Pd Decoration with Synergistic High Oxygen Mobility Boosts Hydrogen Sensing Performance at Low Working Temperature on WO3 Nanosheet.

Pd-based materials have received remarkable attention and exhibit excellent H2 sensing performance due to their superior hydrogen storage and catalysis behavior. However, the synergistic effects originated from the decoration of Pd on a metal oxide support to boost the sensing performance are ambiguous, and the deep investigation of metal support interaction (MSI) on the H2 sensing mechanism is still unclear. Here, the model material of Pd nanoparticle-decorated WO3 nanosheet is synthesized, and individual fine structures can be achieved by treating it at different temperatures. Notably, the Pd-WO3-300 materials display superior H2 sensing performance at a low working temperature (110 °C), with a superior sensing response (Ra/Rg = 40.63 to 10 ppm), high sensing selectivity, and anti-interference ability. DFT calculations and detailed structural investigations confirm that the moderate MSI facilitates the generation of high mobility surface O2- (ad) species and a proper ratio of surface Pd0-Pd2+ species, which can significantly boost the desorption of intermediate PdHx species at low temperatures and contribute to enhanced sensing performance. Our work illustrates the effect of MSI on sensing performance and provides insight into the design of advanced sensing materials.

SUMOylation of SIRT1 activating PGC-1α/PPARα pathway mediates the protective effect of LncRNA-MHRT in cardiac hypertrophy.

Long noncoding RNA-Myosin heavy chain associated RNA transcript (LncRNA-MHRT) has been reported to prevent pathological cardiac hypertrophy. However, the underlying inhibition mechanism has not been fully elucidated. Further, whether MHRT inhibits hypertrophy by regulating post-translational modification of certain proteins remains unclear. Therefore, this study aims to find potential role of MHRT in inhibiting cardiac hypertrophy via regulating modification of certain proteins. Here, Angiotensin II (Ang II) -treated neonatal rat cardiomyocytes and transverse aortic constriction (TAC) mice were used to investigate the effect and mechanism of MHRT in cardiac hypertrophy in vitro and in vivo. Moreover, the regulatory effects of MHRT on SUMOylation of NAD-dependent protein deacetylase sirtuin-1 (SIRT1), peroxisome proliferator-activated receptor γ coactivator-1 α (PGC-1α)/peroxisome proliferator-activated receptor-α (PPARα), specificity protein 1 (SP1)/histone deacetylase 4 (HDAC4) pathway were investigated. Here, we found that MHRT improved heart function by attenuating pathological cardiac hypertrophy in vivo and in vitro. MHRT also promoted the SUMOylation of SIRT1 protein that activated PGC1-α/PPAR-α pathway. Furthermore, MHRT enhanced SUMOylation of SIRT1 by upregulating SP1/HDAC4. Our findings suggested that SUMOylation of SIRT1 could mediate the protective effect of MHRT in cardiac hypertrophy. The new regulatory pathway provides a potential new therapeutic target for pathological cardiac hypertrophy.