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Ischemic stroke is a serious cerebrovascular disease with high morbidity and mortality. As a result of ischemia-reperfusion, a cascade of pathophysiological responses is triggered by the imbalance in metabolic supply and demand, resulting in cell loss. These cellular injuries follow various molecular mechanisms solely or in combination with this disorder. Mitochondria play a driving role in the pathophysiological processes of ischemic stroke. Once ischemic stroke occurs, damaged cells would respond to such stress through mitophagy. Mitophagy is known as a conservatively selective autophagy, contributing to the removal of excessive protein aggregates and damaged intracellular components, as well as aging mitochondria. Moderate mitophagy may exert neuroprotection against stroke. Several pathways associated with the mitochondrial network collectively contribute to recovering the homeostasis of the neurovascular unit. However, excessive mitophagy would also promote ischemia-reperfusion injury. Therefore, mitophagy is a double-edged sword, which suggests that maximizing the benefits of mitophagy is one of the direction of future efforts. This review emphasized the role of mitophagy in ischemic stroke, and highlighted the crosstalk between mitophagy and apoptosis/necroptosis.

This article has been retracted. Please see the Retraction Notice for more detail: https://doi.org/10.1186/s13046-022-02409-y.

Avicennia marina is a pioneer mangrove species widely distributed along the southeast coast of China. It suffers, especially in the seedling stage, from the tidal flooding and anaerobic surroundings as it closes to the seaward side. The aim of this study is to assess the ability of A. marina seedlings to withstand different tidal inundations by physiological and proteomic approaches. To accomplish this, the artificial tidal inundations were mimicked as 0, 4, and 8 h per tidal cycle about 1 week. The physiological approaches and two-dimensional electrophoresis coupled with MALDI-TOF/TOF-MS technology were used to reveal the adaptive alterations of A. marina seedlings to tidal inundation. There were profound changes in photosynthesis and chlorophyll fluorescence characteristics of A. marina seedling leaves under inundation treatment. Particularly, photosynthetic rate increased at 4 h inundation, while decreasing at 8 h inundation treatment compared with control (0 h). The results highlighted that A. marina seedlings could greatly upregulate the abundances of photosynthesis-related proteins, activate antioxidant and defense systems to efficiently suppress the reactive oxygen species (ROS) burst and cell damages, mobilize carbohydrate metabolism associated proteins, and then maintain cellular homeostasis, resulting in well adaptation to short-term tidal inundation. Overall, our results demonstrated that short-term inundation is beneficial, while long-term inundation is detrimental to A. marina. The results allow us to recognize the roles of specific proteins in molecular tolerance to tidal inundation in mangrove plants.

Calcium oxalate (CaOx) is a common biomineral found in the plant kingdom. Crystals of CaOx occur in different plant tissues, such as leaves and stems. However, little is known about the biosynthesis of CaOx in oxalate-accumulating plants. Moreover, the literature on genes related to CaOx formation under high-calcium environment is scarce. In the present study, the physiological parameters and the transcript profiles of Medicago lupulina leaves treated with 0.1 and 25 mM Ca2+ were analyzed to study the genes involved in the biosynthesis of CaOx. We demonstrated that exposure to high external calcium concentration induced H2O2 production, ascorbic acid degradation, and CaOx accumulation in M. lupulina leaves. Moreover, we identified 1715 differentially expressed genes (DEGs) (1322 up-regulated and 393 down-regulated genes) in leaves treated with 25 mM Ca2+ compared with the leaves treated with 0.1 mM Ca2+. We further demonstrated the involvement of DEGs in oxalic acid production, calcium transport, and calcium buffering. These results revealed that a high calcium promoted oxalic acid biosynthesis by inducing the expression of NADPH oxidase and ascorbate oxidase genes. In addition, several genes encoding cyclic nucleotide-gated channel, Ca2+-ATPase, H+/Ca2+ exchangers, and calcium-binding proteins were found to be differentially expressed and involved in calcium transport and calcium buffering. Our transcriptome analyses provide a comprehensive insight into the biosynthesis of CaOx in oxalate-accumulating plants.

Incorporating fluorophores into polymeric nanoparticles has been testified as a feasible way to improve the emitting property and bio-compatibility of nano-emitters, which can be applied as fluorescent probes in labeling cells for imaging. Plenty of efforts have been made on the above direction. However, the size effect of nano-emitters has not been addressed yet mainly given the difficulties in controlling morphology and size of the assemblies. In our preceding study, we employed post-polymerization modification method for preparing amphiphilic copolymers, and obtained core-shell (the hydrophobic fluorophores are wrapped inside the nanoparticle to form the core) assemblies in aqueous solution. By this method, we are able to regulate the ratio of the hydrophilic/hydrophobic moieties, and thus alternate the size of the assemblies in a rather simple way. In this study, we synthesized a series of random copolymers by changing the ratio of poly(ethylene glycol) to tetraphenylethylene groups. Notably, the number of repeating units of the polymer was controlled constant for all the copolymers. The self-assembly of these copolymers resulted in different sizes of nanoparticles, and the size decreased with the decreasing fraction of poly(ethylene glycol). Interestingly, the emission of the nanoparticles showed size dependence, and smaller diameter corresponded to stronger emission. Being cultured with HeLa cells, either the large (diameter of ∼300 nm) or the small (diameter of ∼180 nm) nano-emitters allowed for very high cell viabilities up to 25 µg·mL−1. Both of them can be applied in cell imaging and provide high contrast fluorescent images.

