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Thickness control of 2D nanosheets assembled from precise side-chain giant molecules.

ABSTRACT: The performance of 2D nanomaterials hinges on both the chemical compositions and the morphological structures across different length scales. Among all the three dimensions, thickness is the only one that falls into the nanometer scale and, to some extent, determines the intrinsic properties of 2D nanomaterials. In this study, we report the preparation and precise thickness control of 2D nanosheets assembled from a library of monodispersed amphiphilic giant molecules composed of functional polyhedral oligomeric silsesquioxanes (POSSs) as the side groups. Solution self-assembly of such giant molecules resulted in 2D nanosheets with similar structural configurations, where a bilayer of hydrophobic isobutyl POSS (BPOSS) is sandwiched by two monolayers of hydrophilic POSS bearing carboxylic acid groups (APOSS). The thickness of the obtained nanosheets could be tuned through adjusting the chemical compositions of the pendant POSS cages. Intriguingly, we found that the thickness of the 2D nanosheets was not necessarily proportional to the contour length of the giant molecule nor the total number of POSS cages tethered to the main chain. Indeed, the number ratio of BPOSS to APOSS, rather than the exact number, played a deterministic role in the thickness control. To explain the unusual thickness dependence, we built up a structure model with an in-plane orientation of the giant molecules in the nanosheets, from which a formula was further deduced to semi-quantitatively describe the inverse relationship between the overall thickness and the number ratio of BPOSS to APOSS.

SUBMITTER: Feng F

PROVIDER: S-EPMC8179583 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:The peripheral nervous system has an astonishing ability to regenerate following a compression or crush injury; however, the potential for full repair following a transection injury is much less. Currently, the major clinical challenge for peripheral nerve repair come from long gaps between the proximal and distal nerve stumps, which prevent regenerating axons reaching the distal nerve. Precise axon targeting during nervous system development is controlled by families of axon guidance molecules including Netrins, Slits, Ephrins and Semaphorins. Several recent studies have indicated key roles of Netrin1, Slit3 and EphrinB2 signalling in controlling the formation of new nerve bridge tissue and precise axon regeneration after peripheral nerve transection injury. Inside the nerve bridge, nerve fibroblasts express EphrinB2 while migrating Schwann cells express the receptor EphB2. EphrinB2/EphB2 signalling between nerve fibroblasts and migrating Schwann cells is required for Sox2 upregulation in Schwann cells and the formation of Schwann cell cords within the nerve bridge to allow directional axon growth to the distal nerve stump. Macrophages in the outermost layer of the nerve bridge express Slit3 while migrating Schwann cells and regenerating axons express the receptor Robo1; within Schwann cells, Robo1 expression is also Sox2-dependent. Slit3/Robo1 signalling is required to keep migrating Schwann cells and regenerating axons inside the nerve bridge. In addition to the Slit3/Robo1 signalling system, migrating Schwann cells also express Netrin1 and regenerating axons express the DCC receptor. It appears that migrating Schwann cells could also use Netrin1 as a guidance cue to direct regenerating axons across the peripheral nerve gap. Engineered neural tissues have been suggested as promising alternatives for the repair of large peripheral nerve gaps. Therefore, understanding the function of classic axon guidance molecules in nerve bridge formation and their roles in axon regeneration could be highly beneficial in developing engineered neural tissue for more effective peripheral nerve repair.

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Thickness control of 2D nanosheets assembled from precise side-chain giant molecules.

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