Extracellular vesicles from hypoxia-preconditioned mesenchymal stem cells alleviates myocardial injury by targeting thioredoxin-interacting protein-mediated hypoxia-inducible factor-1α pathway.

BACKGROUND: Extracellular vesicles (EVs) derived from hypoxia-preconditioned (HP) mesenchymal stem cells (MSCs) have better cardioprotective effects against myocardial infarction (MI) in the early stage than EVs isolated from normoxic (NC)-MSCs. However, the cardioprotective mechanisms of HP-EVs are not fully understood. AIM: To explore the cardioprotective mechanism of EVs derived from HP MSCs. METHODS: We evaluated the cardioprotective effects of HP-EVs or NC-EVs from mouse adipose-derived MSCs (ADSCs) following hypoxia in vitro or MI in vivo, in order to improve the survival of cardiomyocytes (CMs) and restore cardiac function. The degree of CM apoptosis in each group was assessed by the terminal deoxynucleotidyl transferase dUTP nick end-labeling and Annexin V/PI assays. MicroRNA (miRNA) sequencing was used to investigate the functional RNA diversity between HP-EVs and NC-EVs from mouse ADSCs. The molecular mechanism of EVs in mediating thioredoxin-interacting protein (TXNIP) was verified by the dual-luciferase reporter assay. Co-immunoprecipitation, western blotting, and immunofluorescence were performed to determine if TXNIP is involved in hypoxia-inducible factor-1 alpha (HIF-1α) ubiquitination and degradation via the chromosomal region maintenance-1 (CRM-1)-dependent nuclear transport pathway. RESULTS: HP-EVs derived from MSCs reduced both infarct size (necrosis area) and apoptotic degree to a greater extent than NC-EVs from CMs subjected to hypoxia in vitro and mice with MI in vivo. Sequencing of EV-associated miRNAs showed the upregulation of 10 miRNAs predicted to bind TXNIP, an oxidative stress-associated protein. We showed miRNA224-5p, the most upregulated miRNA in HP-EVs, directly combined the 3' untranslated region of TXNIP and demonstrated its critical protective role against hypoxia-mediated CM injury. Our results demonstrated that MI triggered TXNIP-mediated HIF-1α ubiquitination and degradation in the CRM-1-mediated nuclear transport pathway in CMs, which led to aggravated injury and hypoxia tolerance in CMs in the early stage of MI. CONCLUSION: The anti-apoptotic effects of HP-EVs in alleviating MI and the hypoxic conditions of CMs until reperfusion therapy may partly result from EV miR-224-5p targeting TXNIP.

Circular RNA Fbxl5 Regulates Cardiomyocyte Apoptosis During Ischemia Reperfusion Injury via Sponging microRNA-146a.

Objective: Cardiomyocyte apoptosis critically contributes to ischemia reperfusion injury (IRI), which lacks effective therapeutic strategies. Circular RNAs (circRNAs) serve as novel diagnostic and therapeutic targets in various cardiovascular diseases. CircRNA Fbxl5 is one of the abundantly expressed circRNAs in the heart and its role in myocardial IRI remains elusive. Materials and Methods: Wild-type (WT) mice and neonatal mice ventricular myocytes (NMVMs) were used and subjected to myocardial IRI and anoxia reoxygenation (AR), respectively. Molecular and histological analyses and echocardiography were used to determine the extent of apoptosis, infarct size, and cardiac function. Results: We found that circRNA Fbxl5 was significantly upregulated in the myocardium, as well as in NMVMs subjected to AR. Knockdown of circRNA Fbxl5 ameliorated cardiomyocyte apoptosis, thereby decreasing infarct size and preserving cardiac function. Additionally, in vitro knockdown of circRNA Fbxl5 in NMVMs subjected to AR recapitulated the in vivo findings. Mechanistically, we identified that circRNA Fbxl5 directly sponged and suppressed the endogenous microRNA-146a (miR-146a), thereby weakening its inhibitory effect on MED1, which could further promote the apoptosis of cardiomyocytes. Conclusion: Our findings revealed a novel and critical role for circRNA Fbxl5 in regulating cardiomyocyte apoptosis, and added additional insight into circRNAs mediated during myocardial IRI. The underlying miR-146a-MED1 signaling serves as an important cascade in regulating the apoptosis of cardiomyocytes.

