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Biology subjects

Descroix, S.

Publications and source records attributed to Descroix, S..

12 recordsLinked to original sources

Fluid transport properties dominate blastocyst expansion over mechanics

Lumens populate most of our organs and their size, which dynamically changes throughout the day and lifetime, can influence their function. During mammalian development, the first lumen appears in the blastocyst. Surface epithelial cells pump ions to build an osmotic gradient that draws water, which inflates the embryo and stretches the epithelium as well as the zona pellucida, an elastic shell protecting the embryo. Blastocyst expansion is not steady and instead undergoes cycles of expansion interrupted by collapses during which the lumen leaks out. Early studies identified the critical role of osmotic pressure difference in regulating the expansion of the blastocyst whereas recent studies proposed that mechanical stresses would set the size of the embryo. However, the relative contributions of osmotic and mechanical stresses to lumen expansion dynamics remain unclear. Here, we investigate this using microfluidics, biophysics, machine learning and modelling on mouse embryos. Breaking down the expansion dynamics of mouse embryos, we discovered that fluid pumping rate accelerates, compensating for the increased frequency of collapses interrupting episodes of expansion. We reasoned that fluid transport could be rate limited by osmotic pumping, water permeability and/or mechanical constraints. Removing the mechanical constraint from the zona pellucida only marginally affected these expansion dynamics. Forcing fluid exchange with osmotic shocks we measured that water permeability is large enough not to restrict fluid accumulation rates. Finally, we estimate ion pumping for mouse blastocysts and interfere with it using inhibitors to measure how it quantitatively sets blastocyst expansion rates. Together, we propose that osmotic pressure differences, regulated by fluid transport properties, dominate over mechanical stresses in controlling blastocyst expansion dynamics.

developmental biology↗

Tumor-on-Chip as a Personalised Platform for Rapid Drug-Testing in Breast Cancer

Breast cancer (BC) remains one of the most common malignancies worldwide and continues to pose major therapeutic challenges, emphasizing the need for functional models that can inform fast treatment selection. Currently, patient-derived xenografts (PDXs) and organoids (PDOs) are valuable biological models for functional precision oncology; however, variable success rates of establishment and prolonged timelines limit their clinical application for real-time drug testing. To overcome this, we developed a Tumor-on-Chip (ToC) platform that enables functional drug sensitivity profiling within a clinically actionable 4-day timeframe. We compared ToC models with PDX results, and demonstrated high reproducibility and strong concordance with in vivo PDX responses. Drug sensitivity was correctly identified ex vivo in 88% of PDX-responsive cases, while resistance was detected in 91%, with no false positives at clinically relevant drug concentrations. To facilitate clinical translation, we engineered a custom microfluidic chip optimized for minimal breast cancer biopsy material, yielding results similar to those obtained from resection samples. We ultimately demonstrated the proof-of-concept for applying this platform to patient samples as a further tool for guiding clinical decision-making and discriminated between resistance and sensitive profiles among patients. These findings demonstrate the feasibility and translational potential of ToC models for personalized drug profiling in breast cancer, laying the groundwork for their integration into real-time clinical decision-making workflows.

bioengineering↗

Shaping and probing living tissues with magnetic bioprinting

Mechanical and geometric cues play a crucial role in vivo, regulating both morphogenetic processes and proper tissue function. This is particularly evident in skeletal muscle, where aligned architecture is essential for myogenesis and functional force generation. However, precisely engineering tissue geometry at both macroscopic and microscopic scales while simultaneously controlling internal mechanical forces remains a significant challenge. In this study, we introduce a magnetic tissue engineering platform based on a magnetic bioprinting technique, enabling precise control of biophysical cues that guide in vitro tissue morphogenesis. Applied here to skeletal muscle, this approach allows for the rapid fabrication of cohesive tissues in any desired shape using cells labeled with magnetic nanoparticles. Additionally, multiple cell types can be incorporated and spatially organized within the same construct through magnetic segregation. Optimizing tissue geometry further enables magnetic actuation, including the ability to trap and maintain tissue shape over time. Furthermore, this magnetic platform facilitates the investigation of how tissue architecture influences mechanical properties, such as resistance to rupture. Overall, this study highlights the significant potential of magnetic bioprinting and stimulation for controlling tissue morphology and advancing biomechanical research.

