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Woodward, O. M.

Publications and source records attributed to Woodward, O. M..

5 recordsLinked to original sources

Transcriptome-based cell type assignment for kidney cell culture models

BackgroundKidney cell lines are widely used to model kidney physiology and disease; however, their gene expression profiles may differ from primary cells due to immortalization, culture conditions, or experimental treatments. Determining whether a cell line resembles its native cell type is critical for interpreting in vitro findings. We developed a transcriptome-based approach that matches bulk RNA-seq data from kidney cell lines, primary cells, or tissues to reference cell types derived from single-cell RNA-seq (scRNA-seq) datasets. MethodsReference transcriptomic profiles were generated from two human and two murine kidney scRNA-seq datasets by pseudobulk aggregation. Bulk RNA-seq data from microdissected kidney tissue, non-kidney negative controls, and kidney cell lines were matched to these references using three statistical similarity measures (Spearman correlation, Euclidean distance, Poisson distance) and three machine learning classifiers (Random Forest, XGBoost, TabPFN). Each was assessed with global gene expression, curated kidney marker gene lists, and the most variable genes. Matching accuracy was evaluated through a three-step validation strategy: within-dataset matching, cross-reference comparison, and validation against primary kidney tissue and negative controls. ResultsGene expression rank-based Spearman correlation and TabPFN, a foundation model for tabular data, emerged as the most accurate and specific approaches, particularly with curated kidney marker gene lists. Both methods correctly identified microdissected kidney tubule segments and were robust against non-kidney negative controls. Applied to commonly used kidney cell lines, OK cells retained proximal tubule identity, particularly under shear stress, while other proximal tubule lines (HK-2, HKC-8, HKC-11) showed inconsistent matching. Collecting duct-derived mIMCD-3 maintained stable similarity across passages, culture conditions, and genetic modifications. ConclusionWe provide two complementary implementations: CellMatchR, an accessible web-based tool using Spearman correlation for routine use, and comprehensive scripts for TabPFN-based matching (link will be added after peer reviewed publication). Together, these resources enable researchers to make informed decisions about kidney cell culture model selection, interpretation, and stability. Translational StatementKidney cell lines are fundamental tools in nephrology research, yet their transcriptomic similarity to native cell types is rarely validated systematically. We demonstrate that combining bulk RNA-seq data with single-cell reference datasets enables robust assessment of cell line identity using gene expression-rank-based correlation and machine learning approaches. By providing a comprehensive evaluation of matching methods, curated kidney marker gene lists, and reference datasets, our study serves as both a practical resource and a methodological framework for the kidney research community, facilitating informed selection of cell culture models, quality control of experimental conditions, developing new experimental cell culture models, and more reliable translation of in vitro findings to kidney physiology and disease.

bioinformatics↗

Extra-ciliary role for polycystins in regulation of Ezrin and renal tubular morphology

Full understanding of the functions of the polycystin proteins, PC1 and PC2, in renal epithelial cells is obscured by signaling complexity and renal injury that occurs in Autosomal Dominant Polycystic Kidney Disease (ADPKD). The polycystins likely function as a complex in the primary cilium, yet previous work hinted at a critical role for PC1 function outside of the primary cilium (extra-ciliary) during tubule development. Here, we investigate an extra-ciliary role for the polycystins in regulating renal cell and tubular morphology. First, we found acute loss of polycystins significantly increased the circularity of renal epithelial cells and tubuloids grown in 3D culture. Next, we demonstrated that both PC1 and PC2 can immunoprecipitate Ezrin, an ERM protein important for apical compartment shape. In human ADPKD renal cystic tissue, and after acute inducible knockout of Pkd1 or Pkd2, we found that Ezrin protein abundance is significantly reduced, with the remaining Ezrin protein mis-localized. Immunofluorescence in 2D cells and 3D tubuloids suggested acute polycystin loss specifically reduced the active form of Ezrin at the apical surface, leaving inactive Ezrin colocalized with ZO1 in the cell junctions. A specific ERM phosphorylation inhibitor, NSC668394, phenocopied the increased circularity observed in the Pkd1 knockout spheroids, as did inhibition of PKC activity, implicating the polycystin complex in regulating Ezrin phosphorylation. Our data strongly support a role for the polycystin complex in regulating renal cell and tubular shape via interactions with the ERM protein Ezrin, interactions that do not require trafficking to the primary cilium.

