Strategies To Modify the Surface and Bulk Properties of 3D-Printed Solid Scaffolds for Tissue Engineering Applications.

3D printing is one of the effective scaffold fabrication techniques that emerged in the 21st century that has the potential to revolutionize the field of tissue engineering. The solid scaffolds developed by 3D printing are still one of the most sought-after approaches for developing hard-tissue regeneration and repair. However, applications of these solid scaffolds get limited due to their poor surface and bulk properties, which play a significant role in tissue integration, loadbearing, antimicrobial/antifouling properties, and others. As a result, several efforts have been directed to modify the surface and bulk of these solid scaffolds. These modifications have significantly improved the adoption of 3D-printed solid scaffolds and devices in the healthcare industry. Nevertheless, the in vivo implant applications of these 3D-printed solid scaffolds/devices are still under development. They require attention in terms of their surface/bulk properties, which dictate their functionality. Therefore, in the current review, we have discussed different 3D-printing parameters that facilitate the fabrication of solid scaffolds/devices with different properties. Further, changes in the bulk properties through material and microstructure modification are also being discussed. After that, we deliberated on the techniques that modify the surfaces through chemical and material modifications. The computational approaches for the bulk modification of these 3D-printed materials are also mentioned, focusing on tissue engineering. We have also briefly discussed the application of these solid scaffolds/devices in tissue engineering. Eventually, the review is concluded with an analysis of the choice of surface/bulk modification based on the intended application in tissue engineering.

Human satellite-III non-coding RNAs modulate heat-shock-induced transcriptional repression.

The heat shock response is a conserved defense mechanism that protects cells from physiological stress, including thermal stress. Besides the activation of heat-shock-protein genes, the heat shock response is also known to bring about global suppression of transcription; however, the mechanism by which this occurs is poorly understood. One of the intriguing aspects of the heat shock response in human cells is the transcription of satellite-III (Sat3) long non-coding RNAs and their association with nuclear stress bodies (nSBs) of unknown function. Besides association with the Sat3 transcript, the nSBs are also known to recruit the transcription factors HSF1 and CREBBP, and several RNA-binding proteins, including the splicing factor SRSF1. We demonstrate here that the recruitment of CREBBP and SRSF1 to nSBs is Sat3-dependent, and that loss of Sat3 transcripts relieves the heat-shock-induced transcriptional repression of a few target genes. Conversely, forced expression of Sat3 transcripts results in the formation of nSBs and transcriptional repression even without a heat shock. Our results thus provide a novel insight into the regulatory role for the Sat3 transcripts in heat-shock-dependent transcriptional repression.