bioengineering↗

Magnetic printing and actuation of stretchable muscle tissue

While the link between tissue organization, stimulation, and function is now acknowledged as crucial for tissue development, engineering tissues with precise, long-lasting shapes and the capability for mechanical stimulation remains challenging. This study addresses this challenge by developing a next-generation magnetic bioprinting approach to create anisotropic, shape-controlled, scaffold-free, and stretchable skeletal muscle constructs. Murine skeletal muscle cells and human induced pluripotent stem cell-derived skeletal muscle cells, labeled with iron oxide nanoparticles, were magnetically bioprinted into wrench-shaped tissues. Their magnetic properties allowed these tissues to be clipped onto magnetic needles, preserving their shape over two weeks of culture while promoting anisotropic differentiation and myoblast fusion. Additionally, the magnetic tissues could be stretched by up to 100%, enhancing their anisotropy and improving muscle maturation. This magnetic toolbox demonstrates significant advancements in muscle tissue engineering, as evidenced by enhanced indicators of myoblast differentiation, including cell fusion, increased myogenic maturation and contractility. These findings highlight the potential of magnetic-based techniques for developing advanced muscle-on-chip systems and other complex tissue constructs.

bioengineering↗

Magnetite Nanoparticle Photothermal Therapy in a Pancreatic Tumor-on-Chip: A Dual-Action Approach Targeting Cancer Cells and their Microenvironment

The application of magnetite nanoparticles (MagNPs) for photothermal therapy (MagNP-PTT) has recently expanded in cancer treatment. This study introduces MagNP-PTT in a tumor-on-chip model to target highly aggressive pancreatic ductal adenocarcinoma (PDAC). A tumor-on-chip system was developed using PANC-1 PDAC cells embedded in a collagen type I extracellular matrix and cultured for one week to form tumor spheroids. This platform serves as the foundation for applying PTT in a model system that is aimed to mimic the native tumor microenvironment. MagNPs efficiently penetrate the tumor spheroids, achieving controlled heating via near-infrared (NIR) light. By adjusting nanoparticle concentration and laser power, temperature increments of 2{degrees}C between 38-48{degrees}C were established. Temperatures above 44{degrees}C significantly increased cell death, while lower temperatures allowed partial recovery. Beyond inducing cancer cell death, MagNP-PTT altered the extracellular matrix, and triggered a slight epithelial-mesenchymal transition marked by increased vimentin expression. These findings highlight MagNP-PTT as a dual-action therapy, targeting both tumor cells and their microenvironment, offering a novel approach for overcoming stromal barriers in pancreatic cancer treatment. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=99 SRC="FIGDIR/small/636875v1_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@9b9c20org.highwire.dtl.DTLVardef@272c7aorg.highwire.dtl.DTLVardef@1d91021org.highwire.dtl.DTLVardef@1b1ea8d_HPS_FORMAT_FIGEXP M_FIG SYNOPSIS TABLE OF CONTENTS C_FIG

cancer biology↗

PIEZO-dependent mechano-sensing of the niche is essential for intestinal stem cell fate decision and maintenance

Stem cells continuously perceive and respond to various environmental signals to maintain homeostasis. In addition to biochemical factors, the stem cell niche is subjected to mechanical and physical cues. However, it remains unclear how stem cells can sense mechanical signals from their niche in vivo. Since intestinal stem cells constantly and directly face the external environment, we investigated the roles of mechano-sensing PIEZO ion channels in the gut stem cell niche. By employing mouse genetics and performing single-cell RNAseq analysis, we revealed the absolute requirement for PIEZO channels in intestinal stem cell (ISC) state dynamics and maintenance. In vivo measurement of basement membrane region stiffness demonstrated that ISCs reside in a more rigid microenvironment at the bottom of the crypt. Using 3D and 2D organoid systems combined with bioengineered substrates and a cell stretching device, we found that PIEZO channels are activated by high extracellular matrix stiffness and tissue tension to modulate ISC behavior. This study delineates the mechanistic cascade of PIEZO channel activation in ISCs from the upstream extracellular stimuli through the downstream signaling activation that coordinates stem cell fate decision and maintenance.