MicroRNA-221 inhibits the transition of endothelial progenitor cells to mesenchymal cells via the PTEN/FoxO3a signaling pathway.

BACKGROUND: Coronary heart disease is one of the most common cardiovascular diseases worldwide and is often associated with vascular endothelial injury. Endothelial-mesenchymal transition (EndMT) is an important process in vascular endothelial injury. OBJECTIVES: This study investigated the function of miR-221 in the EndMT process of endothelial progenitor cells (EPCs). MATERIAL AND METHODS: Transforming growth factor beta (TGF-ß1) was used to induce EndMT in EPCs, and SM22α expression was detected using immunocytochemistry. Western blot was used to detect alpha smooth muscle actin (αSMA) expression, and miR-221 function was evaluated using inhibitors or mimics of the miR-221 sequences that were transfected into EPCs. Reverse transcription polymerase chain reaction (RT-PCR) was used to detect the expression of miR-221 and western blot was used to detect the expression of αSMA, myocardin, phosphatase and tensin homolog (PTEN), p-FoxO3a, and FoxO3a in EPCs. Finally, the expression of the miR-221 target genes was determined using RT-PCR. RESULTS: The expression of SM22α and αSMA increased in EPCs treated with TGF-ß1, while the expression of miR-221 was decreased in EPCs on the 5th day, when compared with the control. The expression of SM22α increased after inhibiting miR-221 in EPCs treated with TGF-ß1 and this was reversed by the overexpression of miR-221. The expression of αSMA and myocardin was significantly increased after inhibiting miR-221 in EPCs treated with TGF-ß1 and decreased in EPCs overexpressing miR-221. Conversely, PTEN was increased in TGF-ß1-treated EPCs and decreased following the overexpression of miR-221. The decrease in phosphorylated-FoxO3a expression in EPCs was accompanied by an increase in αSMA expression, which was reversed in the presence of miR-221 mimics. This effect was nearly abolished following the addition of PTEN cDNA. CONCLUSIONS: The overexpression of miR-221 inhibits EndMT in EPCs, possibly by interacting with PTEN to regulate FoxO3a signaling, to facilitate the repair of the endothelium by EPCs.

VSTM1 regulates monocyte/macrophage function via the NF-κB signaling pathway.

OBJECTIVE: V-set and transmembrane domain-containing protein 1 (VSTM1) is negatively correlated with inflammation. However, its effect on atherosclerosis (AS) remains largely unexplored. In this study, we aimed to assess the effect of VSTM1 on the biological function of human peripheral blood mononuclear cells /macrophages stimulated by oxidized low-density lipoprotein (ox-LDL). METHODS: U937 cells were divided into three groups as follows: control group, pLenti-VSTM1 shRNA group (VSTM1 depletion), and pLenti-VSTM1 group (VSTM1 overexpression). Cellular migration, chemotaxis, apoptosis, and secretion of inflammatory factors of monocytes/macrophages stimulated by ox-LDL were studied. RESULTS: Overexpression of VSTM1 decreased the proliferation of U937 cells and induced cellular apoptosis. Depletion of VSTM1 enhanced the invasiveness and chemotaxis, increased the inflammatory response, and reduced the incidence of cell necrosis and apoptosis. Nuclear factor κ of B cells (NF-κB) was activated in VSTM1-depleted U937 cells. CONCLUSION: VSTM1 might play an important role in the activation of monocytes/macrophages and participate in the pathogenesis of AS via regulating NF-κB activity.

Predictive and prognostic value of v-set and transmembrane domain-containing 1 expression in monocytes for coronary artery disease.

