Mitophagy receptors mediate the selective recognition and targeting of damaged mitochondria by autophagosomes. The mechanism for the regulation of these receptors remains unknown. Here, we demonstrated that a novel hypoxia-responsive microRNA, microRNA-137 (miR-137), markedly inhibits mitochondrial degradation by autophagy without affecting global autophagy. miR-137 targets the expression of two mitophagy receptors NIX and FUNDC1. Impaired mitophagy in response to hypoxia caused by miR-137 is reversed by re-expression of FUNDC1 and NIX expression vectors lacking the miR-137 recognition sites at their 3′ UTR. Conversely, miR-137 also suppresses the mitophagy induced by fundc1 (CDS+3′UTR) but not fundc1 (CDS) overexpression. Finally, we found that miR-137 inhibits mitophagy by reducing the expression of the mitophagy receptor thereby leads to inadequate interaction between mitophagy receptor and LC3. Our results demonstrated the regulatory role of miRNA to mitophagy receptors and revealed a novel link between miR-137 and mitophagy.

Developing specific flotation collectors to improve the separation and enrichment of copper oxide minerals from their ores is still a challenging job. In this article, a novel chelating collector, 5-(2,4,4-trimethylpentyl)-4-amino-1,2,4-triazolidine-3-thione (TMATT), was designed to separate and recover copper oxide minerals, and its flotation response to malachite, calcite, and quartz was compared with that of the traditional collector n-octyl hydroxamic acid (OHA). The findings of contact angle and micro-flotation indicated that TMATT exhibited stronger hydrophobization and better flotation performances to malachite than OHA, and also held the high flotation selectivity against quartz and calcite. The bench-scale flotation outcomes showed that TMATT achieved the high-efficient flotation separation and enrichment of copper oxide minerals from the mixed sulfide-oxide copper ore. XPS, FTIR, AFM, and zeta potential deduced that the adsorption of malachite toward TMATT was related to the reduction of surface Cu(Ⅱ) to Cu(Ⅰ) and the formation of TMATT-Cu(Ⅰ) surface complexes in which the exocyclic N and S atoms of TMATT bonded with the surface Cu(Ⅰ) on malachite. The superior hydrophobicity of TMATT-Cu(I) surface complexes in comparison to that of OHA-Cu(Ⅱ) surface complexes, the favorable five-membered ring bonding mode on malachite surfaces and the preferable chelating selectivity to soft acid Cu(Ⅰ) rather than to hard acid Ca(Ⅱ), deserved TMATT to possess better flotation response to malachite against calcite than OHA.

Angiotensin II (AngII), a vasoactive peptide that elevates arterial blood pressure and results in hypertension, has been reported to directly induce vascular endothelial cell apoptosis. Recent work has demonstrated that propofol pre-treatment attenuates angiotensin II-induced apoptosis in human coronary artery endothelial cells. However, the underlying mechanism remains largely unknown. Here, we investigated human umbilical vein endothelial cells (HUVECs) subjected to angiotensin II-induced apoptosis in the presence or absence of propofol treatment and found that angiotensin II-induced apoptosis was attenuated by propofol in a dose-dependent manner. Furthermore, ELISA assays demonstrated that the ratio of angiotensin (1–7) (Ang (1–7)) to Ang II was increased after propofol treatment. We examined the expression of ACE2, Ang (1–7) and Mas and found that the ACE2-Ang (1–7)-Mas axis was up-regulated by propofol, while ACE2 overexpression increased phosphorylated endothelial nitric oxide synthase (phosphorylated eNOS) expression and siACE2 resulted in the repression of endothelial nitric oxide synthase (eNOS) phosphorylation. In conclusion, our study revealed that propofol can inhibit endothelial cell apoptosis induced by Ang II by activating the ACE2-Ang (1–7)-Mas axis and further up-regulating the expression and phosphorylation of eNOS.

Endothelial microvesicles (EMVs), released after endothelial cell (EC) apoptosis or activation, may carry many adverse signals and propagate injury by intercellular transmission. Caveolae are 50–100 nm cell surface plasma membrane invaginations involved in many pathophysiological processes. Recent evidence has indicated EMVs and caveolae may have functional effects in cells undergoing H/R injury. Propofol, a widely used anaesthetic, confers antioxidative stress capability in the same process. But the connection between EMVs, H/R, and caveolae remains largely unclear. Here, we found that H/R significantly increased the release of EMVs, the expression of CAV‐1 (the structural protein responsible for maintaining the shape of caveolae), oxidative stress, and the mitochondrial damage, and all these changes were inhibited by propofol preconditioning. Interestingly, the caveolae inhibitor Mβ‐CD strengthened the protective effect of propofol preconditioning. We further found that the release of EMVs is more significantly reduced under propofol preconditioning in the presence of the caveolae inhibitor Mβ‐CD. EMVs released from H/R‐treated cells caused a substantially increased mitochondrial and cellular damage to normal HUVECs after 4 hours of coculture. Thus, we conclude that inhibition of caveolae contributes to propofol preconditioning‐suppressed microvesicles release and cell injury by H/R.