In Situ Growth of Cs3Bi2Br9 Quantum Dots on Bi-MOF Nanosheets via Cosharing Bismuth Atoms for CO2 Capture and Photocatalytic Reduction.

Given the global warming caused by excess CO2 accumulation in the atmosphere, it is essential to reduce CO2 by capturing and converting it to chemical feedstock using solar energy. Herein, a novel Cs3Bi2Br9/bismuth-based metal-organic framework (Bi-MOF) composite was prepared via an in situ growth strategy of Cs3Bi2Br9 quantum dots (QDs) on the surface of Bi-MOF nanosheets through coshared bismuth atoms. The prepared Cs3Bi2Br9/Bi-MOF exhibits bifunctional merits for both the high capture and effective conversion of CO2, among which the optimized 3Cs3Bi2Br9/Bi-MOF sample shows a CO2-CO conversion yield as high as 572.24 µmol g-1 h-1 under the irradiation of a 300 W Xe lamp. In addition, the composite shows good stability after five recycles in humid air, and the CO2 photoreduction efficiency does not decrease significantly. The mechanistic investigation uncovers that the intimate atomic-level contact between Cs3Bi2Br9 and Bi-MOF via the coshared atoms not only improves the dispersion of Cs3Bi2Br9 QDs over Bi-MOF nanosheets but also accelerates interfacial charge transfer by forming a strong bonding linkage, which endows it with the best performance of CO2 photoreduction. Our new finding of bismuth-based metal-organic framework/lead-free halide perovskite by cosharing atoms opens a new avenue for a novel preparation strategy of the heterojunction with atomic-level contact and potential applications in capture and photocatalytic conversion of CO2.

Control of anterior GRadient 2 (AGR2) dimerization links endoplasmic reticulum proteostasis to inflammation.

Anterior gradient 2 (AGR2) is a dimeric protein disulfide isomerase family member involved in the regulation of protein quality control in the endoplasmic reticulum (ER). Mouse AGR2 deletion increases intestinal inflammation and promotes the development of inflammatory bowel disease (IBD). Although these biological effects are well established, the underlying molecular mechanisms of AGR2 function toward inflammation remain poorly defined. Here, using a protein-protein interaction screen to identify cellular regulators of AGR2 dimerization, we unveiled specific enhancers, including TMED2, and inhibitors of AGR2 dimerization, that control AGR2 functions. We demonstrate that modulation of AGR2 dimer formation, whether enhancing or inhibiting the process, yields pro-inflammatory phenotypes, through either autophagy-dependent processes or secretion of AGR2, respectively. We also demonstrate that in IBD and specifically in Crohn's disease, the levels of AGR2 dimerization modulators are selectively deregulated, and this correlates with severity of disease. Our study demonstrates that AGR2 dimers act as sensors of ER homeostasis which are disrupted upon ER stress and promote the secretion of AGR2 monomers. The latter might represent systemic alarm signals for pro-inflammatory responses.

Integrative Network-based Analysis of Colonic Detoxification Gene Expression in Ulcerative Colitis According to Smoking Status.

BACKGROUNDS AND AIMS: The effect of cigarette smoking [CS] is ambivalent since smoking improves ulcerative colitis [UC] while it worsens Crohn's disease [CD]. Although this clinical relationship between inflammatory bowel disease [IBD] and tobacco is well established, only a few experimental works have investigated the effect of smoking on the colonic barrier homeostasis focusing on xenobiotic detoxification genes. METHODS: A comprehensive and integrated comparative analysis of the global xenobiotic detoxification capacity of the normal colonic mucosa of healthy smokers [n = 8] and non-smokers [n = 9] versus the non-affected colonic mucosa of UC patients [n = 19] was performed by quantitative real-time polymerase chain reaction [qRT PCR]. The detoxification gene expression profile was analysed in CD patients [n = 18], in smoking UC patients [n = 5], and in biopsies from non-smoking UC patients cultured or not with cigarette smoke extract [n = 8]. RESULTS: Of the 244 detoxification genes investigated, 65 were dysregulated in UC patients in comparison with healthy controls or CD patients. The expression of ≥ 45/65 genes was inversed by CS in biopsies of smoking UC patients in remission and in colonic explants of UC patients exposed to cigarette smoke extract. We devised a network-based data analysis approach for differentially assessing changes in genetic interactions, allowing identification of unexpected regulatory detoxification genes that may play a major role in the beneficial effect of smoking on UC. CONCLUSIONS: Non-inflamed colonic mucosa in UC is characterised by a specifically altered detoxification gene network, which is partially restored by tobacco. These mucosal signatures could be useful for developing new therapeutic strategies and biomarkers of drug response in UC.