CDKN2B-AS1 mediates proliferation and migration of vascular smooth muscle cells induced by insulin.

Excessive proliferation and migration of vascular smooth muscle cells (VSMCs) contribute to the intimal hyperplasia in type 2 diabetes mellitus (T2DM) patients after percutaneous coronary intervention. We aimed to investigate the role of lncRNA cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) in VSMC proliferation and migration, as well as the underlying mechanism. T2DM model mice with carotid balloon injury were used in vivo and mouse aortic vascular smooth muscle cells (MOVAS) stimulated by insulin were used in vitro to assess the role of CDKN2B-AS1 in VSMC proliferation and migration following vascular injury in T2DM state. To investigate cell viability and migration, MTT assay and Transwell assay were conducted. To elucidate the underlying molecular mechanisms, the methylation-specific polymerase chain reaction, RNA immunoprecipitation, RNA-pull down, co-immunoprecipitation, and chromatin immunoprecipitation were performed. In vivo, CDKN2B-AS1 was up-regulated in common carotid artery tissues. In vitro, insulin treatment increased CDKN2B-AS1 level, enhanced MOVAS cell proliferation and migration, while the promoting effect was reversed by CDKN2B-AS1 knockdown. CDKN2B-AS1 forms a complex with enhancer of zeste homolog 2 (EZH2) and DNA methyltransferase (cytosine-5) 1 (DNMT1) to regulate smooth muscle 22 alpha (SM22α) methylation levels. In insulin-stimulated cells, SM22α knockdown abrogated the inhibitory effect of CDKN2B-AS1 knockdown on cell viability and migration. Injection of lentivirus-sh-CDKN2B-AS1 relieved intimal hyperplasia in T2DM mice with carotid balloon injury. Up-regulation of CDKN2B-AS1 induced by insulin promotes cell proliferation and migration by targeting SM22α through forming a complex with EZH2 and DNMT1, thereby aggravating the intimal hyperplasia after vascular injury in T2DM.

Magneto-Induced Janus Adhesive-Tough Hydrogels for Wearable Human Motion Sensing and Enhanced Low-Grade Heat Harvesting.

Janus hydrogels with different properties on the two surfaces have considerable potential in the field of material engineering applications. Various Janus hydrogels have been developed, but there are still some problems, such as stress mismatch caused by the double-layer structure and Janus failure caused by material diffusion in the gradient structure. Here, we report a Janus adhesive-tough hydrogel with polydopamine-decorated Fe3O4 nanoparticles (Fe3O4@PDA) at one side induced by magnetic field to avoid uncontrollable material diffusion in the cross-linking polymerization of acrylamide with alginate-calcium. The magneto-induced Janus (MIJ) hydrogel has an adhesive surface and a tough bulk without an obvious interface to avoid stress mismatch. Due to the intrinsic dissipative matrix and the abundant catechol groups on the adhesive surface, it shows strong adhesion onto various substrates. The MIJ hydrogel has high sensitivity (GF = 0.842) in detecting tiny human motion. Owing to the synergy of Fe3O4@PDA-enhanced interfacial adhesion and heat transfer, it is possible to quickly generate effective temperature differences when adhering to human skin. The MIJ hydrogel achieves a Seebeck coefficient of 13.01 mV·K-1 and an output power of 462.02 mW·m-2 at a 20 K temperature difference. This work proposes a novel strategy to construct Janus hydrogels for flexible wearable devices in human motion sensing and low-grade heat harvesting.

Associations between gut microbiota and sleep: a two-sample, bidirectional Mendelian randomization study.

Introduction: Previous research has reported that the gut microbiota performs an essential role in sleep through the microbiome-gut-brain axis. However, the causal association between gut microbiota and sleep remains undetermined. Methods: We performed a two-sample, bidirectional Mendelian randomization (MR) analysis using genome-wide association study summary data of gut microbiota and self-reported sleep traits from the MiBioGen consortium and UK Biobank to investigate causal relationships between 119 bacterial genera and seven sleep-associated traits. We calculated effect estimates by using the inverse-variance weighted (as the main method), maximum likelihood, simple model, weighted model, weighted median, and MR-Egger methods, whereas heterogeneity and pleiotropy were detected and measured by the MR pleiotropy residual sum and outlier method, Cochran's Q statistics, and MR-Egger regression. Results: In forward MR analysis, inverse-variance weighted estimates concluded that the genetic forecasts of relative abundance of 42 bacterial genera had causal effects on sleep-associated traits. In the reverse MR analysis, sleep-associated traits had a causal effect on 39 bacterial genera, 13 of which overlapped with the bacterial genera in the forward MR analysis. Discussion: In conclusion, our research indicates that gut microbiota may be involved in the regulation of sleep, and conversely, changes in sleep-associated traits may also alter the abundance of gut microbiota. These findings suggest an underlying reciprocal causal association between gut microbiota and sleep.