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Pramotton, F. M.

Publications and source records attributed to Pramotton, F. M..

3 recordsLinked to original sources

ETV2 mediated differentiation of human pluripotent stem cells results in functional endothelial cells for engineering advanced vascularized microphysiological models

Patient-specific microphysiological models, exemplified by organs-on-a-chip and organoids, have become a valuable tool for broad applications, revolutionizing biomedical research. However, limitations persist, with functional vasculature being a significant challenge. Generating functional human induced pluripotent stem cell (h-iPSC) derived endothelial cells (h-iECs) represent an urgent need. With the discovery of ETV2s determinant role in specifying EC lineages during differentiation, researchers have adopted techniques involving ETV2 overexpression to produce h-iECs more efficiently and consistently. However, the capacity of these cells to form functional vasculatures has not yet been thoroughly investigated. Here, we generated multiple h-iPSC lines with inducible ETV2 expression, and subsequently differentiated them into h-iECs, which were validated functionally and by key endothelial markers and RNA-seq analysis. These cells are capable of self-organizing into stable microvascular networks (MVNs) in a microfluidic chip reproducibly, forming lumenized and functional vessels that mimic the in vivo capillary bed in both morphology and function - a result not achieved using h-iECs differentiated with conventional two-step methods using the same h-iPSC lines. Furthermore, complex microphysiological models featuring perfusable vasculature were also successfully developed using ETV2 activated h-iECs, demonstrated with vascularized tumor and blood-brain barrier (BBB) models. Additionally, by pooling genetically engineered h-iPSCs with inducible ETV2, we effectively employed an orthogonally induced differentiation approach to enhance vascularization of an organoid model. Our methodology opens avenues in precision medicine, leading to personalized microphysiological models with perfusable vasculature for various applications.

bioengineering↗

Force-biased nuclear import sets nuclear-cytoplasmic volumetric coupling by osmosis

In eukaryotes, cytoplasmic and nuclear volumes are tightly regulated to ensure proper cell homeostasis. However, the detailed mechanisms underlying nucleus-cytoplasm volumetric coupling remain unknown. Recent evidence supports a primary role of osmotic mechanisms in determining a tight link between nuclear and cytoplasmic volume, but this hypothesis remains largely untested in mammalian cells. We approach the question in single cultured adhering human cells, by jointly measuring cytoplasmic and nuclear volumes, in real time and across cell cycles. Surprisingly, we find that cytoplasmic and nuclear volumes follow different average growth laws: while the cytoplasm grows exponentially, the nucleus grows linearly. Moreover, by combining several experimental perturbations and analyzing a mathematical model including osmotic effects and tension, we conclude that the mechanical forces exerted by the cytoskeleton on the nuclear envelope can strongly affect nucleus-cytoplasm volumetric coupling by biasing nuclear import. Our results unveil how osmo-mechanical equilibrium regulates nuclear size in mammalian cells. One-Sentence SummaryCytoskeletal forces exerted on the nuclear envelope impact on nuclear volume through modulation of force-coupled nucleo-cytoplasmic transport, affecting osmosis.

cell biology↗

PIP4K2B is a mechanosensor and induces heterochromatin-driven nuclear softening through UHRF1.

Phosphatidylinositol-5-phosphate (PtdIns5P)-4-kinases (PIP4Ks) are stress-regulated phosphoinositide kinases able to phosphorylate PtdIns5P to PtdIns(4, 5)P2. In cancer patients their expression is typically associated with bad prognosis. Among the three PIP4K isoforms expressed in mammalian cells, PIP4K2B is the one with more prominent nuclear localization. Here, we unveil the role for PIP4K2B as mechanosensor. PIP4K2B protein level, indeed, strongly decreases in cells growing on soft substrates. Its direct silencing or pharmacological inhibition, mimicking cell response to soft, triggers a concomitant reduction of the epigenetic regulator UHRF1 and induces changes in nuclear polarity, nuclear envelope tension and chromatin compaction. This substantial rewiring of the nucleus mechanical state drives YAP cytoplasmic retention and impairment of its activity as transcriptional regulator, finally leading to defects in cell spreading and motility. Since YAP signalling is essential for initiation and growth of human malignancies, our data suggest that potential therapeutic approaches targeting PIP4K2B could be beneficial in the control of the altered mechanical properties of cancer cells.

cell biology↗