MicroRNA对不完全变态昆虫变态及生殖调控作用的研究进展

MicroRNAs(miRNAs)是一类在真核生物中由内源基因编码的小分子RNA,参与昆虫变态、生殖发育、细胞分化等多种重要生物学过程,在转录水平上发挥重要作用.在完全变态昆虫中,大量调控其变态及生殖的miRNA被广泛报道且进行了深入的研究,但miRNA调控不完全变态昆虫的变态及生殖发育的研究仍比较少,对其具体的调控机制也需要进一步阐明.为此,本文综述了近年来miRNA在调控不完全变态昆虫(以直翅目飞蝗Locusta migratoria、半翅目褐飞虱Nilaparvata lugens和蚜虫以及部分蜚蠊目昆虫为代表)的变态及生殖方面的研究进展,以期深化理解miRNA对不完全变态昆虫变态和生殖发育方面的机制,为害虫生态治理和综合防控提供科学依据.     

Maternal serum-derived exosomal lactoferrin as a marker in detecting and predicting ventricular septal defect in fetuses

Among different types of congenital heart diseases, ventricular septal defect is the most frequently diagnosed type and is frequently missed in early prenatal screening programs. Herein, we explored the role of maternal serum-derived exosomes in detecting and predicting ventricular septal defect in fetuses in the early stage of pregnancy. A total of 104 pregnant women consisting of 52 ventricular septal defect cases and 52 healthy controls were recruited. TMT/iTRAQ proteomic analysis uncovered 15 maternal serum exosomal proteins, which showed differential expression between ventricular septal defect and control groups. Among these, four down-regulated proteins, lactoferrin, SBSN, DCD, and MBD3, were validated by Western blot. The protein lactoferrin was additionally verified by ELISA which was able to distinguish ventricular septal defects from controls with area under the ROC curve (AUC) 0.804 (p < 0.001). Our findings reveal that lactoferrin in maternal serum-derived exosomes may be a potential biomarker for non-invasive prenatal diagnosis of fetal ventricular septal defects.     

Clear and independent associations of several HLA-DRB1 alleles with differential antibody responses to hepatitis B vaccination in youth

To confirm and refine associations of human leukocyte antigen (HLA) genotypes with variable antibody (Ab) responses to hepatitis B vaccination, we have analyzed 255 HIV-1 seropositive (HIV⁺) youth and 80 HIV-1 seronegatives (HIV^?) enrolled into prospective studies. In univariate analyses that focused on HLA-DRB1, -DQA1, and -DQB1 alleles and haplotypes, the DRB1*03 allele group and DRB1*0701 were negatively associated with the responder phenotype (serum Ab concentration ≥ 10 mIU/mL) (P = 0.026 and 0.043, respectively). Collectively, DRB1*03 and DRB1*0701 were found in 42 (53.8%) out of 78 non-responders (serum Ab <10 mIU/mL), 65 (40.6%) out of 160 medium responders (serum Ab 10–1,000 mIU/mL), and 27 (27.8%) out of 97 high responders (serum Ab >1,000 mIU/mL) (P < 0.001 for trend). Meanwhile, DRB1*08 was positively associated with the responder phenotype (P = 0.010), mostly due to DRB1*0804 (P = 0.008). These immunogenetic relationships were all independent of non-genetic factors, including HIV-1 infection status and immunodeficiency. Alternative analyses confined to HIV⁺ youth or Hispanic youth led to similar findings. In contrast, analyses of more than 80 non-coding, single nucleotide polymorphisms within and beyond the three HLA class II genes revealed no clear associations. Overall, several HLA-DRB1 alleles were major predictors of differential Ab responses to hepatitis B vaccination in youth, suggesting that T-helper cell-dependent pathways mediated through HLA class II antigen presentation are critical to effective immune response to recombinant vaccines.     

Research of Iron Reduction and the Iron Reductase Localization of Anammox Bacteria

The iron-reducing capability of anammox bacteria was examined in this study using Percoll purified anammox bacteria. Anammox bacteria could reduce Fe(III) to Fe(II) with organic matters as the electron donor. The activity of anammox iron-reducing process was dependent on different electron donor, acceptor and pH. The highest iron-reducing activity of anammox bacteria was achieved with Fe(III)-NTA (nitrilotriacetic acid) as electron acceptor and formate as the electron donor at pH7. Similar to other iron reducers, 80 % of the iron reductase in anammox bacteria was located in the membrane fraction. Due to the chemical oxidant of NO₂ ^? and the NO₃ ^? dependent ferrous iron oxidation by anammox bacteria, the iron-reducing activity of anammox bacteria could be severely inhibited when iron-reducing pathway and the anammox process were coupled. However, the total nitrogen removal efficiency was not significantly affected in the presence of Fe(III). The iron-reducing capability of anammox bacteria could influence both N and Fe cycle on earth, and it is a potential way for wastewater treatment.     

Proteomic Analysis of High Temperature Stress-Responsive Proteins in Chrysanthemum Leaves

Chrysanthemum is one of the most important ornamental flowers in the world, and temperature has a significant influence on its field production. In the present study, differentially expressed proteins were investigated in the leaves of Dendranthema grandiflorum ‘Jinba’ under high temperature stress using label-free quantitative proteomics techniques. The expressed proteins were comparatively identified and analyzed. A total of 1,463 heat-related, differentially expressed proteins were successfully identified by Liquid Chromatography-tandem Mass Spectrometry (LC-MS/MS), and 1,463 heat-related, differentially expressed proteins were successfully identified by mass spectrometry after a high temperature treatment. Among these, 701 proteins were upregulated and 762 proteins were downregulated. The in-depth bioinformatics analysis of these differentially expressed proteins revealed that these were involved in energy metabolism pathways, protein metabolism, and heat shock. In the present study, the investigators determined the changes in the levels of some proteins, and their expression at the protein and molecular levels in chrysanthemum to help reveal the mechanism of heat resistance in chrysanthemum. Furthermore, the present study elucidated some of the proteins correlated to heat resistance in chrysanthemum, and their expression changes at the protein and molecular levels to help reveal the mechanism of heat resistance in this flower species. These results provide a theoretical basis for the selection of new heat resistant varieties of chrysanthemum in the field.     