The aim of this study was to investigate the correlation between v-set and transmembrane domain-containing 1 (VSTM1) expression and incidence of major adverse cardiac events (MACE) in patients with coronary heart disease (CHD). A total of 310 patients were divided into a non-acute coronary syndrome (non-ACS) group (containing the stable angina group, and the asymptomatic coronary artery diseaseand other patients group) and an ACS group (containing unstable angina and acute myocardial infarction patients). Monocytic VSTM1 expression levels (assessed via average fluorescence intensity derived from antibody binding to VSTM1) in each group were detected and analyzed. The cut-off value of monocytic VSTM1 expression to predict the onset of ACS and MACE was confirmed. VSTM1 expression in monocytes from the ACS group was lower than that of the non-ACS group. The incidence of MACEs in the high VSTM1-expression group was much less than that of those in the low VSTM1 expression group at the 1 year follow-up stage. VSTM1 expression had an independent-inversed association with increased incidence of MACE and ACS. VSTM1 expression in monocytes may help to predict the occurrence of ACS in patients with CHD, and moreover it may provide the means to evaluate MACE prognosis during CHD patient follow-up.

Effect of lgals3a on embryo development of zebrafish.

Our study was aimed to investigate the effects of lgals3a (Gal-3 encoding gene) on the development of zebrafish embryo and its underlying mechanisms. Morpholino (MO) technology was used to inhibit the expression of zebrafish lgals3a, and the effect of lgals3a gene knockdown on zebrafish embryo development and the number of monocyte macrophages was observed. Effect of lgals3a-e3i3-MO on apoptosis of zebrafish was detected by acridine orange staining. In addition, the mRNA expression levels of Wnt/ß-catenin signaling pathway-related genes were detected by RT-qPCR. Compared with control-MO group, the zebrafish embryos injected with lgals3a-e3i3-MO had obvious defects in the head, eyes, and tail, and pericardial edema. Lgals3a-e3i3-MO significantly reduced the number of mononuclear macrophages in zebrafish embryos compared with the control-MO group. The results of acridine orange staining showed that compared with the control-MO group, lgals3a-e3i3-MO promoted cardiomyocyte apoptosis in zebrafish. Furthermore, lgals3a-e3i3-MO significantly up-regulated the expression of dkk1b, wnt9a, lrp5, fzd7a, ß-catenin, Gsk-3ß, mycn, myca in the Wnt/ß-catenin pathway, and decreased the expression of lef1. These results indicate that lgals3a-e3i3-MO inhibits zebrafish embryo development, reduces the number of mononuclear macrophages, activates Wnt/ß-catenin signaling pathway and promotes cardiomyocyte apoptosis.

Nicotine exacerbates atherosclerosis through a macrophage-mediated endothelial injury pathway.

Evidence suggests that nicotine intake promotes atherosclerosis. We enrolled 100 patients with coronary heart disease (CHD) and found that plaque burden, TXNIP expression, and inflammatory chemokine levels were higher in smokers than non-smokers. Additionally, patients with higher TXNIP expression in peripheral blood mononuclear cells (PBMCs) had a higher Gensini Scores and higher plasma IL-1ß and IL-18 levels. Treating bone marrow-derived macrophages (BMDMs) with nicotine in vitro led to enhanced lipid phagocytosis, chemotaxis, and increased production of reactive oxygen species (ROS), which activated TXNIP/NLRP3 inflammasome signaling and promoted pyroptosis, as evidenced by caspase-1 cleavage and increased production of IL-1ß, IL-18, and gasdermin D. Nicotine intake by ApoE(-/-) mice fed a high-fat diet recapitulated those phenotypes. The effects of nicotine on pyroptotic signaling were reversed by N-acetyl-cysteine, a ROS scavenger. Silencing TXNIP in vivo reversed the effects of nicotine on macrophage invasion and vascular injury. Nicotine also induced pyroptotic macrophages that contributed to the apoptotic death of endothelial cells. These findings suggest that nicotine accelerates atherosclerosis in part by promoting macrophage pyroptosis and endothelial damage. Therefore, targeting the TXNIP/NLRP3-mediated pyroptotic pathway in macrophages may ameliorate nicotine-induced endothelial damage.

Extracellular vesicles from anoxia preconditioned mesenchymal stem cells alleviate myocardial ischemia/reperfusion injury.

