DNA-coated colloids hold great promise for self-assembly of programmed heterogeneous microstructures, provided they not only bind when cooled below their melting temperature, but also rearrange so that aggregated particles can anneal into the structure that minimizes the free energy. Unfortunately, DNA-coated colloids generally collide and stick forming kinetically arrested random aggregates when the thickness of the DNA coating is much smaller than the particles. Here we report DNA-coated colloids that can rearrange and anneal, thus enabling the growth of large colloidal crystals from a wide range of micrometre-sized DNA-coated colloids for the first time. The kinetics of aggregation, crystallization and defect formation are followed in real time. The crystallization rate exhibits the familiar maximum for intermediate temperature quenches observed in metallic alloys, but over a temperature range smaller by two orders of magnitude, owing to the highly temperature-sensitive diffusion between aggregated DNA-coated colloids.

Colloids with well-defined multicavities are synthesized through the hydrolytic removal of silica cluster templates from organo-silica hybrid patchy particles. The geometry of the cavities stems from the originally assembled cluster templates, displaying well-defined three-dimensional symmetries, ranging from spherical, linear, triangular, tetrahedral, trigonal dipyramidal, octahedral, to pentagonal dipyramidal. The concave surface of the cavities is smooth, and the cavity shallowness and size can be varied. These particles with multicavities can act as "lock" particles with multiple "key holes". Up to n "key" particles can self-assemble into the lock particles via depletion interaction, resulting in multivalent, site-specific, reversible, and flexible bonding.

We report on synthetic strategies to fabricate DNA-coated micrometer-sized colloids that, upon thermal annealing, self-assemble into various crystal structures. Colloids of a wide range of chemical compositions, including poly(styrene), poly(methyl methacrylate), titania, silica, and a silica-methacrylate hybrid material, are fabricated with smooth particle surfaces and a dense layer of surface functional anchors. Single-stranded oligonucleotides with a short sticky end are covalently grafted onto particle surfaces employing a strain-promoted alkyne-azide cycloaddition reaction resulting in DNA coatings with areal densities an order of magnitude higher than previously reported. Our approach allows the DNA-coated colloids not only to aggregate upon cooling but also to anneal and rearrange while still bound together, leading to the formation of colloidal crystal compounds when particles of different sizes or different materials are combined.

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BackgroundChronic muscle injury is characteristics of fatty infiltration and fibrosis. Recently, fibro/adipogenic progenitors (FAPs) were found to be indispensable for muscular regeneration while were also responsible for fibrosis and fatty infiltration in muscle injury. Many myokines have been proven to regulate the adipose or cell proliferation. Because the fate of FAPs is largely dependent on microenvironment and the regulation of myokines on FAPs is still unclear. We screened the potential myokines and found Interleukin-15 (IL-15) may regulate the fatty infiltration in muscle injury. In this study, we investigated how IL-15 regulated FAPs in muscle injury and the effect on muscle regeneration.MethodsCell proliferation assay, western blots, qRT-PCR, immunohistochemistry, flow cytometric analysis were performed to investigate the effect of IL-15 on proliferation and adipogensis of FAPs. Acute muscle injury was induced by injection of glycerol or cardiotoxin to analyze how IL-15 effected on FAPs in vivo and its function on fatty infiltration or muscle regeneration.ResultsWe identified that the expression of IL-15 in injured muscle was negatively associated with fatty infiltration. IL-15 can stimulate the proliferation of FAPs and prevent the adipogenesis of FAPs in vitro and in vivo. The growth of FAPs caused by IL-15 was mediated through JAK-STAT pathway. In addition, desert hedgehog pathway may participate in IL-15 inhibiting adipogenesis of FAPs. Our study showed IL-15 can cause the fibrosis after muscle damage and promote the myofiber regeneration. Finally, the expression of IL-15 was positively associated with severity of fibrosis and number of FAPs in patients with chronic rotator cuff tear.ConclusionsThese findings supported the potential role of IL-15 as a modulator on fate of FAPs in injured muscle and as a novel therapy for chronic muscle injury.Electronic supplementary materialThe online version of this article (10.1186/s12964-018-0251-0) contains supplementary material, which is available to authorized users.