Activation of JNK/c-Jun is required for the proliferation, survival, and angiogenesis induced by EET in pulmonary artery endothelial cells

Pulmonary artery endothelial plexiform lesion is responsible for pulmonary vascular remodeling (PVR), a basic pathological change of pulmonary arterial hypertension (PAH). Recent evidence suggests that epoxyeicosatrienoic acid (EET), which is derived from arachidonic acid by cytochrome p450 (CYP) epoxygenase, has an essential role in PAH. However, until now, most research has focused on pulmonary vasoconstriction; it is unclear whether EET produces mitogenic and angiogenic effects in pulmonary artery endothelial cells (PAEC). Here we found that 500 nM/l 8,9-EET, 11,12-EET, and 14,15-EET markedly augmented JNK and c-Jun activation in PAECs and that the activation of c-Jun was mediated by JNK, but not the ERK or p38 MPAK pathway. Moreover, treatment with 8,9-EET, 11,12-EET, and 14,15-EET promoted cell proliferation and cell-cycle transition from the G0/G1 phase to S phase and stimulated tube formation in vitro. All these effects were reversed after blocking JNK with Sp600125 (a JNK inhibitor) or JNK1/2 siRNA. In addition, the apoptotic process was alleviated by three EET region isomers through the JNK/c-Jun pathway. These observations suggest that 8,9-EET, 11,12-EET, and 14,15-EET stimulate PAEC proliferation and angiogenesis, as well as protect the cells from apoptosis, via the JNK/c-Jun pathway, an important underlying mechanism that may promote PAEC growth and angiogenesis during PAH.     

植物内生菌增强植物对生物胁迫抗性的研究进展

植物在生长发育过程中因遭遇多种逆境的威胁而出现营养流失、产量大幅下降等问题，而使用传统的化学农药调控植物抗逆作用会对环境造成严重污染甚至危及人类健康，因此需要从天然成分中寻找合适的农药代替品。生活在每种植物体内的内生菌几乎都是植物微生态系统中的天然成分，因其特殊的生态位而可能对植物具有更加积极和直接的影响。然而目前，关于内生菌在提高宿主生物胁迫抗性等方面的作用机制还知之甚少。该文就植物内生菌的来源、多样性和对生物胁迫的抗性展开叙述。首先，总结了植物内生菌传播的主要方式，即水平传播和垂直传播；其次对内生菌种类的多样性以及在植物中的分布多样性进行了归纳与分析；最后，详细阐述了植物内生菌增强植物对生物胁迫应激耐受性(抗致病菌病害、抗虫害)的基本特点与作用机制，即植物内生菌可利用生态位竞争或营养位竞争产生的诱导抗性遏制病原菌感染，或合成抗生素类、生物碱类、几丁质类等次生代谢产物抑制病原菌或线虫的生长，从而防治病虫害。此外，基于内生菌增强植物生物胁迫抗性的研究现状进行了展望，为更加环保的生物防治制剂的开发与利用提供了参考。     

MicroRNA‐29b‐3p suppresses oral squamous cell carcinoma cell migration and invasion via IL32/AKT signalling pathway

Oral squamous cell carcinoma (OSCC) is aggressive accompanied with poor prognosis. We previously isolated the most invasive cells resembling the invasive tumour front by microfluidic technology and explored their differentially expressed microRNAs (miRNAs) in our previous work. Here, we verified the miR‐29b‐3p as a guarder that suppressed migration and invasion of OSCC cells and was down‐regulated in the most invasive cells. Besides that, the invasion suppression role of miR‐29b‐3p was achieved through the IL32/AKT pathway. Thus, miR‐29b‐3p and IL32 might serve as therapeutic targets for blocking the progression and improving the outcome of OSCC.     

Fibroblast growth factor 21 alleviates acute pancreatitis via activation of the Sirt1‐autophagy signalling pathway

Fibroblast growth factor 21 (FGF21), a metabolic hormone with pleiotropic effects on glucose and lipid metabolism and insulin sensitivity, alleviates the process of acute pancreatitis (AP). However, its mechanism remains elusive. The pathological and physiological characteristics of FGF21 are observed in both patients with AP and cerulein‐induced AP models, and the mechanisms of FGF21 in response to AP are investigated by evaluating the impact of autophagy in FGF21‐treated mice and cultured pancreatic cells. Circulating levels of FGF21 significantly increase in both AP patients and cerulein‐induced AP mice, which is accompanied by the change of pathology in pancreatic injury. Replenishment of FGF21 distinctly reverses cerulein‐induced pancreatic injury and improves cerulein‐induced autophagy damage in vivo and in vitro. Mechanically, FGF21 acts on pancreatic acinar cells to up‐regulate Sirtuin‐1 (Sirt1) expression, which in turn repairs impaired autophagy and removes damaged organs. In addition, blockage of Sirt1 accelerates cerulein‐induced pancreatic injury and weakens the regulative effect in FGF21‐activated autophagy in mice. These results showed that FGF21 protects against cerulein‐induced AP by activation of Sirtuin‐1‐autophagy axis.