Mangroves are critical in global carbon budget while vulnerable to exotic plant invasion. Spartina alterniflora, one of typical salt marsh plant grows forcefully along the coast of China, has invaded the native mangrove habitats in Zhangjiang Estuary. However, the effects of S. alterniflora invasion on soil carbon gases (CH4 and CO2) emission from mangroves are not fully understood. Accordingly, we conducted a field experiment to investigate the soil CH4 and CO2 emission during growing seasons in 2016 and 2017 at four adjacent wetlands, namely bare mudflat (Mud), Kandelia obovata (KO), Avicennia marina (AM) and S. alterniflora (SA). Potential methane production (PMP), potential methane oxidation (PMO), functional microbial abundance and soil biogeochemical properties were measured simultaneously. Our results indicate that S. alterniflora invasion could dramatically increase soil CH4 emissions mainly due to the enhancement in PMP which facilitated by soil EC, MBC, TOC and mcrA gene abundance. Additionally, S. alterniflora invasion decreases soil CO2 emission. Both heterotrophic microbial respiration (16S rRNA) and methane oxidation (pmoA and ANME-pmoA) are responsible for CO2 emission reduction. Furthermore, S. alterniflora invasion greatly increases GWP by stimulating CH4 emissions. Thus, comparing with mangroves, invasive S. alterniflora significantly (p 4 emission while reduces CO2 emission.

Background Chemoresistance is a major obstacle that limits the benefits of 5-Fluorouracil (5-Fu)-based chemotherapy for colon cancer patients. Autophagy is an important cellular mechanism underlying chemoresistance. Recent research advances have given new insights into the use of natural bioactive compounds to overcome chemoresistance in colon cancer chemotherapy. As one of the multitargeted and safer phytomedicines, curcumin has been reported to work as cancer-specific chemosensitizer, presumably via induction of autophagic signaling pathways. The precise therapeutic effect of curcumin on autophagy in determining tumorous cells’ fate, however, remains unclear. This study was conducted to investigate the differential modulations of the treatments either with 5-Fu alone or 5-Fu combined with curcumin on cellular autophagic responses and viabilities in the human colon cancer cells HCT116 and HT29, and explore molecular signaling transductions underlying the curcumin-mediated autophagic changes and potentiation of 5-Fu’s cytotoxicity in vitro and in vivo. Methods Cell proliferation assay and morphology observation were used to identify the cytotoxicity of different combinations of curcumin and 5-Fu in HCT116 and HT29 cells. Cell immunofluorescence assay, Flow cytometry and Western blot were employed to detect changes of autophagy and the autophagy-related signaling pathways in the colon cancer cells and/or xenograft mice. Results Curcumin could significantly augment the cytotoxicity of 5-Fu to the tumorous cells, and the pre-treatment with curcumin followed by 5-Fu (pre-Cur) proved to be the most effective one compared to other two combinations. The chemosensitizing role of curcumin might attribute to the autophagy turnover from being activated in 5-Fu mono-treatment to being inhibited in the pre-Cur treatment as indicated by the changes in expression of beclin-1, p62 and LC3II/LC3I and the intensity of Cyto-ID Green staining. The autophagic alterations appeared to be contributed by down-regulation of not only the phospho-Akt and phospho-mTOR expressions but the phospho-AMPK and phospho-ULK1 levels as well. The cellular activation of AMPK by addition of A-769662 to the pre-Cur combination resulted in reversed changes in expressions of the autophagy protein markers and apoptotic status compared to those of the pre-Cur combination treatment. The findings were validated in the xenograft mice, in which the tumor growth was significantly suppressed in the mice with 25-day combination treatment, and meanwhile expressions of the autophagy markers, P-AMPK and P-ULK1 were all reversely altered in line with those observed in HCT116 cells. Conclusion Pre-treatment with curcumin followed by 5-Fu may mediate autophagy turnover both in vitro and in vivo via AMPK/ULK1-dependent autophagy inhibition and AKT modulation, which may account for the increased susceptibility of the colon cancer cells/xenograft to the cytotoxicity of 5-Fu.

Effects of alloy elements Cr, W, Ce, and Si on oxidation behavior at 750 °C in air and stress-rupture properties of P92 steel have been investigated. The proper increase in elements Cr, W, and Ce improved to varying degrees both oxidation resistance by either facilitating more protective Cr2O3 or modifying surface morphologies and stress-rupture life largely attributed to the formation of fine Laves phase. The excessive addition of Si significantly improved oxidation resistance of P92 steel, but dramatically impaired the stress-rupture life due to the formation and coarsening of Laves phase. The results indicate that proper additions of Cr, W, and Ce are beneficial for the comprehensive property of P92 steel.