Extracellular vesicles (EVs) produced by anoxia-preconditioned mesenchymal stem cells (MSCs) may afford greater cardioprotection against myocardial ischemia-reperfusion injury (MIRI) than EVs derived from normoxic MSCs. Here, we isolated EVs from mouse adipose-derived MSCs (ADSCs) subjected to anoxia preconditioning or normoxia and evaluated their ability to promote survival of mouse cardiomyocytes following MIRI in vivo and anoxia/reoxygenation (AR) in vitro. Injection of anoxia-preconditioned ADSC EVs (Int-EVs) reduced both infarct size and cardiomyocyte apoptosis to a greater extent than normoxic ADSC EVs (NC-EVs) in mice subjected to MIRI. Sequencing EV-associated miRNAs revealed differential upregulation of ten miRNAs predicted to bind thioredoxin-interacting protein (TXNIP), an inflammasome- and pyroptosis-related protein. We confirmed direct binding of miRNA224-5p, the most upregulated miRNA in Int-EVs, to TXNIP and asserted through western blotting and apoptosis assays a critical protective role for this miRNA against AR-induced cardiomyocyte death. Our results suggest that ischemia-reperfusion triggers TXNIP-induced inflammasome activation in cardiomyocytes, which leads to apoptosis rather than pyroptosis due to low basal levels of the pyroptosis executioner protein gasdermin D in these cells. The antiapoptotic effect of EV-associated miRNA224-5p would in turn result from TXNIP downregulation, which prevents caspase-1-mediated degradation of GATA4 and sustains the expression of Bcl-2.

MicroRNA-21 Mediates a Positive Feedback on Angiotensin II-Induced Myofibroblast Transformation.

OBJECTIVE: Post myocardial infarction (MI) fibrosis has been identified as an important factor in the progression of heart failure. Previous studies have revealed that microRNA-21 (miR-21) plays an important role in the pathogenesis of fibrosis. The purpose of this study was to explore the role of miR-21 in post-MI cardiac fibrosis. MATERIAL AND METHODS: MI was established in wild-type (WT) and miR-21 knockout (KO) mice. Primary mice cardiac fibroblasts (CFs) were isolated from WT and miR-21 KO mice and were treated with angiotensin II (Ang II) or Sprouty1 (Spry1) siRNA. Histological analysis and echocardiography were used to determine the extent of fibrosis and cardiac function. RESULTS: Compared with WT mice, miR-21 KO mice displayed smaller fibrotic areas and decreased expression of fibrotic markers and inflammatory cytokines. In parallel, Ang II-induced myofibroblasts transformation was partially inhibited upon miR-21 KO in primary CFs. Mechanistically, we found that the expression of Spry1, a previously reported target of miR-21, was markedly increased in miR-21 KO mice post MI, further inhibiting ERK1/2 activation. In vitro studies showed that Ang II activated ERK1/2/TGF-ß/Smad2/3 pathway. Phosphorylated Smad2/3 further enhanced the expression of α-SMA and FAP and may promote the maturation of miR-21, thereby downregulating Spry1. Additionally, these effects of miR-21 KO on fibrosis were reversed by siRNA-mediated knockdown of Spry1. CONCLUSION: Our findings suggest that miR-21 promotes post-MI fibrosis by targeting Spry1. Furthermore, it mediates a positive feedback on Ang II, thereby inducing the ERK/TGF-ß/Smad pathway. Therefore, targeting the miR-21-Spry1 axis may be a promising therapeutic option for ameliorating post-MI cardiac fibrosis.

In vivo Screening of Natural Products Against Angiogenesis and Mechanisms of Anti-Angiogenic Activity of Deoxysappanone B 7,4'-Dimethyl Ether.

