Leukemia (AML). It arises in utero and results in ectopic overexpression of homeobox gene MNX1. Using a 3-dimensional (3D) model of blood development, we recently showed that t(7;12)-AML originates at the endothelial-to-hematopoietic transition, explaining its characteristic gene expression signature. Herein, we employ that signature to interrogate the transcriptional profiles of hundreds of human cell lines against the GDSC database of drug sensitivities to identify candidate drugs against t(7;12)-AML. We employ a cell line in which we engineered t(7;12) and systematically test the candidate drugs by cell surface phenotype and clonogenic assays. Importantly, we identify HSP90 inhibitor SNX.2112 as a potential therapeutic agent against t(7;12)-AML. SNX.2112 selectively eliminates colony-initiating leukemia progenitors in vitro and decreases MNX1 expression, effects recapitulated by other HSP90 inhibitors. SNX.2112 acts at least partly through destabilisation of STAT5 signalling. Critically, SNX.2112-differential signatures uniquely map to progenitors with hemato-endothelial characteristics in t(7;12)-AML patient blasts, suggesting targeting of leukemia-initiating cells. Combinatorial treatment with chemotherapeutic agents indicates synergy, suggesting SNX.2112 potential as a targeted and cytotoxicity-sparing therapeutic approach. Overall, we successfully use an integrated computational and multi-model experimental approach to identify a drug vulnerability of t(7;12)-AML. Key pointsO_LIClassifier-based in silico drug screening identifies vulnerabilities of t(7;12)-infant leukemia C_LIO_LI2D and 3D models of t(7;12)-leukemia match HSP90 inhibition cellular and molecular responses to candidate leukemia stem cells in t(7;12) patient analysis. C_LI

cancer biology↗

Macrophage-like vascular smooth muscle cells dominate early atherosclerosis and are inhibited by targeting iron regulation

Vascular smooth muscle cells (VSMCs) contribute dynamically to atherosclerosis at all stages but the molecular drivers of their phenotypic switching, especially during early plaque development, and how they contribute to plaque progression remain unclear. We performed spatial transcriptomics on 12 human aortic tissues with and without atherosclerotic plaque. Macrophage-like SMCs were the predominant cell-type in the atheroma, displaying high iron storage and dysregulation, confirmed by spatial elemental mapping with nuclear microscopy. The combination of soluble iron and oxidized LDL promoted foamy macrophage-like VSMC cell state transition, while chelation inhibited this switching. In vivo, iron dysregulation induced neointimal thickening and macrophage-like switching in wire-injured Ldlr-/- mice, which was significantly reversed by ferrostatin-1, a ferroptosis inhibitor. These data show how targeting iron regulation modifies the macrophage-like VSMC cell state, and inhibits disease progression in atherogenesis.

genomics↗