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Biology subjects

Lazarus, K. A.

Publications and source records attributed to Lazarus, K. A..

4 recordsLinked to original sources

Compound screening in primary human airway basal cells identifies Wnt pathway activators as potential pro-regenerative therapies

Regeneration of the airway epithelium restores barrier function and mucociliary clearance following lung injury and infection. Basal cells are tissue-resident airway stem cells that enact regeneration, yet the mechanisms regulating their proliferation and differentiation remain incompletely understood. To identify compounds that promote primary human airway basal cell proliferation, we performed phenotype-based compound screening of 1,429 compounds (from the ENZO and Prestwick Chemical libraries) in 384-well format using primary cells transduced with lentiviral luciferase. 16 pro-proliferative compounds validated in independent donor cell cultures, with several hit compounds activating the Wnt signalling pathway. The effects of compounds on proliferation were further explored in concentration-response, colony formation and 3D organoid assays. Structurally and functionally-related compounds that more potently induced both Wnt activation and basal cell proliferation were investigated. One such compound, 1-azakenpaullone, induced Wnt target gene activation and basal cell proliferation in mice in the absence of tracheal injury. Our results demonstrate the pro-proliferative effect of small-molecule Wnt activators on airway basal cells. These findings contribute to the rationale to develop novel approaches to modulate Wnt signalling during airway epithelial repair. Summary statementIshii, Orr and colleagues perform a high-throughput screen of 1,429 compounds in primary human airway epithelial cells, identifying Wnt activating compounds as promoters of proliferation.

cell biology↗

A lentiviral toolkit to monitor airway epithelial cell differentiation using bioluminescence

Basal cells are adult stem cells in the airway epithelium and regenerate differentiated cell populations, including the mucosecretory and ciliated cells that enact mucociliary clearance. Human airway basal cells can proliferate and produce differentiated epithelium in vitro. However, studies of airway epithelial differentiation mostly rely on immunohistochemical or immunofluorescence-based staining approaches, meaning that a quantitative approach is lacking. Here, we use a lentiviral reporter gene approach to transduce primary human basal cells with bioluminescence-based reporter constructs to monitor airway epithelial differentiation longitudinally. We generated three constructs driven by promoter sequences from the TP63, MUC5AC and FOXJ1 genes to quantitatively assess basal cell, ciliated cell and mucosecretory cell abundance, respectively. We validated these constructs by tracking differentiation of basal cells in air-liquid interface and organoid ( bronchosphere) cultures. Transduced cells also responded appropriately to stimulation with interleukin 13 (IL-13; to increase mucosecretory differentiation and mucus production) and IL-6 (to increase ciliated cell differentiation). We anticipate that these constructs will be a valuable resource for researchers monitoring airway epithelial cell differentiation in primary epithelial and/or induced pluripotent stem cell (iPSC) cell cultures. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=78 SRC="FIGDIR/small/579635v1_ufig1.gif" ALT="Figure 1"> View larger version (22K): org.highwire.dtl.DTLVardef@a4e127org.highwire.dtl.DTLVardef@b9c7c5org.highwire.dtl.DTLVardef@ea7bd0org.highwire.dtl.DTLVardef@66a384_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

Cell-intrinsic differences between human airway epithelial cells from children and adults

The airway epithelium is a key protective barrier, the integrity of which is preserved by the self-renewal and differentiation of basal stem cells. Epithelial cells are central to the pathogenesis of multiple lung diseases. In chronic lung diseases, increasing age is a principle risk factor. Few studies have explored the differences between airway epithelial cells in children and adults and how the function of basal stem cells changes during ageing is poorly understood. Here, we analyze airway epithelial cells from children and adults in homeostatic conditions (laser capture-microdissected whole epithelium and fluorescence-activated cell-sorted basal cells) and in proliferation-inducing cell culture conditions. We find that, while the cellular composition of the pediatric and adult tracheobronchial epithelium is broadly similar, in cell culture, pediatric airway epithelial cells displayed higher colony-forming ability, sustained in vitro growth and outcompeted adult cells in competitive proliferation assays. In RNA sequencing experiments, we observed potentially important differences between epithelium from children and adults, including higher baseline interferon-associated gene expression in pediatric epithelium. Our results demonstrate cell-intrinsic differences in transcriptional profile and regenerative capacity between proximal airway epithelial cells of children and adults. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=178 SRC="FIGDIR/small/027144v2_ufig1.gif" ALT="Figure 1"> View larger version (33K): org.highwire.dtl.DTLVardef@b7a680org.highwire.dtl.DTLVardef@1145543org.highwire.dtl.DTLVardef@1e9a86aorg.highwire.dtl.DTLVardef@12fe0bf_HPS_FORMAT_FIGEXP M_FIG C_FIG

cell biology↗

BCL11A interacts with SOX2 to control the expression of epigenetic regulators in lung squamous cell carcinoma

Patients diagnosed with lung squamous cell carcinoma (LUSC) have limited targeted therapeutic options. We report here the identification and characterisation of the transcriptional regulator, BCL11A, as a LUSC oncogene. Analysis of cancer genomics datasets revealed BCL11A to be upregulated in LUSC but not lung adenocarcinoma (LUAD). We demonstrated that knockdown of BCL11A in LUSC cell lines abolished xenograft tumour growth and its overexpression in vivo led to lung airway hyperplasia and the development of reserve cell hyperplastic lesions. In addition, deletion of Bcl11a in the tracheal basal cells abolished the development of tracheosphere organoids while its overexpression led to solid tracheospheres with a squamous phenotype. At the molecular level we found BCL11A to be a target of SOX2 and we show that it is required for the oncogenic role of SOX2 in LUSC. Furthermore, we showed that BCL11A and SOX2 interact at the protein level and that together they co-regulated the expression of several transcription factors. We demonstrate that pharmacological inhibition of SETD8, a gene co-regulated by BCL11A and SOX2, alone or in combination with cisplatin treatment, shows significant selectivity to LUSC in comparison to LUAD cells. Collectively, these results indicate that the disruption of the BCL11A-SOX2 transcriptional program provides a future framework for the development of targeted therapeutic intervention for LUSC patients.

cancer biology↗