cell biology↗

Decoupling shear stress and pressure effects in the biomechanics of autosomal dominant polycystic kidney disease using a perfused kidney-on-chip.

Kidney tubular cells are submitted to two distinct mechanical forces generated by the urine flow: shear stress and hydrostatic pressure. In addition, the mechanical properties of the surrounding extracellular matrix modulate tubule deformation under constraints. These mechanical factors likely play a role in the pathophysiology of kidney diseases as exemplified by autosomal dominant polycystic kidney disease, in which pressure, flow and matrix stiffness have been proposed to modulate the cystic dilation of tubules with PKD1 mutations. The lack of in vitro systems recapitulating the mechanical environment of kidney tubules impedes our ability to dissect the role of these mechanical factors. Here we describe a perfused kidney-on-chip with tunable extracellular matrix mechanical properties and hydrodynamic constraints, that allows a decoupling of shear stress and flow. We used this system to dissect how these mechanical cues affect Pkd1-/- tubule dilation. Our results show two distinct mechanisms leading to tubular dilation. For PCT cells (proximal tubule), overproliferation mechanically leads to tubular dilation, regardless of the mechanical context. For mIMCD-3 cells (collecting duct), tube dilation is associated with a squamous cell morphology but not with overproliferation and is highly sensitive to extracellular matrix properties and hydrodynamic constraints. Surprisingly, flow alone suppressed Pkd1-/- mIMCD-3 tubule dilation observed in static conditions, while the addition of luminal pressure restored it. Our in vitro model emulating nephron geometrical and mechanical organization sheds light on the roles of mechanical constraints in ADPKD and demonstrates the importance of controlling intraluminal pressure in kidney tubule models.

biophysics↗

Cilia to basement membrane signalling is a biomechanical driver of autosomal dominant polycystic kidney disease

Autosomal dominant polycystic kidney disease (ADPKD), which affects around 4 million patients worldwide, is characterized by the formation of multiple tubule derived cysts, which grossly enlarge both kidneys and progressively compromise renal function. ADPKD mainly results from mutations in PKD1, leading to the loss of polycystin-1 protein, which localizes to primary cilia. Primary cilia are required for cyst formation but the biomechanical changes underlying cystogenesis upon loss of polycytin-1 are unknown. We find that cilia and polycystin-1 shape the tubular basement membrane (TBM). Combining orthologous mouse models with a tubule-on-chip approach allowing manipulations of TBM stiffness, we find that cilia regulate the composition and biomechanical properties of the TBM. In the setting of polycytin-1 loss, reduced TBM stiffness and increased luminal pressure act as biomechanical drivers of cyst formation. These findings suggest a novel biomechanical model for ADPKD and unveil that cilia to TBM signalling controls kidney shape.

physiology↗

Magnetic Microtweezers for High-Throughput Bioseparation in Sub-Nanoliter Droplets

Multiomics studies at single-cell level require small volume manipulation, high throughput analysis and multiplexed detection, characteristics that droplet microfluidics can tackle. However, the initial step of molecules bioseparation remains challenging. Here, we describe a unique magnetic device to trap and extract magnetic particles in sub-nanoliter droplets, for compartmentalisation of detection steps. Relying on electrodeposition of NiFe structures and microfluidic manipulation, this technology has allowed the purification of genetic material at single-cell scale and was able to reach an extraction rate of 72% for a sample of purified oligonucleotides.