cell biology↗

Multi-omics profiling of mouse polycystic kidney disease progression at a single cell resolution

Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disease and causes significant morbidity, ultimately leading to end-stage kidney disease. PKD pathogenesis is characterized by complex and dynamic alterations in multiple cell types during disease progression, hampering a deeper understanding of disease mechanism and the development of therapeutic approaches. Here, we generate a single nucleus multimodal atlas of an orthologous mouse PKD model at early, mid and late timepoints, consisting of 125,434 single-nucleus transcriptomic and epigenetic multiomes. We catalogue differentially expressed genes and activated epigenetic regions in each cell type during PKD progression, characterizing cell-type-specific responses to Pkd1 deletion. We describe heterogeneous, atypical collecting duct cells as well as proximal tubular cells that constitute cyst epithelia in PKD. The transcriptional regulation of the cyst lining cell marker GPRC5A is conserved between mouse and human PKD cystic epithelia, suggesting shared gene regulatory pathways. Our single nucleus multiomic analysis of mouse PKD provides a foundation to understand the earliest changes molecular deregulation in a mouse model of PKD at a single-cell resolution.

genomics↗

Defining cellular complexity in human autosomal dominant polycystic kidney disease by multimodal single cell analysis

Autosomal dominant polycystic kidney disease (ADPKD) is the leading genetic cause of end stage renal disease and is characterized by the formation and progressive expansion of kidney cysts. Most ADPKD cases arise from mutations in either the PKD1 or PKD2 gene but the precise downstream signaling pathways driving cyst growth are not well understood, and relatively few studies investigate human cystic kidney due to sample scarcity. In order to better understand the cell types and states driving human ADPKD progression, we analyzed eight ADPKD and five healthy human kidney samples, generating a single cell multiomic atlas consisting of ~100,000 single nucleus transcriptomes and ~50,000 single nucleus epigenomes. The integrated datasets identified 11 primary cell clusters including most epithelial cell types as well as large endothelial and fibroblast cell clusters. Proximal tubular cells from ADPKD kidneys expressed a failed repair transcriptomic signature characterized by profibrotic and proinflammatory transcripts. We identified the G protein-coupled receptor GPRC5A as specifically upregulated in cyst lining cells derived from collecting duct. The principal cell subpopulation enriched for GPRC5A expression also exhibited increased transcription factor binding motif availability for NF-{kappa}B, TEAD, CREB and retinoic acid receptor families and we identified and validated a distal enhancer regulating GPRC5A expression containing these transcription factor binding motifs. This study establishes the single cell transcriptomic and epigenomic landscape of ADPKD, revealing previously unrecognized cellular heterogeneity.

genomics↗

Trans-epithelial Fluid Pumping Performance of Renal Epithelial Cells and Mechanics of Cystic Expansion

Using a novel microfluidic platform to recapitulate fluid absorption activity of kidney cells, we report that renal epithelial cells can actively generate hydraulic pressure gradients across the epithelium. The fluidic flux declines with increasing hydraulic pressure until a stall pressure, at which the fluidic flux vanishes--in a manner similar to mechanical fluidic pumps. The developed pressure gradient translates to a force of 50-100 nanoNewtons per cell. For normal human kidney cells, the fluidic flux is from apical to basal, and the pressure is higher on the basal side. For human polycystic kidney disease (PKD) cells, the fluidic flux is reversed from basal to apical with a significantly higher stall pressure. Molecular studies and proteomic analysis reveal that renal epithelial cells are highly sensitive to hydraulic pressure gradients, developing different expression profiles and spatial arrangements of ion exchangers and the cytoskeleton in different pressure conditions. These results, together with data from osmotic and pharmacological perturbations of fluidic pumping, implicate mechanical force and hydraulic pressure as important variables during morphological changes in epithelial tubules, and provide further insights into pathophysiological mechanisms underlying the development of high luminal pressure within renal cysts.

biophysics↗