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Consoli, C.

Publications and source records attributed to Consoli, C..

2 recordsLinked to original sources

Deep learning-based image quantification of epithelial cell shapes and its application to polycystic kidney disease

Cell shape is a fundamental determinant of tissue architecture and organ function. In epithelial tissues, cytoskeletal organization and tight junctions regulate cell geometry, shaping functional tissue units. Disruption of these mechanisms may cause diseases such as autosomal dominant polycystic kidney disease (ADPKD), in which cyst formation is characterized by abnormal regulation of epithelial cell shape. The mechanisms of cystogenesis remain incompletely understood, highlighting the need for robust, high-throughput methods to quantify the morphology of epithelial cells. Here, we present a fully automated, deep learning-based image analysis pipeline to quantify epithelial cell shape and tight junction morphology from immunofluorescence images. Our approach employs a U-Net convolutional neural network for accurate segmentation of fluorescence labeled tight junctions. We introduce novel algorithms to quantify overall cell shape and tight junction morphology, as well as to estimate cytoskeletal traction at shared cell borders. Our analysis pipeline objectively identifies subtle morphogenetic changes associated with disease-related mutations, applied to a genetically modified Madin-Darby Canine Kidney cell model of ADPKD. The method enables high-throughput, standardized analysis, reduces observer bias, and facilitates comparison across experiments. We further demonstrate the pipelines generalizability by applying it to Drosophila egg chamber epithelia. Our results establish a robust and scalable framework for analyzing cell shape and mechanical interactions in epithelial tissues, with broad applications in phenotypic screening, disease modeling, and morphogenesis research. Author SummaryThe shape of epithelial cells is critical for organ function. In the kidney, properly shaped epithelial cells assemble to tubules ensuring efficient waste excretion as well as body electrolyte and water balance. Disruption of cell shape regulation can lead to diseases such as autosomal dominant polycystic kidney disease (ADPKD), characterized by cyst formation and displacement of normal kidney tissue. Traditionally, analysis of epithelial cell morphology has relied on manual, low-throughput methods, which are time-consuming and prone to error. To overcome these limitations, we developed a fully automated, artificial intelligence-based pipeline that rapidly and reliably quantifies cell shape and junctional organization from microscopic images. We validated our approach using a cellular model of ADPKD, demonstrating clear differences in cell shape and junctional structure between normal and mutant cells harboring mutations in PKD-related genes. Our method enables efficient, objective analysis of large datasets and provides a powerful tool for understanding the mechanisms underlying cell shape regulation in health and disease.

bioinformatics↗

Small molecule intervention of actin-binding protein profilin1 reduces tumor angiogenesis in renal cell carcinoma

Angiogenesis plays a key role in the development and progression of renal cell carcinoma (RCC). Actin-binding protein profilin-1 (Pfn1) is overexpressed in clear cell RCC predominantly in tumor-associated vascular endothelial cells (ECs). We previously demonstrated that that EC-selective (over)expression of Pfn1 accelerates RCC progression, and conversely, genetic loss of EC-Pfn1 dramatically inhibits tumor angiogenesis impeding tumor initiation and/or progression in RCC, suggesting that Pfn1 could be an actionable therapeutic target in RCC. In this study, we demonstrate that 4,4-((4-bromophenyl)methylene)bis(3,5-dimethyl-1H-pyrazole), a small molecule that we had previously identified as an inhibitor of Pfn1-actin interaction, directly binds to Pfn1 and attenuates tumor angiogenesis when directly administered into subcutaneous RCC tumors. Next, we undertook a chemical optimization approach to design and synthesize 4,4-((4-(trifluoromethyl)phenyl)methylene)bis(3,5-dimethyl-1H-pyrazole), a structural analog of our originally identified inhibitor, that exhibits improved anti-angiogenic efficacy in vitro and in vivo. Finally, we demonstrate that Pfn1 inhibitor is amenable to lipid microbubble encapsulation and release in the tumor microenvironment (TME) by ultrasound-mediated disruption of circulating microbubbles to achieve anti-angiogenic and anti-tumor benefit. In summary, our findings suggest that tumor-localized release of Pfn1 inhibitor could be a potential therapeutic strategy in RCC.

cell biology↗