Magnetic-microcontact printing based ECM nano-patterning allows homogeneous controlling of cell growth and behavior
Poster Dec 12, 2017
Marc Botcherby1*, Julie Foncy2, Adriana Lagraulet3**, Benjamin Berteloite3**, Aurore Esteve2, Marie-Charline Blatche4, Laurent Malaquin2 & Christophe Vieu2,5
Surface nano-patterning with biochemical cues has been shown to be a very powerful tool to control cell growth and attachment. However, manual patterning methods are unable to assure pattern homogeneity in large surface, introducing biases in the analysis of cell response face to external stimuli such as drugs, toxins or others. Here we present a new patterning method that allows to automatically pattern large surfaces such as whole microscope slides or 4in wafers. Using magnetic-microcontact printing, microscope slides were printed with different 50-150 µm patterns of extracellular matrix proteins (ECM) with a pitch of 40-220 µm. PC3-GFP cells were cultured on patterned slides. Fluorescence detection was used to evaluate cell spread homogeneity on nano-patterns. Results show homogeneous cell growth and attachment on defined patterns all along the patterned surface. Using this new methodology, the study of cell behavior in response to well-controlled biochemical surface cues can be studied. In the context of multiplexed assays for high-throughput screening, automated magnetic-microcontact printing is a method of choice providing a high level of reproducibility and homogeneity over large surface of analysis.
Genome-wide association studies (GWAS) have identified more than 100 genetic loci associated with type 2 diabetes. The majority of these are located in the intergenic or intragenic regions suggesting that the implicated variants may alter chromatin conformation. This, in turn, is likely to influence the expression of nearby or more remotely located genes to alter beta cell function. At present, however, detailed molecular and functional analyses are still lacking for most of these variants. We recently analysed one of these loci and mapped five causal variants in an islet-specific enhancer cluster within the STARD10 gene locus. Here, we aimed to understand how these causal variants influence b-cell function by alteration of the chromatin structure of enhancer clusterREAD MORE