INTRODUCTION: The aim of this study was to screen the leading compounds of natural origin with anti-angiogenic potential and to investigate their anti-angiogenic mechanism preliminarily. MATERIALS AND METHODS: An initial screening of 240 compounds from the Natural Products Collection of MicroSource was performed using the transgenic zebrafish strain Tg [fli1a: enhanced green fluorescent protein (EGFP)]y1 . The zebrafish embryos at 24 h post-fertilization were exposed to the natural compounds for an additional 24 h; then, morphological changes in the intersegmental vessels (ISVs) were observed and quantified under a fluorescence microscope. The expression profiles of angiogenesis-related genes in the zebrafish embryos were detected using quantitative real-time PCR. RESULTS: Five compounds were identified with potential anti-angiogenic activity on the zebrafish embryogenesis. Among them, deoxysappanone B 7.4'-dimethyl ether (Deox B 7,4) showed anti-angiogenic activity on the formation of ISVs in a dose-dependent manner. The inhibition of ISV formation reached up to 99.64% at 5 µM Deox B 7,4. The expression of delta-like ligand 4 (dll4), hes-related family basic helix-loop-helix transcription factor with YRPW motif 2, ephrin B2, fibroblast growth factor receptor (fgfr) 3, cyclooxygenase-2, protein tyrosine phosphatase, receptor type B (ptp-rb), phosphoinositide-3-kinase regulatory subunit 2, slit guidance ligand (slit) 2, slit3, roundabout guidance receptor (robo) 1, robo2, and robo4 were down-regulated, while vascular endothelial growth factor receptor-2, fgfr 1, and matrix metallopeptidase 9 were up-regulated in the zebrafish embryos treated with Deox B 7,4. CONCLUSION: Deox B 7,4 has a therapeutic potential for the treatment of angiogenesis-dependent diseases and may exert anti-angiogenic activities by suppressing the slit2/robo1/2, slit3/robo4, cox2/ptp-rb/pik3r2, and dll4/hey2/efnb2a signaling pathways as well as activation of vegfr-2/fgfr1/mmp9.

MicroRNA-146a protects against myocardial ischaemia reperfusion injury by targeting Med1.

BACKGROUND: Myocardial ischaemia reperfusion injury (MIRI) is a difficult problem in clinical practice, and it may involve various microRNAs. This study investigated the role that endogenous microRNA-146a plays in myocardial ischaemia reperfusion and explored the possible target genes. METHODS: MIRI models were established in microRNA-146a deficient (KO) and wild type (WT) mice. MicroRNA-146a expression was evaluated in the myocardium of WT mice after reperfusion. The heart function, area of myocardium infarction and in situ apoptosis were compared between the KO and WT mice. Microarray was used to explore possible target genes of microRNA-146a, while qRT-PCR and dual luciferase reporter assays were used for verification. Western blotting was performed to detect the expression levels of the target gene and related signalling molecules. A rescue study was used for further testing. RESULTS: MicroRNA-146a was upregulated 1 h after reperfusion. MicroRNA-146a deficiency decreased heart function and increased myocardial infarction and apoptosis. Microarray detected 19 apoptosis genes upregulated in the KO mice compared with the WT mice. qRT-PCR and dual luciferase verified that Med1 was one target gene of microRNA-146a. TRAP220, encoded by Med1 in the KO mice, was upregulated, accompanied by an amplified ratio of Bax/Bcl2 and increased cleaved caspase-3. Inhibition of microRNA-146a in H9C2 cells caused increased TRAP220 expression and more apoptosis under the stimulus of hypoxia and re-oxygenation, while knockdown of the increased TRAP220 expression led to decreased cell apoptosis. CONCLUSIONS: MicroRNA-146a exerts a protective effect against MIRI, which might be partially mediated by the target gene Med1 and related to the apoptosis signalling pathway.

MicroRNA-21 deficiency attenuated atherogenesis and decreased macrophage infiltration by targeting Dusp-8.

BACKGROUND AND AIMS: Atherosclerosis is a chronic inflammatory disorder mediated by macrophage activation. MicroRNA-21 (miR-21) is a key regulator in the macrophage inflammatory response. However, the functional role of miR-21 in atherogenesis is far from clear. METHODS AND RESULTS: Here, we report that miR-21 is significantly upregulated in mouse atherosclerotic plaques and peripheral monocytes from patients with coronary artery disease. Compared with miR-21+/+apoE-/- mice (apoE-/- mice), miR-21-/-apoE-/- (double knockout, DKO) mice showed less atherosclerotic lesions, reduced presence of macrophages, decreased smooth muscle cells(SMC) and collagen content in the aorta. We further explored the role of miR-21 in macrophage activation in vitro. Bone marrow-derived macrophages (BMDMs) from DKO mice not only exhibit impaired function of migration induced by chemokine (C-C motif) ligand 2 (CCL2) but also a weakened macrophage-endothelium interaction activated by tumor necrosis factor-α (TNF-α). However, atherogenic inflammatory cytokine secretion was not affected by miR-21 in vitro or in vivo. Additionally, miR-21 knockdown in BMDMs directly derepressed the expression of dual specificity protein phosphatase 8 (Dusp-8), a previously validated miR-21 target in cardiac fibroblasts, which negatively regulates mitogen-activated protein kinase (MAPK) signaling, particularly the p38-and c-Jun N-terminal kinase (JNK)-related signaling pathways. CONCLUSIONS: These data demonstrate that inhibition of miR-21 may restrict the formation of atherosclerotic plaques partly by regulating macrophage migration and adhesion, while, reduced SMCs and collagen content in plaques may lead to a less stable phenotype with the progression of atherosclerosis. Thus, the absence of miR-21 reduces atherosclerotic lesions but may not represent all benefit in atherosclerosis development.

