Search bioRxiv⌕ Search

bioRxiv · 10.1101/2024.10.26.619288

Systematic standardization of organ-on-a-chip under controlled flow conditions: use case with Caki-1 and A549 cell lines

Abstract

New in vitro models are an urgent need for to improve both the research data and the preclinical development of new drugs. Current standardized cellular models are mainly based in 2D cell culture, which lacks flow conditions and with complex co-culture settings. In this way, advanced cell culture models, such as organ-on-a-chip (OoC), aim to solve these limitations. OoC systems are composed by a microfluidic chip functionalized with different combinations of extracellular matrixes, coatings and cell cultures to mimic the physiological conditions of human organs. Advantages of OoC include the possibility to add 3D structures, delimited regions for co-culture and dynamic flow conditions to cell cultures. However, to perform reproducible and controlled experiments with OoC, it is necessary to systematically standardize the cell culture conditions in the microfluidic channels. For this is necessary to test both the combination of flow and extracellular matrix (ECM) coating to reliably mimic the human organ physiology. In this work, we standardized both conditions, ECM coating and the flow conditions to functionalize OoC with cell lines from kidney (Caki-1) and from lung (A549) to develop OoC systems beyond the Vessel-on-a-chip setting. In this way, the protocol detailed in this work will allow to standardize cell culture on different optimized OoC types with different cell types from different origins.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Balsa-Diaz, A., Vazquez-Vazquez, L., Ferreiro-Vila, E., Rivas-Meizoso, L., Martinez, A. L., Brea, J., Loza, M. I., Perez Rodriguez, S., Sinde, E., Alvarez, E., Rodino-Janeiro, B. K.. 2024-10-27. Systematic standardization of organ-on-a-chip under controlled flow conditions: use case with Caki-1 and A549 cell lines. https://doi.org/10.1101/2024.10.26.619288

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

HUH-tag conjugation enables accessible, site-specific functionalization of DNA origami with signaling-competent proteins

DNA origami enables precise nanometer scale control over the number, spacing, and geometry of biomolecules, making it a powerful tool for dissecting spatially organized biological processes such as receptor signaling. However, functionalizing origami with proteins remains a bottleneck restricting the technology to specialized laboratories. Here we show that viral-derived HUH endonuclease tags, small (~10 kDa) domains that form a covalent phosphotyrosine bond with short unmodified ssDNA, provide a simple and cost-effective route to decorating DNA origami with functional proteins. Using interleukin-1{beta} (IL-1{beta}) as a model ligand, we generated recombinant IL-1{beta}-HUH, achieved efficient site-specific conjugation to unmodified ssDNA within minutes, and coupled the conjugates to a DNA origami pegboard with tunable stoichiometry. IL-1{beta}-functionalized origami triggered ligand-dependent signalling in living cells and allowed visualization of the recruitment of downstream signaling molecules, confirming that HUH-tag conjugation preserves functionality. Because this strategy requires only standard molecular biology equipment and unmodified DNA, it lowers a technical and financial barrier to DNA origami-based experimentation, opening the approach to a broader range of biological questions and laboratories outside the DNA nanotechnology field.

cell biology↗

Global mapping of VEGF-A driven changes in the RNA bound phospho-proteome reveals a molecular switch to coordinate angiogenesis in endothelial cells

RNA binding proteins (RBPs) serve as upstream master regulators of cellular fate transitions at the post-transcriptional level. RBP-RNA interactions are dynamically regulated by post-translational modifications to coordinate cellular responses. We hypothesised that changes in RBP phosphorylation will play a key role in coordinating angiogenesis, the formation of new blood vessels, in endothelial cells (ECs). Therefore, we used phospho-proteomic analysis of the mRNA bound proteome to identify global phosphorylation changes in mouse cardiac ECs during acute and prolonged VEGF-A stimulation. Of the differentially phosphorylated RBPs, we found that the phosphorylation of serine 199 within mRNA bound Phf6 (PHD finger protein 6) was consistently increased following VEGF-A stimulation. Phf6 phosphorylation at this specific site was sufficient and required to induce a pro-angiogenic phenotype, facilitating a change in Phf6 conformation promoting interaction with distinct RNAs. We show here that Phf6 phosphorylation at serine 199, downstream of VEGF-A, acts as a molecular switch to differentially coordinate a decrease of anti-angiogenic RNAs (i.e. extracellular matrix genes) and an increase in pro-angiogenesis related RNAs, in part by differentially regulating their stability, to promote angiogenesis.

cell biology↗

Metaplasia Orchestrates Tissue Recovery and Immune Remodeling Through CD73 in Chronic Pancreatitis

Chronic inflammatory injury promotes epithelial metaplasia, and progression from metaplasia to dysplasia is a recognized initiating event in carcinogenesis, as metaplastic cells exhibit heightened susceptibility to genetic alterations. In the pancreas, persistent acinar-to-ductal metaplasia (ADM) can progress to pancreatic intraepithelial neoplasia (PanIN), yet the mechanisms that determine whether ADM resolves or persists with fibrosis and sustained inflammation remain poorly defined. Here, we identify CD73 as a central regulator of ADM fate, tissue repair, and immune microenvironment remodeling during chronic pancreatic injury. Analysis of previously published single-cell RNA sequencing dataset from chronic pancreatitis (CP) tissues identified enrichment of Nt5e, which encodes CD73, within Hnf1{beta} ADM populations. Hnf1bCreERT2 and CD73fl/fl;Hnf1bCreERT2 mice were treated with caerulein for 4 weeks to induce pancreatitis and ADM prior to tamoxifen-induced deletion of CD73 in HNF1B-expressing metaplastic epithelial cells. Histologic phenotyping and immune profiling were performed using immunohistochemistry and imaging mass cytometry. Metaplasia-specific CD73 deletion exacerbated pancreatic injury and fibrosis, impaired epithelial proliferation and recovery of the acinar compartment, and altered the abundance and spatial organization of inflammatory cells. Ex vivo ADM assays further demonstrated that CD73 loss increased ADM formation and the production of MCP-1 and TIMP-1. These findings identify CD73 as a context-dependent checkpoint linking epithelial plasticity and immune modulation during chronic pancreatic injury and tissue repair.

cell biology↗