SRGN, a new identified shear-stress-responsive gene in endothelial cells.

Endothelial cells (ECs) play an important role in the pathogenesis of cardiovascular disease, especially atherosclerosis (AS). The abnormal wall shear stress (WSS) which directly contacts with ECs is the key stimulating factor leading to AS. However, the underlying mechanism of ECs responding to WSS is still incompletely understood. This study aims to explore the novel mechano-sensitive genes and its potential mechanism in response to WSS in ECs by employing bioinformatics methods based on previously available high-throughput data from zebrafish embryos, both before and after blood flow formation. Six common differentially expressed genes (DEGs) (SRGN, SLC12A3, SLC25A4, PVALB1, ITGAE.2, zgc:198419) were selected out from two high-throughput datasets (GSE126617 and GSE20707) in the GEO database. Among them, SRGN was chosen for further verification through the in vitro shear stress loading experiments with human umbilical vein endothelial cells (HUVECs) and the in vivo partial ligation of carotid artery in mice. Our data indicated that low shear stress (LSS) could enhance the expression of SRGN via the PKA/CREB-dependent signaling pathway. The proportion of Ki67+ cells and the concentration of nitric oxide (NO) were high in SRGN high expression cells, suggesting that SRGN may be involved in the proliferation of HUVECs. Furthermore, in the partial ligation of the carotid artery mice model, we observed that the expression of SRGN was significantly increased in atherosclerotic plaques induced by abnormal shear stress. Taken together, this study demonstrated that SRGN is a key gene in the response of ECs to WSS and could be involved in AS.

Site-specific variations in surface structure and Young's modulus of human hair surfaces at the nanometer scale as induced through bleach treatment.

The effect of bleach treatments on the morphology and mechanical properties of hair surfaces was measured at the nanometer scale using atomic force microscopy. We used an ultrahigh-precision relocation technique to observe the variations in these properties at precise locations on hair surfaces in their virgin state and then after each of the two bleach treatments, to rule out position-dependent fluctuations. We demonstrate that statistically significant variations in roughness and Young's modulus are observed as a result of exposure to bleach, which is known to disrupt the disulfide linkage network throughout the fiber. The rate at which surface roughness changes increased with the number of treatments, with very little effect seen after 10 min, and an increase of up to 65% was observed after a further 10 min. The Young's modulus decreased by up to 40% after each treatment. We also investigate micropores and show that they are subsurface, but revealed through bleaching, and oriented along the direction of the hair shaft with a characteristic aspect ratio. This work demonstrates the profound effect bleaching has on the molecular structure of hair, which manifests as changes in morphology and stiffness, and this should be taken into account in the formulation of future hair-care products.

Nanoparticles retard immune cells recruitment in vivo by inhibiting chemokine expression.

The large-scale utilization of nanotechnology depends on public and consumer confidence in the safety of this new technology. Studying the interaction of nanoparticles with immune cells plays a vital role in the safety assessment of nanomedicine. Although some researches have indicated that the immune cells undergo severe interfere after phagocytosis of nanoparticles, the impact on immune system of the whole body are still unclear. Here, we use immune cells labeled transgenic zebrafish to study the mechanisms of nanoparticles on zebrafish immune cells. We demonstrate that gold nanoparticles (Au NPs) phagocytized by immune cells can reduce and retard the sensitivity of immune response, resulting nanoparticle-induced bluntness in immune cell (NIBIC). RNA-seq and functional analysis reveal that NIBIC is mainly induced by the inhibiting expression of chemokine receptor 5 (CCR5). Furthermore, PVP-modified Au NPs can eliminate NIBIC by inhibiting the cell phagocytosis. Our results highlight the potential risk for Au NPs in vivo and further the understanding of the mechanism of the interaction between Au NPs and the immune response. We should consider this factor in future material design and pay more attention to the process of using nanomedicines on immune diseases.

Photooxidation crosslinking to recover residual stress in decellularized blood vessel.

Decellularization method based on trypsin-digestion is widely used to construct small diameter vascular grafts. However, this method will reduce the opening angle of the blood vessel and result in the reduction of residual stress. Residual stress reduced has an adverse effect on the compliance and permeability of small diameter vascular grafts. To improve the situation, acellular blood vessels were treated with glutaraldehyde and photooxidation crosslinking respectively, and the changes of opening angle, circumferential residual strain of native blood vessels, decellularized arteries and crosslinked blood vessels were measured by means of histological examination, scanning electron microscopy (SEM) and transmission electron microscopy (TEM) in this study. The opening angle of decellularized arteries significantly restored after photooxidation crosslinking (P = 0.0216), while that of glutaraldehyde crosslinking blood vessels reduced. The elastic fibers inside the blood vessels became densely rearranged after photooxidation crosslinking. The results of finite element simulation showed that the residual stress increased with the increase of opening angle. In this study, we found at the first time that photooxidation crosslinking method could significantly increase the residual stress of decellularized vessels, which provides biomechanical support for the development of new biomaterials of vascular grafts.