Evaluation of Gas Formation and Consumption Driven by Crossover Effect in High-Voltage Lithium-Ion Batteries with Ni-Rich NMC Cathodes.

Gas formation during lithium-ion battery (LIB) cycling impacts the stability and safety of these batteries, especially for those containing Ni-rich NMC cathodes. In this paper, the cycling performance and gassing behavior of NMC811/graphite full cells with 4.2 and 4.4 V upper cutoff voltages were first compared. Cells with a 4.2 V upper cutoff voltage had good cycling stability, exhibiting a capacity retention of 96.8% after 100 cycles and generated little gas. On the other hand, cells with a 4.4 V upper cutoff voltage lost over 25% of initial capacity after 100 cycles and generated large amounts of gas in the first 10 cycles. Electrochemical cycling of anode and cathode symmetric cells was implemented to isolate gases formed at the electrode. Gas chromatography-mass spectrometry, Fourier transform infrared spectroscopy, X-ray photoelectron spectroscopy, and scanning transmission electron microscopy were used to characterize the gas formation and associated material surfaces and structural properties. It was found that CO2 and fluorinated alkanes were the dominant gases evolved on the cathode side during cycling to 4.4 V. Gas crossover to the anode led to the depletion of gaseous products, which stabilized the cell performance to some extent. However, the growing surface reconstruction layer at the cathode, the thickening of the solid electrolyte interphase layer at the anode, and the gradual depletion of lithium inventory collectively contributed to the continuous capacity loss of full cells cycled to 4.4 V.

Integrating Zeolite-Type Chalcogenide with Titanium Dioxide Nanowires for Enhanced Photoelectrochemical Activity.

Developing photoanodes with efficient visible-light harvesting and excellent charge separation still remains a key challenge in photoelectrochemical water splitting. Here zeolite-type chalcogenide CPM-121 is integrated with TiO2 nanowires to form a heterostructured photoanode, in which crystalline CPM-121 particles serve as a visible light absorber and TiO2 nanowires serve as an electron conductor. Owing to the small band gap of chalcogenides, the hybrid electrode demonstrates obvious absorption in visible-light range. Electrochemical impedance spectroscopy (EIS) shows that electron transport in the hybrid electrode has been significantly facilitated due to the heterojunction formation. A >3-fold increase in photocurrent is observed on the hybrid electrode under visible-light illumination when it is used as a photoanode in a neutral electrolyte without sacrificial agents. This study opens up a new avenue to explore the potential applications of crystalline porous chalcogenide materials for solar-energy conversion in photoelectrochemistry.

Selective Ion Exchange and Photocatalysis by Zeolite-Like Semiconducting Chalcogenide.

The development of novel photocatalysts usually centers on features such as band structures, various nano-, micro-, or macro-forms, and composites in efforts to tune their light absorption and charge separation efficiency. In comparison, the selectivity of photocatalysts with respect to features of reactants such as size and charge has received much less attention, in part due to the difficulty in designing semiconducting photocatalysts with uniform pore size. Here, we use crystalline porous chalcogenides as a platform to probe reactant selectivity in photocatalytic processes. The 3-in-1 integration of high surface area, uniform porosity, and favorable band structures in such chalcogenides makes them excellent candidates for efficient and selective photocatalytic processes. We show that their photocatalytic activity and selectivity are closely related to their differing affinity and selectivity for different guest species. In particular, unlike common solid-state photocatalysts with neutral framework, the anionic nature of the porous chalcogenide framework used here endows them with a high degree of selectivity for cationic species in both guest exchange and closely coupled photocatalytic transformation of such guests. Another interesting discovery is the observation of an unusual ion exchange process involving a transient state of over-saturation of exchanged ions, which can be explained by a transition from an initially kinetically controlled process to a subsequent thermodynamically controlled one. This work is part of ongoing efforts to contribute to the development of a new generation of crystalline porous photocatalysts with custom-designed selectivity for various reactants or products.