bioengineering↗

Arp2/3 inhibition switches Eps8's network associations to favour longer actin filament formation necessary for tunneling nanotubes

Tunneling nanotubes (TNTs) connect distant cells and mediate cargo transfer for intercellular communication in physiological and pathological contexts. How cells generate these actin-mediated protrusions to span lengths beyond those attainable by canonical filopodia remains unknown. Through a combination of micropatterning, microscopy and optical tweezer-based approaches, we demonstrate that TNTs forming through the outward extension of actin (not through cellular dislodgement) achieve distances greater than the mean length of filopodia, and that branched Arp2/3-dependent pathways attenuate the extent to which actin polymerizes in nanotubes, limiting TNT occurrence. Proteomic analysis using Epidermal growth factor receptor kinase substrate 8 (Eps8) as a positive effector of TNTs showed that upon Arp2/3 inhibition, proteins enhancing filament turnover and depolymerization were reduced and Eps8 instead exhibited heightened interactions with the inverted Bin/Amphiphysin/Rvs (I-BAR) domain protein IRSp53 that provides a direct connection with linear actin polymerases. Our data reveals how common protrusion players (Eps8 and IRSp53) form TNTs, and that when competing pathways overutilizing such proteins and monomeric actin in Arp2/3 networks are inhibited, processes promoting linear actin growth dominate to favour TNT formation. Thus, this work reinforces a general principle for actin network control for cellular protrusions where simple shifts in the balance between processes that inhibit actin growth versus those that promote growth dictate protrusion formation and the ultimate length scales protrusions achieve.

cell biology↗

Evolution of a confluent gut epithelium under cyclic stretching

The progress of food in the gastrointestinal (GI) tract is driven by a peristaltic motion generated by the muscle belt surrounding the GI tract. In turn, the response of the intestinal epithelial cells to the peristaltic stresses affects the dynamics of the epithelial structure. In this work, we study the effect of cyclic stretching (0.125 Hz, 10% strain) on the spatial organization of the intestinal epithelium using intestinal cells deposited on a flat elastomeric substrate to mimic the peristaltic motion in vitro. A confluent monolayer of Caco-2 cells is grown on a PDMS chip to probe the morphological and orientational response of the tissue to cyclic stretching. The PDMS chips are either covalently or non-covalently coated with laminin to recapitulate the basement membrane. We observe a significant orientational response where the cells rearrange their long axes perpendicular to the stretching direction for both coating conditions. The experiment is modeled by a vertex model where the cells store elastic energy with varying strain and effectively have a rotational diffusive motion through rearrangements of their shapes. The model also predicts a transition between the perpendicular orientation and orientation at an oblique angle determined by the level of the cell elastic anisotropy. It provides a general framework to study cell response and relaxation dynamics under cyclic stretching across different cell types. We also discuss potential relevance of peristalsis in determining planar cell polarity in 3D architectures.

biophysics↗

Cancer-associated fibroblasts actively compress cancer cells and modulate mechanotransduction

During tumor progression, cancer-associated fibroblasts (CAFs) accumulate in tumors and produce excessive extracellular matrix (ECM), forming a capsule that enwraps cancer cells. This capsule is a barrier that restricts tumor growth leading to the buildup of intratumoral pressure. Combining genetic and physical manipulations in vivo with microfabrication and force measurements in vitro, we found that the CAFs capsule is not a passive barrier but instead actively compresses cancer cells using actomyosin contractility. Cancer cells mechanosense CAF compression, resulting in an altered localization of the transcriptional regulator YAP. Abrogation of CAFs contractility in vivo leads to the dissipation of compressive forces and impairment of capsule formation. By mapping CAF force patterns in 3D, we show that compression is a CAF-intrinsic property independent of cancer cell growth. Supracellular coordination of CAFs is achieved through fibronectin cables that serve as scaffolds allowing force transmission. Our study unveils that the contractile capsule actively compresses cancer cells, modulates their mechanical signaling, and reorganizes tumor morphology.

cell biology↗