Visible-Light-Mediated [4+2] Annulation of N-Cyclobutylanilines with Alkynes Catalyzed by Self-Doped Ti3+ @TiO2.

We herein report a visible-light-mediated heterogeneous [4+2] annulation of N-cyclobutylanilines with alkynes catalyzed by self-doped Ti3+ @TiO2 . The self-doped Ti3+ @TiO2 is stable under photooxidation conditions, easy to recycle, and can be used multiple times without appreciable loss of activity. Extensive mechanistic studies suggest that the annulation reaction is mediated by singlet oxygen, which is generated through the photosensitization of oxygen in the air by the self-doped Ti3+ @TiO2 . In contrast, the homogeneous variant catalyzed by a far more expensive iridium complex proceeds under an inert atmosphere, which indicates a different mechanism. The substrate scopes of the two processes are comparable.

Multivariable Modular Design of Pore Space Partition.

Pore space partition, especially the one using C3-symmetric 2,4,6-tri(4-pyridyl)-1,3,5-triazine as pore-partition agent in MIL-88 type (the acs net), has been shown to dramatically enhance CO2 uptake to near-record values. The continued advance in property engineering via pore space partition would depend on intelligent design of both framework components and pore-partition agent. Here, we report a new advance in the design of pore-partition agent by demonstrating a symmetry-guided pathway to develop a large variety of di- and trinuclear 1,2,4-triazolate-based clusters for use as pore-partition agent. The use of metal-organic clusters (instead of organic ligands) as pore-partition agent gives rise to many new pore-partitioned materials with huge compositional variety. The full assembly involves the simultaneous formation of two separate coordination architectures (i.e., the 3-D acs framework and 0-D triazolate clusters) and the eventual welding between the acs framework and triazolate clusters. The wide range of new compositions and structures provides a high degree of tunability in gas sorption properties.

An ultra-tunable platform for molecular engineering of high-performance crystalline porous materials.

Metal-organic frameworks are a class of crystalline porous materials with potential applications in catalysis, gas separation and storage, and so on. Of great importance is the development of innovative synthetic strategies to optimize porosity, composition and functionality to target specific applications. Here we show a platform for the development of metal-organic materials and control of their gas sorption properties. This platform can accommodate a large variety of organic ligands and homo- or hetero-metallic clusters, which allows for extraordinary tunability in gas sorption properties. Even without any strong binding sites, most members of this platform exhibit high gas uptake capacity. The high capacity is accomplished with an isosteric heat of adsorption as low as 20 kJ mol-1 for carbon dioxide, which could bring a distinct economic advantage because of the significantly reduced energy consumption for activation and regeneration of adsorbents.

Hexagonal@Cubic CdS Core@Shell Nanorod Photocatalyst for Highly Active Production of H2 with Unprecedented Stability.

A highly effective, low-cost strategy for improved photocatalytic efficiency and stability of CdS is described. Based on the integration of hexagonal-cubic core-shell architecture with nanorod morphology, the concentric CdS nanorod phase junctions (NRPJs) obtained demonstrate extremely high H2 production rate and unprecedented photocatalytic stability.

Open framework metal chalcogenides as efficient photocatalysts for reduction of CO2 into renewable hydrocarbon fuel.

Open framework metal chalcogenides are a family of porous semiconducting materials with diverse chemical compositions. Here we show that these materials containing covalent three-dimensional superlattices of nanosized supertetrahedral clusters can function as efficient photocatalysts for the reduction of CO2 to CH4. Unlike dense semiconductors, metal cations are successfully incorporated into the channels of the porous semiconducting materials to further tune the physical properties of the materials such as electrical conductivity and band gaps. In terms of the photocatalytic properties, the metal-incorporated porous chalcogenides demonstrated enhanced solar energy absorption and higher electrical conductivity and improved photocatalytic activity.